3025 Textbook

CHAPTER 1
Conceptual issues in
abnormal psychology
Marianna Szabó
CHAPTER OUTLINE
● The definitions of abnormal behaviour and mental disorder
● Perspectives on the classification, causation and treatment of mental disorders
● The classification and diagnosis of mental disorders
● Summary
LEARNING OBJECTIVES (LO)

1.1 Describe the difficulties inherent in defining abnormality and mental disorder.
1.2 Distinguish among the main theoretical approaches to understanding the classification, aetiology and treatment
of mental disorders.
1.3 Evaluate the changes made in psychiatric classification over time.
ABNORMAL PSYCHOLOGY: AN AUSTRALASIAN FOCUS

Copyright © 2017. McGraw-Hill Education (Australia) Pty Limited. All rights reserved.
In 1929, Henry Tasman Lovell, whose interest was in abnormal psychology, became the first Professor of Psychology in
Australia at the University of Sydney. A more recent, yet also momentous, milestone for the field of abnormal psychology
occurred in November 2006 when the Federal Government introduced the Better Access to Mental Health Care program,
which, for the first time in Australia, allowed people to receive Medicare rebates for psychological treatment provided
by trained mental health professionals. As a result of this program, access to psychological services is now available to
people who would not otherwise be able to afford it. The introduction of the Better Access initiative signalled a significant
recognition of the effectiveness of psychological treatments.
A 2017 report by the Australian Psychological Society entitled ‘Ten Years of Better Access’ provides a review of the
first decade of the Better Access program (Littlefield, 2017). The report highlights the program’s success in providing
accessible, effective and affordable treatment for psychological problems to many Australians. For example, by 2013
psychological services provided through Better Access had been accessed by more than three million people. In
addition, while only 35 per cent of Australians with mental disorders sought treatment prior to the introduction of Better
Access, this rate had increased to 46 per cent by 2010. Researchers attributed this increase in the treatment rate to the
availability of affordable psychological services through the Medicare system, and the de-stigmatisation of help-seeking
for mental health encouraged by this system (Pirkis, Harris, Hall, & Ftanou, 2011). A client satisfaction survey of more
than 2000 clients indicated that psychological treatment provided through Better Access resulted in significant or very
significant improvement for 91 per cent of clients, thus supporting the program’s effectiveness.
Nevertheless, the ‘Ten Years of Better Access’ report also highlights important limitations and challenges associated
with the program. For instance, it was announced in the 2011–2012 Federal Budget that the number of Medicare-
supported psychological consultations would be reduced from a possible maximum of 18 to 10 sessions per calendar year.
continued
Rieger, Elizabeth. Abnormal Psychology : Leading Researcher Perspectives, McGraw-Hill Education (Australia) Pty Limited, 2017. ProQuest Ebook Central,
http://ebookcentral.proquest.com/lib/anu/detail.action?docID=5471261.
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2 Abnormal psychology 4e
Unfortunately, this number of sessions is inadequate to treat many

psychological disorders. A study investigating mental health outcomes
found that among individuals receiving psychological treatment,
65 per cent continued to have severe symptoms after 10 treatment
sessions, but that only 22 per cent continued to report severe symptoms
after receiving up to 18 sessions (see Littlefield, 2013). As many
individuals do not improve sufficiently after receiving the 10 treatment
COURTESY THE UNIVERSITY OF SYDNEY ARCHIVES

sessions available under Better Access, psychologists and clients alike
experience difficulty in achieving adequate client care. Among the less
than optimal options available to psychologists and their clients when
the maximum 10 sessions per year has been reached are: postponing
further treatment until the following year, when the client can once again
access Medicare-supported sessions; extending the interval between
sessions so that treatment can be available for a longer period of time,
even though more frequent sessions might be beneficial; or receiving
treatment from a public mental health service, which often entails long
waiting periods.
As well as summarising some of the key achievements and
difficulties of Better Access to date, the ‘Ten Years of Better Access’
report also highlights future potential challenges for the program.
Among these is the Federal Government’s proposal to limit access
Henry Tasman (Tassie) Lovell (pictured
to Better Access to those with moderately severe mental disorders,
with his son) was the first Professor of
while directing those with milder and more severe disorders to other
Psychology in Australia, taking up his
programs. However, these alternative programs raise concerns about
position in the Department of Psychology at
those with milder disorders having services delivered by inadequately
the University of Sydney in 1929.
trained practitioners and about those with more severe and complex
disorders receiving sufficient funds to meet their needs. The ability to
address the mental health needs of all groups in society therefore remains a significant challenge.
This chapter traces the development of abnormal psychology and the mental health professions from their beginnings to
the present and looks at possible future directions. Abnormal psychology is commonly defined as the field of psychology that
aims to understand and modify abnormal behaviours. Most of the field of abnormal psychology today, however, is concerned
only with a special subset of abnormal behaviours, a subset labelled ‘mental disorders’ or ‘psychological disorders’. Indeed,
most of the following chapters focus upon a specific category of mental/psychological disorder. The present chapter serves
as an introduction to some of the fundamental concepts of abnormal psychology. First, definitions of abnormality and mental
disorder will be discussed. The bulk of the chapter will focus on the main theoretical perspectives that have shaped current
knowledge in abnormal psychology. In this section, the biological perspective (the oldest and currently dominant approach
to understanding mental disorders) will be contrasted with various psychological perspectives to underline the differences
in their approaches to the conceptualisation, classification, explanation and treatment of mental disorders. The chapter will
end with a description of one of the major systems for diagnosing mental disorders, and a consideration of the directions for
future developments in the field of psychiatric classification.
LO 1.1 The definitions of abnormal behaviour

and mental disorder
Abnormality
Although the distinction between ‘normal’ and ‘abnormal’ behaviours seems intuitively clear to most
people, a more careful consideration reveals that this distinction is often difficult to make. Although
no clear rules have yet been identified to differentiate normality and abnormality, several elements
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Chapter 1 Conceptual issues in abnormal psychology 3
have been proposed. The most common ones

are statistical rarity and the ‘three Ds’: deviance,
distress and dysfunction.
STATISTICAL RARITY
Statistical rarity is one criterion that has been used
to define abnormality. Individuals who possess a
characteristic that is rarely found in society can be
said to be abnormal, in the sense that they deviate
from the average to a large extent. This element
of abnormality, of course, can include positive
deviations as well. So, according to this definition,
people who are known for their musical or scientific
genius, for example, can be considered abnormal.
Clearly, the field of abnormal psychology cannot
DAL
be defined on the basis of statistical rarity alone,
otherwise individuals such as Wolfgang Amadeus The definition of abnormality often includes an element of statistical
Mozart or Albert Einstein would be prime candidates rarity. However, individuals whose statistically rare characteristics or
for treatment! abilities (such as those of a concert pianist or an Olympic athlete) are
positively evaluated by society would not be described as abnormal.
DEVIANCE OR NORM VIOLATION
Unlike the criterion of statistical rarity, the criterion of ‘deviance’ includes a value component.
According to this criterion, a behaviour is considered to be abnormal if it is negatively evaluated by
society. The ‘abnormal’ abilities of famous musicians, sportspeople or scientists are positively valued
by society and thus would not be defined as abnormal according to this criterion. On the other hand,
being unable to socialise because of extreme anxiety, avoiding all forms of public transport, hearing
voices, physically assaulting one’s spouse, or making a living by armed robbery are generally seen as
violating social expectations.
While adding the element of norm violation to statistical rarity can give a more precise definition of
abnormality, it still leaves a very broad class of behaviours for abnormal psychology to be concerned
with. Norm-violating behaviours encompass a diverse range of behaviours. These may include
instances of harmless eccentricity and serious criminal acts, as well as instances of mental disorder.
Moreover, using norm violation as a sole requirement to define abnormality can be dangerous as it
can be used to oppress any non-conformist behaviours. For example, homosexuality and a range of
other sexual behaviours such as masturbation were seen as both statistically rare and unacceptable by
society only a few decades ago. Therefore, people engaging in these behaviours were viewed as in
need of either punishment or treatment (Szasz, 1961).
DISTRESS
A third important element in defining abnormality, which is sometimes used to differentiate the
field of abnormal psychology from that of forensic psychology or criminology, is that the abnormal
behaviour causes distress to the person. At first sight, this would appear to be a necessary element in
defining psychological abnormality. In addition, this element allows the individual to self-define their
behaviours as abnormal or not, rather than allowing society at large to make that decision. People
who are happy and content with their lives tend to consider themselves normal, while those who are
distressed by their own thoughts, feelings or behaviours tend to seek treatment.
Unfortunately, this element also has its limitations and dangers in attempting to define abnormality.
On the one hand, some individuals cause themselves a great deal of personal suffering, for example,
by starving themselves to near death for religious, political or other reasons. Should these individuals
(e.g., great national leaders such as Mahatma Gandhi) be considered abnormal and requiring treatment?
On the other hand, many people whose behaviours come to the attention of mental health professionals
do not experience distress. For example, one of the defining features of a manic episode in bipolar
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disorder (as discussed in Chapter 6) is abnormally elevated mood, self-esteem and creativity, all of
which are experienced as very pleasant by the individual.
DYSFUNCTION
maladaptive The fourth element in defining abnormality asks whether the behaviour is dysfunctional or maladaptive.
Behaviour that In other words, does the behaviour interfere with the person’s ability to meet the requirements of
interferes with a everyday life? For instance, is s/he able to have a job, a family, a social network and a necessary level
person’s ability
of financial security? This element is widely accepted among mental health professionals as crucial
to meet the
requirements of
in defining abnormality and is often incorporated in the diagnostic criteria for the various mental
everyday life. disorders. So, the person who experiences a manic episode with abnormally elevated mood, self-
esteem and creativity may not be distressed but may be making decisions that interfere with his/her
ability to function effectively in everyday life. During manic episodes, individuals often make risky
financial investments or engage in sexual or aggressive behaviours that they would normally see as
foolhardy and dangerous. In that sense, the behaviour is maladaptive or dysfunctional. On the other
hand, according to the dysfunction criterion, a person with an extreme snake phobia who never leaves
the city would not be considered abnormal because his/her fear of snakes does not interfere with the
ability to meet the requirements of everyday life.
The maladaptiveness criterion is highly practical and liberal in that it can accommodate an
individual’s life circumstances (as in the case of the urban-dwelling person with a fear of snakes).
However, it also has its limitations. Most importantly, it greatly overlaps with the concept of norm
violation: how functional an individual is considered to be is often based on how well s/he meets
social expectations. It is a social expectation that individuals should have a job, a family, financial
security and a social network, and not to do so is seen as dysfunctional. As such, this criterion suffers
from the same limitation as the criterion of norm violation: it may be the social expectations that are
wrong rather than the individual’s failure to adapt to these.
A commonly cited illustration of how a particular society’s values influence the idea of what
is dysfunctional is the mental disorder drapetomania (Szasz, 1971; Wakefield, 1992). Drapetomania
was described by Dr Samuel Cartwright in 1851 as a mental disorder. It was used to describe
African American slaves who repeatedly attempted to run away from slavery, even though running
away resulted in severe punishment for those who were caught. So, this behaviour was thought to be
causing distress to the individual (as it elicited punishment), as well as being ‘dysfunctional’ (as it was
inconsistent with what was thought to be the normal function of African Americans in society, that is,
to be a slave). Therefore, running away was seen as a type of insanity requiring treatment.
Clearly, neither rarity, norm violation, distress or dysfunction on its own is sufficient or necessary
for the definition of abnormality. Therefore, a common approach is to consider all of these elements
together: it is the accumulation of these elements that assists in defining behaviour as abnormal.
Nevertheless, it is important to remember that each of the criteria suffers from being closely tied with
societal norms and expectations that change over time and cultures. No clear, universally accepted
definition of ‘abnormality’ has yet been established.
Mental disorder
The field of abnormal psychology concerns itself with a wide range of behaviours that are considered
‘abnormal’. However, not all of them are currently defined as mental disorders. For example, much
research effort has been focused on understanding the reasons behind domestic violence or the eating
behaviours leading to obesity. Yet neither domestic violence nor obesity is currently classified as a
mental disorder.
Unfortunately, similar to the concept of abnormality, a precise definition of the general concept
of mental disorder continues to be elusive. Several theorists have offered their views on how to
differentiate mental from physical disorders (Brülde & Radovic, 2006), while others have concentrated
on attempting to clearly define the concepts of disease, illness and disorder (Wakefield, 1992).
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One of the most contentious issues has been whether disease, illness and disorder are purely
factual, medical terms, or whether they are purely value judgments based on social norms.
The label ‘mental disorder’ in its most common usage today implies that the abnormal behaviour is
not only statistically rare, unacceptable to society, causes distress and/or is maladaptive, but that it also
stems from an underlying dysfunction or illness. For example, the current edition of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-5) defines mental disorder as follows:
A mental disorder is a syndrome characterized by clinically significant disturbance in an clinically
individual’s cognition, emotion regulation, or behavior that reflects a dysfunction in the significant
psychological, biological, or developmental processes underlying mental functioning. Mental Meaning the
disorders are usually associated with significant distress or disability in social, occupational, or disorder causes
other important activities. An expectable or culturally approved response to a common stressor substantial
or loss, such as the death of a loved one, is not a mental disorder. Socially deviant behavior impairment
in social,
(e.g., political, religious, or sexual) and conflicts that are primarily between the individual and
occupational or
society are not mental disorders unless the deviance or conflict results from a dysfunction in the other areas of
individual, as described above. functioning.
American Psychiatric Association (APA), 2013, p. 20
Each specific mental disorder identified in the DSM must meet this general definition.
Wakefield (1992; 1999) proposes that the concept of mental disorder, as stated in the DSM,
involves both a factual component (there is an underlying dysfunction) and a value component (it
is seen by society as harmful). The factual component specifies that there is an internal dysfunction
present: that a psychological mechanism has failed to carry out its natural evolutionary function. For
example, the evolutionary function of anxiety may be to warn the individual of objective danger.
When anxiety occurs in the absence of objective danger, this psychological mechanism has failed to
perform its natural function. Therefore, the individual’s fear of harmless objects can be said to occur
as a result of an internal dysfunction. It is important to note that the meaning of the term ‘dysfunction’
in Wakefield’s approach is different from its usage in relation to the ‘three Ds’ above, where it refers
to an individual’s inability to carry out his/her social roles.
The ‘internal dysfunction’ specification helps demarcate instances of mental disorder from
instances of social deviance, non-conformity or crime. For example, individuals who go on hunger
strikes and starve themselves for political reasons do not do so as a result of an internal dysfunction
but as a means of effecting social change. On the other hand, individuals with anorexia nervosa may
be said to severely limit their food intake as a result of an internal psychological dysfunction: the
internal mechanisms that contribute to maintaining a minimum healthy weight do not perform their
natural function. Similarly, individuals who carry out violent, illegal or otherwise antisocial acts may
do so as a result of an internal dysfunction (e.g., a lack of impulse control or an inability to feel
empathy for others) and thus they may qualify for the diagnosis of a mental disorder (in this case,
antisocial personality disorder). Some of these individuals, however, may engage in such acts as a
result of belonging to a gang so as to protect themselves in a violent neighbourhood or simply because
they find it easier and more acceptable to earn a living by illegal means. Such cases would not qualify
for a diagnosis of mental disorder as no internal dysfunction is present.
However, according to Wakefield’s approach, for a behaviour resulting from an internal dysfunction
to qualify as a mental disorder it needs an additional value component: it needs to be causing harm to
the individual. So, hallucinating that results from an internal dysfunction is not necessarily seen as a
disorder in societies where hallucinating is evaluated positively, perhaps as a sign of psychic abilities.
In these societies, hallucinating causes no harm or social disadvantage to the person.
According to Wakefield’s analysis, therefore, mental disorders are best conceptualised as lying
somewhere between the concept of physical disorder, which involves mainly a factual component
(e.g., having a broken leg or a viral infection are facts that exist in nature, independent of any
evaluations) and the concept of social deviance, which involves mainly a value component (e.g., being a
nudist, taking recreational drugs, living in a commune or running away from slavery can be considered
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instances of social deviance, as they are evaluated as right or wrong in relation to changing social
norms). The concept of mental disorder involves a bit of both.
Wakefield’s conceptualisation of mental disorder has received several criticisms, most of which
concentrate on the difficulty in ascertaining the normal evolutionary function of psychological
processes and the consequent difficulty in identifying when such processes are not carrying out their
functions (Lilienfeld & Marino, 1995; McNally, 2001). For example, while the function of anxiety is
likely to be to warn the organism of impending danger, the possible evolutionary function of sadness is
the subject of ongoing debate. It is difficult, therefore, to offer a conceptualisation of major depression
in terms similar to that of anxiety disorders. Further, some cognitive abilities, such as reading, have
been acquired too recently in human history to be regarded as natural functions designed by evolution.
According to an evolutionary analysis, therefore, reading disabilities such as dyslexia could not be
classified as a disorder. Although Wakefield’s analysis and the subsequent responses to it have made
important contributions, the ongoing debate regarding the most appropriate definition of mental
disorder continues to pose a fundamental conceptual challenge to the field of abnormal psychology
(Rounsaville et al., 2002).
LO 1.2 Perspectives on the classification, causation

and treatment of mental disorders
To appreciate how the understanding of mental disorders has developed to its current stage and in what
directions it may be developing in the future, an introduction to the main theoretical perspectives for
mental disorders is needed. These perspectives propose different conceptualisations of what a mental
disorder is, how many and what kinds of different mental disorders there are, what their primary causes
may be, and what the best treatments are.
The discussion will begin with the currently dominant (and oldest) biological/medical perspective,
followed by the main psychological perspectives, the sociocultural perspective and the integration of
these various perspectives in the biopsychosocial model. Such integration emphasises that the various
perspectives on mental disorders are not mutually exclusive. There is not one right way of explaining
mental disorders. Rather, the various perspectives emphasise different levels of explanation and are
best seen as complementing, rather than competing with, each other.
The biological perspective

HISTORICAL BACKGROUND OF THE BIOLOGICAL PERSPECTIVE
Before the emergence of psychoanalytic thinking and behaviourism in the early twentieth century,
the concept of mental illness was virtually identical with the concepts of madness or insanity. These
terms were applied to individuals with extremely severe disturbances involving hallucinations and
affect delusions, or severe disorganisation of speech, affect (emotion), thinking or behaviour. Most of these
Experience symptoms would today be summarised under the term ‘psychosis’ (as discussed in Chapter 7), while
of feeling or others might resemble dementia (as discussed in Chapter 15).
emotion.
Patients who displayed such severe disturbances were treated in mental asylums by ‘mad doctors’
or ‘alienists’, the forerunners of today’s psychiatrists. Until the early nineteenth century, a large
proportion of those treating the mentally ill were not even medically trained, let alone specialists in the
dementia study of mental illness—some were general physicians or surgeons, but others were simply charlatans.
Neurological
Madness was seen as a state that anyone could recognise, and often it was left to local magistrates to
disorder in which
a gradual decline
certify a person’s sanity or lack thereof (Routh, 1998).
of intellectual Psychiatry became recognised as a legitimate speciality within medicine only about 150 years ago
functioning (Barton, 1987). The forerunner of the American Psychiatric Association—the Association of Medical
occurs. Superintendents of American Institutions for the Insane—was established in 1844. The American
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Journal of Insanity, later called the American Journal of Psychiatry, was also first published in 1844,
and remains one of the leading journals in psychiatry to this day. By the end of the nineteenth century,
most of those treating mentally ill people were medically trained physicians who believed that symptoms
of madness arose from underlying biological diseases affecting the brain or the nervous system.
CLASSIFICATION AND CAUSATION FROM THE BIOLOGICAL PERSPECTIVE

There is only one kind of mental disease, we call it insanity.
Heinrich Neumann, 1859, cited in Hecker, 1871/2004, p. 351
Prior to the twentieth century, the symptoms of the various mental disorders (as currently defined)
were not usually seen as indicators of separate disorders. Instead, many doctors in the nineteenth
century agreed with Heinrich Neumann, believing insanity to be a single disease that progressed from
one major symptom to another over time, with the symptoms becoming increasingly severe. Thus,
the first symptom of insanity was thought to be depression, followed by agitation, then confusion,
paranoia and finally dementia (Misbach & Stam, 2006).
Others, however, believed that there were in fact several different mental diseases. The basis for this
belief was the observation that some individuals displayed groups of symptoms (called syndromes) syndrome
that others did not, or that people with certain types of symptoms got better while others with different Set of symptoms
symptoms got worse, or that some symptoms began early in life and others began later, or that some that tend to occur
together.
symptoms were more often seen in men while others were more often seen in women. The ultimate
aim of such observations was to identify symptoms that clustered together to form syndromes because
they had a common cause. Once the causal agents underlying these symptom clusters were identified,
it was hoped that it would become possible to discover an effective treatment that targeted those
underlying causes. In other words, the ultimate aim of psychiatric classification was, and still is,
to describe symptom clusters that have common causes and respond to common treatments. Such
symptom clusters are then labelled as ‘disorders’ or ‘diseases’.
An example of a similar process in the history of physical illnesses pertains to the treatment of
‘the fevers’. Such treatment had limited success. This was partly because people did not understand
that a high fever was not a disease in its own right, but that it could be a symptom of a diverse
range of disorders, caused by a diverse range of underlying pathologies that were unknown at the
time. However, once doctors noticed that some fevers were accompanied by red spots on the body,
while others were accompanied by abdominal pain, they were in a position to describe two different
syndromes or categories of illness (e.g., measles and appendicitis, respectively). They could then
begin to look for the specific causes and treatments of these different illnesses.
Unfortunately, the causes of most diseases were unknown for much of human history so that
classification of illnesses into separate categories was often based on hypothesised causes. The earliest
known attempt at such classification was offered by the ancient Greek physician Hippocrates (c. 460–
377 BCE), who is often referred to as the father of modern medicine given his emphasis on natural
(rather than supernatural) causation. He hypothesised that mental and physical health required the
balance of four ‘humours’ or fluids in the body: blood, yellow bile (choler), black bile (melancholer)
and phlegm. Too much of any of these was believed to result in certain personality types, such as a
melancholic or depressed personality arising from excessive black bile. An extreme imbalance of the
humours was thought to result in mental illness.
Another mental illness identified at the time was ‘hysteria’, which was thought to be caused by a
detached womb wandering in the body (and which, therefore, by definition, could afflict only women).
About 2000 years later, in the sixteenth century, the famous Swiss physician Paracelsus proposed that
there were three classes of mental illnesses: vesania, thought to be caused by poisons; lunacy, believed
to be influenced by phases of the moon; and insanity, a disease believed to be caused by heredity
(Charney et al., 2002). Unfortunately, because the assumed causation underlying these proposed
disorders was manifestly wrong, the treatments targeting the presumed causes also had limited success.
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However, by the end of the nineteenth century the medical profession was optimistic that it was
only a matter of time before the biological causes of mental illnesses would be precisely known.
A number of important scientific discoveries gave impetus to this optimism. Foremost among
these were Louis Pasteur’s germ theory of diseases, which stated that tiny creatures, invisible
to the naked eye, could invade the body and cause illness. This seemingly strange idea received
empirical support in the late nineteenth century and was followed by the discovery of various
bacterial microorganisms.
Concerning mental illness specifically, one of the most important early discoveries within the
biological perspective was the identification of the cause of a mysterious mental illness: ‘general
paralysis of the insane’, also known as general paresis (Routh, 1998). In many respects, general paresis
was similar to other types of ‘insanity’: it included bizarre behaviours, persecutory delusions and
hallucinations. However, it had a steadily deteriorating course, while most other types of insanity
tended to remain stable. Patients with general paresis almost invariably got worse, eventually becoming
paralysed and dying within about five years of disease onset.
This suggested that general paresis might be a specific disease category with its own causation and
treatment, different from other types of insanity. Additional descriptive information was then used to
hypothesise about and test various ideas about causation. As the condition was observed more often
in men, especially in sailors, it was initially thought that smoking, drinking alcohol or being in contact
with sea water might cause the illness. Experimental studies were conducted to discover the biological
disease process underlying the syndrome.
To test one hypothesis, in 1897 Richard von Krafft-Ebing, a German neurologist, injected
discharge from syphilitic sores into patients suffering from general paresis. None of the patients
developed symptoms of syphilis, suggesting that they were already infected. This finding gave support
to the notion that general paresis might be caused by syphilis. Indeed, the bacterium Treponema
electroconvulsive pallidum was discovered as the causal agent of syphilis in 1905 and it was found in the brains of
therapy (ECT) patients with general paresis in 1913, confirming the hypothesis. On the basis of this underlying
Treatment for biological causation, the syndrome general paresis was identified as a part of the last stage of syphilis,
mood disorders rather than being a separate category of mental illness with its own specific cause. Of course, after the
that involves
invention of antibiotics, it also became possible to treat it.
the induction of
Other important discoveries at the time included the identification of associations between certain
a brain seizure
by passing an syndromes and localised damage to the brain. The French physician Pierre P. Broca (1824–1880)
electrical current identified the area of the brain damaged in patients with expressive aphasia (an inability to produce
through the meaningful speech) and Carl Wernicke (1848–1905) later found damage in a different part of the brain
patient’s brain associated with receptive aphasia (an inability to understand speech).
while s/he is Following such discoveries, the idea that all mental disorders were caused by biological factors
anaesthetised. became increasingly accepted. Many doctors believed that all mental disturbances would eventually
be identified as having a biological origin, for instance, in the form of some bacterial or viral infection,
psychosurgery contact with toxic agents or structural brain abnormality.
Biological
An enduring contribution to the classification of mental disorders at this time was made by the
treatment (such
as lobotomy) for German psychiatrist Emil Kraepelin (1856–1926), one of the most influential thinkers to challenge
a psychological the single-disease concept of insanity in the nineteenth century. In the first edition of his great work
disorder in which of psychiatric classification, the Compendium of Psychiatry in 1883, he initially distinguished two
a neurosurgeon main mental illnesses: manic-depressive psychosis and dementia praecox. These historical definitions
attempts to are close to today’s concepts of bipolar disorder and schizophrenia, respectively. After a further
destroy small 30 years of work, in the final edition of his Compendium published in 1915, Kraepelin distinguished
areas of the
13 categories of mental illness.
brain thought
to be involved A crucial feature of Kraepelin’s classification system was that mental illnesses were either
in producing categorised according to their known causes (e.g., intoxication psychosis or infectious psychosis) or
the patient’s remained at the level of description (e.g., manic-depressive insanity or dementia praecox). Kraepelin
symptoms. expected that biological causes would eventually be identified for each mental illness. Where such
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causes were not yet known, Kraepelin adopted a descriptive approach.

That is, instead of classifying disorders in terms of hypothesised causes, he
simply described diagnostic categories of unknown causation in terms of
their symptoms, onset, duration or other characteristics until such time as
their causation was discovered.
Consistent with the idea that mental illness involves hallucinations,
delusions or other severe psychological disturbances, most of the
categories of mental illness in Kraepelin’s classification system referred
to some form of psychosis or dementia. Similarly, the first official
psychiatric classification system published in the United States in 1918
contained 22 categories of mental illness, 21 of which referred to different
forms of psychosis with presumably different causes. Until the middle of
the twentieth century, most classification systems included one residual
category, usually labelled ‘general neuroses’. This one category contained
most of the symptoms of anxiety, phobias, obsessions and other non-
WIKIPEDIA CREATIVE COMMONS

psychotic but psychologically abnormal states that psychologists treat
today (Horwitz, 2003).
TREATMENT FROM THE BIOLOGICAL PERSPECTIVE

In spite of the important discoveries and optimism of the nineteenth century,
the first biological treatments yielded disappointing results. Doctors
attempted to treat mentally ill patients in insane asylums using hot and
cold baths, bleeding, removal of teeth, electric shocks and drug treatments The work of Emil Kraepelin was an influential
including opium and alcohol. In the absence of effective treatments, forerunner of contemporary psychiatric
physical constraints, including straitjackets and solitary confinement, were classification.
also used to control patients.
The twentieth century saw the emergence of more enduring and effective treatments. After pre-frontal cortex
initial experiments with dogs and pigs, electroconvulsive therapy (ECT) was first tried on a Region at the
human patient in 1938 to treat schizophrenia. It was subsequently found to have a calming effect front of the
on many patients and became part of the standard treatment for a variety of mental disorders, brain important
in language,
until it was superseded by drug treatments in the 1960s. ECT is still in use, having proven emotional
to be an effective treatment for severe depression that is not responsive to other, less invasive expression, the
treatments. However, the action on the brain by which ECT produces its effects remains unclear planning and
(Fink, 2001). production of
Another commonly used treatment in the early part of the twentieth century was psychosurgery. new ideas, and
Pre-frontal lobotomy was developed by Egas Moniz in 1937 and involved severing the neural fibres the mediation of
connecting the pre-frontal cortex to the rest of the brain. As with ECT, this procedure was found to social interactions.
have a calming effect on patients and became widely used in mental hospitals, with several thousand
patients receiving psychosurgery each year. The use of psychosurgery declined rapidly after the 1950s,
partly as a result of the introduction of more effective, less expensive and less invasive drug therapies
(Routh, 1998). biological
approach
CONTEMPORARY BIOLOGICAL PERSPECTIVES Theories that
explain abnormal
Mental illnesses are real, diagnosable, treatable brain disorders. behaviours
in terms of
Hyman, 1998, p. 38 a biological
dysfunction
The biological model proposes that symptoms result from disturbances of the physical (also called
body. The above quote from Hyman (1998) is an illustration of the biological model applied the medical
to mental illness. In their traditional and strictest forms, the biological approach and the approach).
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medical model of diseases are synonymous. However, it is important to point out that not all
contemporary biological approaches subscribe to the strict traditional model. In general,
contemporary biological perspectives focus on uncovering the interactions between behaviour
and biological functions, implying that behaviour influences biology as much as biology
influences behaviour. Nevertheless, contemporary psychiatry as a medical profession largely
upholds the biological model in its focus on seeking to find the causes of mental disorders in
underlying biological malfunctions.
There are two main areas that contemporary biological theories focus upon in trying to
identify the causes of mental disorders. These areas are (1) structural brain abnormalities and (2)
neurochemical imbalances. In turn, two main causes for brain abnormalities or neurochemical
imbalances are proposed: (1) a person’s genetic makeup and (2) trauma affecting the brain or
nervous system. For example, in the case of schizophrenia, researchers have discovered associations
between certain forms of the illness and abnormalities in specific areas of the brain. Using various
brain-scanning techniques, it has been shown that individuals who display mainly the negative
symptoms of schizophrenia (e.g., a marked reduction in emotional expression, motivation and
enlarged speech) tend to have enlarged ventricles (the brain cavities that contain cerebrospinal fluid). This
ventricles finding has been interpreted as an indication that nearby parts of the brain have not developed
Fluid-filled spaces properly or have been damaged. Neurochemical imbalances have also been implicated in
in the brain schizophrenia, as well as in many other mental disorders. For instance, excess activity of the
that are larger
dopamine neurotransmitter system is thought to be related to schizophrenia, while imbalances in
than normal
and suggest a the neurotransmitters serotonin and noradrenaline may be involved in severe depression. Genetic
deterioration in research has found evidence for the involvement of heredity in both of these disorders (Andreasen,
brain tissue. 2001; Maj & Sartorius, 2002).
CONTRIBUTIONS AND LIMITATIONS OF THE BIOLOGICAL PERSPECTIVE

The biological model enjoys considerable respect and influence in today’s society. Some
researchers within the biological tradition claim that eventually all human phenomena will be
able to be explained in terms of underlying biological processes. Others, however, warn against
the dangers of this form of reductionism (Valenstein, 1998). They argue that complex human
phenomena such as beliefs, values and interpretations cannot be reduced to basic biological
processes because the essence of the phenomenon is lost in the reduction. The whole is greater
than, and different from, its constituent parts. In addition, when associations between biological
processes and psychological states are found, the direction of causation is often unclear. That is, if
a psychological disorder is linked to a biological abnormality, it is possible that the disorder causes
selective
the abnormality rather than vice versa, or that a third factor causes both the biological abnormality
serotonin
and the psychological disorder.
reuptake
inhibitors (SSRIs)
Indeed, it is important to keep in mind that the evidence for the biological causation of disorders
Class of is often overstated in popular (and sometimes scientific) discourse. Much of the evidence for
antidepressant biological explanations is inconclusive. Many of the studies have been conducted on animals and
drugs (such it is not known how much animal models of depression or anxiety, for example, are applicable to
as fluoxetine) humans. The success of drug therapies has also resulted in erroneous claims about causation. For
that inhibit the example, the success of selective serotonin reuptake inhibitors (SSRIs) such as Prozac® or Zoloft®
reuptake of has been interpreted by some as evidence for the involvement of serotonin in the causation of major
serotonin.
depression (Bell, 2005; Moynihan & Cassels, 2005). It needs to be remembered, however, that the
effectiveness of treatment does not necessarily imply causation. For example, while aspirin is an
psychopharma-
effective treatment for headaches, this of course does not imply that headaches are caused by low
cological
levels of aspirin in the brain.
treatment
The use of One of the most important contributions of the biological perspective is the development of effective
drugs to treat drug treatments in recent decades. Since the discovery of the first effective psychopharmacological
psychological treatment in the 1950s, drug therapy has become a very commonly used treatment for a variety
disturbances. of mental disorders. An increasing number of people, however, now believe that medications are
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overused in the treatment of psychological disorders and, although they are effective in many
cases, they are by no means a universal cure. Perhaps the main drawback associated with drug
therapies is the high likelihood of relapse after the individual stops taking the drug. In addition,
the question as to whether long-term usage of certain medications can produce undesirable,
often very serious, side effects has not always been answered (Bech, 2002; Ma, Lee, & Stafford,
2005). These considerations underscore the importance of expanding treatments beyond a purely
biological approach.
Finally, empirical evidence is mounting to suggest that the traditional medical model of diseases,
where clearly identifiable sets of symptoms are assumed to reflect a common underlying causation, psychoanalysis
may not be applicable to the definition and classification of mental disorders (Krueger & Piasecki, Form of treatment
2002; Widiger & Sankis, 2000). Instead, it has been argued that while most physical disorders are pioneered by
clearly distinguishable from each other on the basis of their symptoms and underlying causes (e.g., Sigmund Freud
cancers are clearly distinguishable from heart disease), many mental disorders overlap and merge into that entails
each other in a continuous fashion (as may be the case, for example, between anxiety and depressive alleviating the
unconscious
disorders). Further, while there may be a clear qualitative difference between physical health and
conflicts driving
illness (e.g., between having cancer and not having cancer), such a difference is not quite so clear in psychological
the case of mental disorders. Instead, it is now increasingly accepted that many mental disorders are symptoms by
best conceptualised on a continuum between normality and abnormality, rather than as qualitatively helping the
distinct states of mental health versus illness. The idea of such continuity between normal and patient gain
abnormal mental states and among different types of psychological abnormality was first popularised insight into his/
by Sigmund Freud, the father of psychoanalysis and one of the forerunners of the contemporary her conflicts
psychological approach. through
techniques
such as dream
analysis and free
Psychological perspectives association.
The psychological approach sees the primary causes of abnormal behaviours not in underlying
biological disturbances, but in underlying psychological processes, including the manner in which psychological
people interpret their environment, their conscious or unconscious beliefs and motivations, or their approach
learning history. In this section, the development of the main psychological approaches to defining, Theories
that explain
understanding and treating mental disorders will be discussed. Traditional and more contemporary
abnormality
forms of the two earliest psychological perspectives—psychoanalysis and behaviourism—will be in terms of
briefly presented, followed by an introduction to the cognitive perspective that is currently dominant psychological
in abnormal psychology. factors such
Many of the mental health professions as they are known today—such as psychotherapists or as disturbed
clinical psychologists treating individuals with less severe, non-psychotic disorders in outpatient personality,
clinics using so-called talking therapies—did not exist until relatively recently. Abnormal psychology behaviour and
ways of thinking.
as a science and clinical psychology as a profession began to develop about 75 years after the
emergence of psychiatry as a specialised field of medicine. The American Psychological Association
was founded in 1892, and its Clinical Psychology Section was established in 1919. The Journal psychotherapy
Treatment for
of Abnormal Psychology, the preeminent journal in the field to this day, was founded in 1906. Its
abnormality
original title was the Journal of Abnormal and Social Psychology, clearly distinguishing it from that consists of
biological approaches to mental illness. In Australia, the development of the profession was somewhat a therapist and
slower. The first professional body of psychologists, the Australian Overseas Branch of the British client discussing
Psychological Society, was established in 1944 (O’Neil, 1987). It had an initial membership of 42, the client’s
slowly rising to about 200 by the 1950s (Turtle, 1995). symptoms;
Until well into the 1950s, psychologists around the world were involved mainly in psychometric the therapist’s
theoretical
assessment (i.e., assessing intellectual abilities) and research in educational or industrial settings,
orientation
rather than in providing psychotherapy. The diagnosis and treatment of mental illness was strictly determines
the domain of psychiatry alone (Benjamin, 2005). The impetus behind the change towards providing the focus of
psychological treatment for mental disorders by non-medical professionals was provided by the discussions with
increasing popularity of psychoanalysis. the client.
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The psychoanalytic perspective

Sigmund Freud (1856–1939) was a medically
trained neurologist with a private practice in Vienna.
He set one of the most important milestones in the
history of the mental health professions in 1895
when, with his colleague Josef Breuer, he published
Studies on Hysteria, marking the beginning of
the psychoanalytic movement (Breuer & Freud,
1895/1955). After the initial reluctance of the
medical establishment to take his ideas seriously, he
became one of the most influential thinkers of the
twentieth century.
Psychoanalysis dominated the mental health field
for more than half a century. It was especially influential
in psychiatry between the 1940s and 1970s. By 1945,
most chairs of departments of psychiatry in medical
schools in the United States were psychoanalysts and
the standard training of psychiatrists included extensive
instruction in psychoanalytic therapy techniques.
However, by the end of the 1970s, the number of
DAL
psychoanalysts acting as the chairs of psychiatry

Sigmund Freud, the founder of psychoanalysis departments had reduced to near zero. Psychiatry
and one of the most influential thinkers of the as a profession returned largely to the biological
twentieth century. Psychoanalysis is both a perspective. As a consequence, psychiatrists now
theory to explain normal and abnormal human receive only a relatively limited training in psychological
functioning and a therapeutic technique to therapies and concentrate more on biological therapies
alleviate abnormal functioning. (Horwitz, 2003).
At the same time, clinical psychologists began
to establish themselves as experts in psychological
therapies, along with other emerging professions such as social workers and counsellors. One important
reason for this change was that psychoanalysis revolutionised the concept of mental illness to include
conditions other than severe psychotic states. As a therapy, psychoanalysis was applied mainly to
neurotic symptoms such as general anxiety, depression or various phobias, and foresaw the current
emphasis of the mental health field on such symptoms and disorders. This represented a significant
unconscious
In psychoanalytic
change from the earlier emphasis on psychotic symptoms described earlier.
theory, the part
of the personality KEY CONCEPTS OF PSYCHOANALYSIS
of which the Psychoanalysis is both a theory to explain normal and abnormal human functioning and a therapeutic
conscious ego is technique to uncover the causes of, and hence alleviate, abnormal functioning. The basic concepts of
unaware. psychoanalysis discussed in this section were initially proposed by Sigmund Freud; they formed the
foundation for the wide variety of contemporary psychoanalytic perspectives, collectively referred to
id as psychodynamic approaches (Freud, 1900/1997; 1923/1960; 1933/1965).
In psychoanalytic
theory, most The unconscious
primitive part of According to psychoanalytic theory, the reasons for much of human behaviour lie hidden in the
the unconscious;
unconscious. Psychoanalysts interpret the surface or manifest content of people’s behaviour (including
consists of
drives and their jokes, dreams, mistakes, choices or works of art) to understand their true meaning or unconscious,
impulses seeking latent content.
immediate What determines people’s behaviour is the complex interaction among the forces of the id, the ego
gratification. and the superego. The id was the collective term Freud used to refer to humans’ most primitive drives.
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According to this theory, human beings are born with two primitive biological drives: the sexual drive libido
and the aggressive drive, with the sexual drive being the most important. The energy stemming from In psychoanalytic
this drive, called libido, was proposed to motivate much of human behaviour. theory, psychical
energy within
The id operates on the pleasure principle—it is driven purely by a need for instant gratification of
the id.
its desires without any reference to logic, reality, morality or the needs of others. In order to respond
adaptively to the world, it is necessary to develop a second component of the mind, the ego (or pleasure principle
conscious self). When the id signals its desire, the ego locates a potential gratifier of that desire in Drive to maximise
the environment and assesses the best ways of attaining it. Therefore, the ego operates on the reality pleasure and
principle. The ego comprises higher cognitive functions such as learning, memory, language and minimise pain
as quickly as
planning, which have developed in order to find ways of satisfying id impulses. Finally, the superego
possible.
is the part of the mind that develops last. It operates on the morality principle, based on the values and
moral standards of society that are often in conflict with the sexual and aggressive drives of the id. It ego
is then the task of the ego to meet the competing demands of external reality, the desires of the id and According to
the ideals of the superego. psychoanalytic
theory, part of
the psyche that
The stages of psychosexual development
channels libido
These three aspects of the human mind develop in a predictable fashion during several stages of acceptable to
psychosexual development. In each of these stages, the motivation to gratify the sexual and aggressive the superego
urges of the id is centred on different pleasure-producing parts of the body: the mouth, the anus and and within the
the genitals. The oral stage (0–2 years), when the primary focus of id gratification is the mouth, begins constraints of
at birth. Gratification and pleasure is achieved by the infant sucking, biting and chewing. During reality.
the anal stage (2–3 years), gratification is derived mainly from the retaining and expelling of faeces.
reality principle
At this stage, toilet training usually interferes with this gratification. Toilet training is seen as an Idea that the
important event in the development of the ego, because this is the first time the child is confronted by ego seeks to
the demands of the external world. satisfy one’s
The phallic stage (3–6 years) in turn is crucial because it sets the scene for the development of the needs within
superego. In boys, this process has been associated with the ‘Oedipus complex’. During this stage, the constraints
boys’ extreme dependence on their mother is said to culminate in a sexual desire for her. This desire of reality rather
then leads to ‘castration anxiety’: boys fear that their fathers will cut off their penis as a punishment. than following the
pleasure principle.
To reduce this anxiety, boys resolve this conflict by repressing their desire for their mother and
identifying with their father instead of competing with him. This internalisation of the father, who superego
represents the values and morals of society, then leads to the development of the superego. In girls, In psychoanalytic
the superego develops with the resolution of the ‘Electra complex’. When girls realise that they lack a theory, part of
penis, they experience ‘penis envy’. This causes them to develop a sexual interest in their father, since the unconscious
that consists
seducing him is the only way to obtain a penis, even if only vicariously. At the resolution of the Electra
of the absolute
complex, girls repress their desire for their father and regress to their earlier identification with the moral standards
mother. Because of their lack of internalisation of the father, girls develop a less sound morality, less internalised from
self-control and a weaker ability to use sublimation as a defence mechanism later in life. Consequently, one’s parents and
women are less able to successfully take part in professional, artistic or political endeavours, according the wider society
to this theory. After a latency period between 6 and 12 years of age, psychosexual development enters during childhood.
the final phase: the ‘genital stage’. With the onset of puberty, young people achieve their ability for
morality principle
mature love and healthy functioning in society. In psychoanalytic
theory, the
CLASSIFICATION AND CAUSATION FROM THE PSYCHOANALYTIC PERSPECTIVE motivational
According to psychoanalytic theory, all behaviours, both normal and abnormal, are the result of conflict force of the
superego, driving
among the id, ego and superego. While the true generator and motivator of behaviour is the id, the ego the individual
controls whether and how the strivings of the id are expressed, trying to keep such expressions consistent to act strictly in
with the moral values contained in the superego. As a result, the three components of the mind are in accordance with
constant conflict. At other times, the id’s own desires can be in conflict with each other or the id’s energy internalised moral
threatens to overwhelm the controls of the ego. At any of these times, the person experiences anxiety. standards.
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Defence mechanisms
In psychoanalysis, anxiety is the ultimate signal of psychic distress. It is very similar to the anxiety
experienced when the ego (the conscious self) is threatened in some way. For example, a person might
feel anxious before an important exam because of the threat of failing. It is possible to reduce this
anxiety by studying harder or by avoiding sitting the exam. However, the anxiety arising from
intrapsychic conflicts between the id, ego and superego is more difficult to deal with. To avoid the
pain of overwhelming anxiety and the feelings of guilt, embarrassment and shame that often
defence accompany intrapsychic conflict, the ego employs defence mechanisms. As shown in Table 1.1,
mechanisms defence mechanisms work by distorting the id impulses into acceptable forms or by rendering them
In traditional unconscious.
psychoanalytic
theory,
strategies (such TABLE 1.1 Some of the defence mechanisms postulated by psychoanalytic theory
as repression
or reaction DEFENCE DESCRIPTION
formation)
the ego uses Repression The person avoids anxiety by not allowing painful or dangerous thoughts to
to disguise become conscious.
or transform
unacceptable, Denial The person reduces anxiety by refusing to perceive the anxiety-provoking aspects
unconscious of external reality.
wishes or
Projection The person attributes his/her own unacceptable thoughts, emotions or desires to
impulses.
another person.
Rationalisation The person creates a socially acceptable reason for an action, thought or emotion
that has unacceptable underlying reasons.
Reaction formation The person acts in a way that is the exact opposite of the impulses s/he is afraid to
consciously acknowledge.
Displacement The person reduces anxiety by shifting sexual or aggressive impulses from an
unacceptable target to an acceptable substitute.
Intellectualisation The person creates an overly logical, rational response to distance him/herself from
anxiety-provoking emotions.
Regression The person retreats to an earlier developmental stage to reduce anxiety in the face
of unacceptable impulses.
Sublimation The person expresses sexual or aggressive impulses in ways that are acceptable to
society, such as in artistic or professional achievements.
Defence mechanisms can be more or less successful in reducing the anxiety caused by unconscious
intrapsychic conflict. If the defence mechanisms fail to control the anxiety, it is directly experienced,
resulting in significant distress. At other times, this anxiety is unconsciously controlled by the
defences, but the defences themselves can then create suffering or interfere with the individual’s
ability to function. For example, depression has often been thought of as resulting from the defence
mechanism of displacement: a person who has unacceptable aggressive or hateful impulses against
another (e.g., his/her father) may try to reduce the anxiety resulting from such unacceptable impulses
by turning this aggression and hatred towards the self. Another way to keep such impulses out of
conscious awareness is to use the defence mechanism of reaction formation: overprotective or
excessively dependent behaviour towards the hated person may be an expression of this defence
mechanism. Finally, the defence mechanism of projection in this situation could cause the individual
to believe that others (especially authority figures symbolically representing the father) hate him/her
(rather than vice-versa), thereby possibly resulting in paranoid beliefs.
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Neuroses and psychoses

The symptoms of anxiety, depression or extreme dependence can be examples of one type of
abnormality, collectively called the neuroses. These symptoms can have relatively milder forms, neurosis
manifesting within the normal range of behaviours. In other words, most people become anxious, sad According to
or dependent on occasion. The dividing line between the normal and abnormal manifestations of these psychoanalytic
theory, set of
behaviours is not clear.
maladaptive
Further, from the psychoanalytic perspective, psychoses that could not be identified as having symptoms caused
a clear physical cause such as toxins or infections were also seen as manifestations of intrapsychic by unconscious
conflict. Psychoses are more serious manifestations than neuroses, occurring when the usual defence conflict and
mechanisms fail to protect the person from the pain of intrapsychic conflict. In these cases, the only its associated
way the ego can cope with such pain is by withdrawing from reality, finding respite in hallucinations, anxiety.
delusions and severe disorganisation of speech, affect and behaviour.
psychosis
Differences between the medical and psychoanalytic models State involving
Several important conceptual differences exist between the medical and the psychoanalytic model of a loss of
classifying mental disorders. First, psychoanalysis sees no qualitative difference between normal and contact with
abnormal functioning—the difference is merely one of degree. Freud believed that all human beings, reality in which
both the sane and the insane, are driven by the same underlying forces originating from the id. Thus, the individual
both normal and abnormal behaviours, including the various forms of neuroses and psychoses, have experiences
symptoms such
the same underlying causes: there is no specific disease process that causes various types of insanity
as delusions and
or that differentiates sanity from insanity. In other words, psychoanalysis introduced and popularised hallucinations.
the idea that normal and abnormal behaviours lie on a continuum, rather than belonging to distinct
categories of health versus illness.
Further, the traditional medical model of diseases held that different symptom profiles were
manifestations of different underlying causes, such as bacteria or toxins. Therefore, it was crucial to
describe categories of mental disorders based on their symptoms and associated characteristics, such
as their onset and course over time, in order to find the specific underlying cause of each proposed
disorder. In contrast, the basic premise of psychoanalysis was that symptoms merely disguise a more
complex, underlying, unconscious reality. No strong one-to-one connection was proposed to exist
between specific underlying conflicts and specific symptoms. According to psychoanalytic thinking,
the same unresolved conflicts could result in widely different symptoms in two different individuals,
depending on the defence mechanisms they employ to keep the conflict (and the anxiety associated
with it) out of conscious awareness. Thus individuals with the same underlying conflicts may respond
to the anxiety arising from this conflict by developing sexual perversions, paranoia, a phobia of
specific animals or situations, or great artistic or scientific achievements. By the same token, two
individuals who present with very similar symptoms may have developed those symptoms as a result
of very different underlying conflicts. Moreover, the same individual may develop different symptom
profiles over time, depending on the primary defence mechanism s/he uses at the time to cope with
the underlying conflict. Symptoms themselves, unlike in the traditional medical model, were not
crucially important to understanding and treating individuals. What was crucial was to uncover the
unconscious conflict kept out of awareness by defence mechanisms, as this was believed to be causing
the symptoms.
TREATMENT FROM THE PSYCHOANALYTIC PERSPECTIVE

According to the psychoanalytic perspective, in order to uncover the true causes of the patient’s
feelings and behaviours it is crucial to reduce the ego’s ability to keep the conflict out of conscious
awareness. Psychoanalytically trained therapists use a variety of techniques to achieve this aim. In
dream analysis, the manifest content of dreams is interpreted in terms of an underlying latent content,
which is thought to be an indication of unconscious id impulses. In the technique of free association,
the patient is encouraged to say freely what comes to mind, without attempting to keep any conscious
control over the content of his/her speech. Again, this technique is thought to provide insight into
the unconscious parts of the mind. Another important technique is the analysis of transference and
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countertransference processes. Psychoanalysts believe that the manner in which people respond to
others is influenced by their unconscious projections. In transference, patients who feel angry or
irritated with their analyst, for example, may experience these feelings because they are transferring
them from another important figure from earlier stages of their lives to the therapist. Such transference
is believed to be helpful in uncovering themes from past relationships. In countertransference, it is the
therapist who unconsciously transfers feelings derived from his/her past into the relationship with the
patient, a problem of which the therapist needs to be aware and must overcome.
Because of the unclear lines between normal and abnormal behaviours, psychoanalytic therapies do
not have clearly defined goals in terms of symptom reduction—it is not easy to tell when someone is
no longer in need of psychoanalysis. Many individuals sought the help of analysts to resolve problems
in their lives, such as their relationship difficulties. Therapy usually proceeded for several years, or
until the patient decided that it was no longer needed, or s/he could no longer afford it.
CONTEMPORARY PSYCHODYNAMIC PERSPECTIVES

Several of Freud’s colleagues and students, such as Alfred Adler (1870–1937), Karen Horney (1885–1952),
Carl Gustaf Jung (1875–1961), as well as his daughter, Anna Freud (1895–1982), developed their own
psychodynamic theories about normal and abnormal human functioning. Although these psychodynamic theories uphold
theories Freud’s fundamental principles, they depart from some of his original ideas in important ways. The most
Theories that significant departure from Freud’s original thinking was a more pronounced emphasis on the processes
focus on the and development of the ego, instead of analysing human behaviour largely in terms of the strivings of
interplay between
the id.
unconscious
psychological ‘Object relations’ is one of the most influential contemporary psychodynamic concepts. According
processes in to theorists of the object relations school, such as Margaret Mahler (1897–1985), ‘objects’ are the people
determining to whom individuals are strongly attached. The primary motive of human behaviour is the need for
thoughts, feelings close relationships with others. The prototype of this strong emotional attachment is the relationship
and behaviours. between an infant and his/her primary caregiver, usually the mother. According to this theory, newborns
have no sense of self separate from their mothers. The crucial process of developing a separate sense
of self and a secure internal image of the mother is called separation-individuation. As the success of
this process strongly influences the nature of attachment in later intimate relationships, disturbance
in the separation-individuation process can result in psychological problems (Mahler, Pine, &
Bergman, 1975).
Contemporary psychodynamic theories have also revised Freud’s original ideas about penis envy
and girls’ moral development. Freud originally proposed that girls have a less well-developed superego
and therefore a weaker sense of morality. The first neo-Freudian theorist to challenge this concept was
Karen Horney (1922/1967), who pointed out that it was social conditions, rather than the lack of a penis,
that doomed females of that era to inferiority and envy. Later theorists such as Carol Gilligan (1982)
proposed that the crucial process in the development of the superego is separation-individuation, rather
than the Oedipus and Electra conflicts. Separation-individuation from the mother is crucial in the
development of masculinity, whereas it is not required for the development of femininity. Therefore,
boys are more strongly motivated to place an emphasis on separation-individuation, while girls have
more difficulty with that process. Thus, it is proposed that males may have difficulty with intimate
relationships, while females may have difficulty with independence during adulthood.
CONTRIBUTIONS AND LIMITATIONS OF THE PSYCHODYNAMIC MODEL

Perhaps one of the most enduring contributions of the psychoanalytic movement to mental health
is that it popularised concepts of mental health and disorder that were radically different from the
hitherto dominant medical model. Psychoanalysis also extended the boundaries of the definition of
mental disorder to include not only symptoms of insanity, but also symptoms of anxiety, depression
and other neuroses. By doing so, psychoanalysis initiated the current proliferation of mental disorder
categories. It also contributed to a radical change in the mental health professions by extending the
client base from a small number of severely psychotic individuals treated in asylums to a large number
of neurotic individuals treated at outpatient clinics (Horwitz, 2003). In addition to taking mental
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health out of the asylum and into the office, psychoanalysis was instrumental in enabling mental case study
health professionals other than psychiatrists to provide treatment. Freud thought of psychoanalysis as method
a field independent of medicine or psychiatry and was willing to train analysts who were not medical Research method
doctors. Mental health became the field not only of doctors but also of the variety of non-medical in which single
individuals are
practitioners seen today, such as psychologists, clinical psychologists, psychotherapists, counsellors studied in detail.
and social workers (Routh, 1998).
Several different factors contributed to the psychoanalytic movement’s loss of dominance during
control group
the 1970s. In spite of contemporary developments addressing some of the shortcomings of classical Group of
Freudian theory (e.g., its gender bias), the main problems of the psychodynamic model remained largely participants in
unresolved. These included pervasive criticisms of the problematic scientific basis of psychoanalysis an experimental
as a theory and data showing its limited success as a treatment (Eysenck, 1952; Firestone, 2002). study whose
Freud developed his theory using the case study method. This was a widely accepted method experience is the
of medical science at the time: most of medical knowledge was based on carefully observed and same as that of
the experimental
comprehensively documented cases of specific individuals with various illnesses. By the second
group in all
half of the twentieth century, however, the norms of medical science moved beyond the case study ways except
method to adopting large samples, control groups, statistical analyses and double-blind experiments that they do not
with placebo medications. Case studies are highly influenced by the interpretative framework of the receive the key
researcher (e.g., psychoanalysts focus on childhood material to a much greater degree than other manipulation;
theorists), do not allow the researcher to rule out competing hypotheses (e.g., did patients improve as this allows for
a result of the uncovering of unconscious material or some other aspect of therapy?) and are based on the effect of the
experimental
individual patients who may not be representative of broader groups. Hence they were increasingly
manipulation to
seen as unreliable and unacceptable as a primary research method. be determined.
Moreover, the theory of psychoanalysis was criticised for being virtually untestable using modern
empirical methods. Psychodynamic concepts are complex, hard to define and operate at a level that
double-blind
is not available to consciousness. Therefore, they are extremely difficult to measure and test using
experiment
reliable and valid empirical techniques. Indeed, there is little controlled research evaluating the Experimental
fundamental concepts of the psychodynamic perspective to this day. study in which
The theory has also been criticised for being unfalsifiable (Popper, 1968). The term ‘falsifiability’ both the
refers to the ability of a theory to be proven wrong. A theory is falsifiable if it can make clear researchers and
predictions that are testable either by collecting empirical data or by conducting a logical analysis. the participants
For example, one of the most important concepts of psychoanalysis is the Oedipus complex. To test are unaware
of which
whether the Oedipus complex exists, a researcher might want to ask a large group of men whether they
experimental
remember that, at about the age of 5, they developed a sexual desire towards their mothers. However, condition the
responding with either yes or no (due to the repression of unacceptable id impulses) is consistent with participants
the theory, rendering the theory unfalsifiable. are in so as to
The complexity and lack of clarity of the concepts involved in psychoanalytic theory also had reduce demand
important implications for the accountability of psychoanalysis as a treatment method. Clear and characteristics.
reliable diagnoses often could not be given, treatment progress and outcomes were very difficult to
specify, and the length and cost of treatment could not be predicted with any precision. With the validity
advent of medical insurance for psychiatric treatment, the demand for clearer and more specific In psychological
diagnoses and outcomes was ever-increasing. In summary, psychoanalysis was unable to meet the testing, degree
to which an
societal demand for greater accountability, as well as the professional demand for increased scientific
instrument
validity, occurring during the second half of the twentieth century (Horwitz, 2003). actually
measures what
it is intended
The behavioural perspective to measure. In
diagnosis, the
Psychoanalysis concerned itself with the subjective experience of the individual and sought to explain
degree to which
human behaviour in terms of unobservable, unconscious processes. The behavioural approach (also diagnostic criteria
known as the learning perspective) differed radically from this school of thought by emphasising that accurately define
the causes of behaviour are observable and identifiable in the immediate environment to the behaviour the features of
itself. These causes are simply stimuli that elicit, reinforce or punish the behaviour. disorders.
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behavioural KEY CONCEPTS OF BEHAVIOURISM

approach John B. Watson (1878–1958) is credited as the founder of behaviourism, not primarily because of
Theories that rely any major theoretical contributions but because of his efforts in popularising this new approach to
on the principles psychology. In 1913 he published the manifesto of radical behaviourism, entitled Psychology as the
of learning to
Behaviourist Views It. In this paper he argued that psychology did not need to concern itself with
explain both
normal and complex, unobservable constructs such as thoughts and sensations. Instead, the proper domain of
abnormal psychology included only observable, readily measurable stimuli and responses. The basic premise
behaviour. of radical behaviourism was that the study of behaviour should be an objective, experimental science,
much like chemistry or physics. To illustrate this approach, he demonstrated experimentally, in the
classical famous case of ‘Little Albert’, that the phobic fear of furry animals and other furry objects could be
conditioning instilled in a child as a result of simple learning processes (Watson & Rayner, 1920).
Form of learning The basic mechanisms of learning were first discovered by the Russian physiologist Ivan Pavlov
in which a neutral (1849–1936), who earned the Nobel Prize in 1904 for his contribution to science. The fundamental
stimulus, through
principle of classical conditioning is that behaviour can be explained in terms of unconditioned
its repeated
association with
responses (UR) and conditioned responses (CR). Unconditioned responses are elicited automatically
a stimulus that by certain stimuli, such as salivating at the sight of food or experiencing fear when attacked. If such
naturally elicits a unconditioned stimuli (US) (food or attack) consistently occur together with some other, previously
certain response, neutral stimulus (such as the place where the attack has occurred), a response similar to the
acquires the unconditioned response will occur. In this example, the place of the attack is a conditioned stimulus
ability to produce (CS) and the response of anxiety upon entering the same place is a conditioned response. This process
the same is summarised in Table 1.2.
response.
unconditioned TABLE 1.2 The procedure for Pavlovian (classical) conditioning

response (UR)
In classical Pre-training
conditioning,
response that Unconditioned and conditioned Unconditioned stimulus (e.g., food) → Unconditioned response
naturally follows stimuli are presented separately. (e.g., salivation)
when a certain Conditioned stimulus does not Conditioned stimulus (e.g., bell) No response
stimulus appears, elicit a response.
such as salivation
in dogs at the Training
smell of food.
Unconditioned and conditioned Unconditioned stimulus (e.g., → Unconditioned response
stimuli are presented together, food) + conditioned stimulus (e.g., salivation)
conditioned several times. (e.g., bell)
response (CR)
Learned response Post-training
that is elicited
Conditioned stimulus is presented Conditioned stimulus (e.g., bell) → Conditioned response
by a conditioned
stimulus following alone. It elicits a response that is (e.g., salivation)
classical the same or similar to the original
conditioning. unconditioned response.
unconditioned
stimulus (US)
The principles of operant conditioning (also known as ‘instrumental conditioning’) were first discovered
In classical by Edward Lee Thorndike (1874–1949) and later refined by B. F. Skinner (1904–1990) and others.
conditioning, The fundamental principle of operant conditioning is that behaviours which are followed by satisfying
stimulus that consequences (‘rewards’) are likely to be repeated, while behaviours that are followed by unsatisfying
naturally elicits a consequences (‘punishments’) are likely to be avoided or decreased. In other words, all organisms,
reaction, such as including humans, are controlled by the consequences of their actions. Positive reinforcement increases a
the smell of food particular behaviour because the behaviour is followed by a reward. Negative reinforcement also increases
eliciting salivation
a particular behaviour because the behaviour is followed by the removal of negative or unpleasant
in dogs.
stimuli. Negative reinforcement should not be confused with punishment, which acts to suppress, rather
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than increase behaviours, through the application of conditioned

negative consequences contingent upon the behaviour stimulus (CS)
occurring. Consistent with the behaviourist emphasis on Previously neutral
observables as the only legitimate objects of scientific stimulus that,
when paired with
study, all reinforcements and punishments were an unconditioned
initially thought of as external environmental stimuli, stimulus,
for example, receiving food (positive reinforcement) or becomes
electric shocks (punishment). sufficient to elicit
a response.
CLASSIFICATION AND CAUSATION FROM
THE BEHAVIOURAL PERSPECTIVE
operant
According to the behavioural perspective, both normal
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(instrumental)
and abnormal behaviour is the product of learning.
conditioning
For example, a child who has been bitten by a dog Form of learning
learns to be more fearful and careful around dogs. in which
This learning is adaptive, as it helps the child to behaviours elicit
avoid future negative consequences. However, such consequences
responses often generalise to cause the child to fear that either
all dogs, all animals, or even to respond to pictures of reinforce or
punish the
dogs with fear and anxiety and consequently to avoid
organism, leading
such stimuli. At this point, the learnt behaviour is said to an increased
to be maladaptive, as it no longer serves the function or decreased
of helping the child avoid objective danger. Indeed, B. F. Skinner, a key proponent of the principles probability
such avoidance learning has been implicated in the of operant conditioning underlying learned respectively of
development of several anxiety disorders. behaviour. the behaviour
However, it is also important to keep in mind occurring in
that strict behaviourists would not use diagnostic labels such as ‘anxiety disorder’. The behaviourist the future
(also known as
perspective has traditionally been highly critical of diagnostic categories, for several reasons. One
‘instrumental
reason is that, as discussed previously, diagnostic categories imply a medical model of mental conditioning’).
disorders, according to which symptoms (such as anxiety) are manifestations of underlying disease
processes. According to the behavioural perspective, however, normal and abnormal behaviour are
both products of the same learning process, and there are no specific underlying disease processes
differentiating one from the other. In other words, behaviourists see normal and abnormal (or adaptive
versus maladaptive) behaviour on a continuum. The difference between the two is only a matter of
degree (i.e., how much fear is experienced in certain situations) rather than being a matter of qualitative
differences. Interestingly, in this matter (if in nothing much else) behaviourists and psychoanalysts aversion therapy
agree with each other. Treatment that
involves the
TREATMENT FROM THE BEHAVIOURAL PERSPECTIVE pairing of an
Consistent with their sceptical approach to diagnostic labelling, traditional behaviourists would argue unpleasant
that in order to reduce maladaptive behaviour, the behaviour needs to be described in objective detail stimulus with
and the environmental stimuli that determine the behaviour need to be identified. This process is a deviant or
called a functional analysis of behaviour: it implies that all behaviours can be understood in terms maladaptive
of their function towards receiving rewards or avoiding punishments. From that point on, the task of source of
pleasure (such as
the therapist is to help the individual to rearrange environmental contingencies in a way that supports
excessive alcohol
adaptive responses. This process also involves learning new responses, extinguishing old responses, or consumption) in
becoming habituated to previously avoided, feared stimuli. order to induce
Many effective treatments have been developed based on learning principles. One of the earliest an aversive
of these was the introduction of aversion therapy in the 1930s to help individuals who were abusing reaction to
alcohol to develop a dislike of the taste of alcoholic drinks through the pairing of drinking cues with the formerly
aversive stimuli (Routh, 1998). In 1958, Joseph Wolpe published an influential book on systematic pleasurable
desensitisation, a technique still widely used in the treatment of anxiety and phobias. In this approach, stimulus.
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systematic individuals learn to associate a relaxation response with imagined feared stimuli. In the 1960s,
desensitisation token economies were introduced in various mental hospitals to encourage persons with mental
Behavioural retardation (an old label for intellectual disability), schizophrenia, and other disorders to increase
technique that their self-care and prosocial behaviours by consistently rewarding such behaviours with tokens that
aims to reduce
the client’s
could be exchanged for various goods and privileges at the hospital (Ayllon & Azrin, 1968). The basic
anxiety through principles of learning theory can still be found to underlie many contemporary treatment programs,
progressive, both for adults and children. These treatments have been empirically evaluated and shown in many
imaginal exposure cases to be more effective than other forms of psychological treatment, as well as being briefer and
to feared stimuli less expensive (Chambless & Ollendick, 2001; Eysenck, 1952).
paired with
the induction
of a relaxation
CONTEMPORARY BEHAVIOURAL PERSPECTIVES
response. Traditionally, behaviourists strongly argued against the idea that non-observable constructs can be legitimate
targets of scientific enquiry. Beliefs, thoughts, feelings, values, interpretations or other mental processes
were seen as inappropriate concepts for scientific scrutiny as they cannot be directly observed or measured
token economy
reliably. By the 1970s, however, increasing amounts of data became available that forced learning theorists
Treatment
application to reconsider this position and admit mental processes into the realm of explanatory constructs.
of operant As early as 1948, Edward Tolman questioned some of the basic principles of operant conditioning
conditioning in and argued that learning occurs through mental processes independent of external reinforcement.
which individuals Reinforcement merely affects the rate of learning by creating thoughts predicting the likelihood of
receive tokens for rewards and punishments in specific situations. Concerning classical conditioning, data from blocking
exhibiting desired design experiments have shown that simple pairing of a conditioned stimulus and an unconditioned
behaviours
stimulus is not sufficient to produce learning (Kamin, 1969). Instead, learning occurs only if the
that can then
be exchanged conditioned stimulus provides new information about the occurrence of the unconditioned stimulus, and
for privileges helps create expectancies (or predictions) about the likelihood of the unconditioned stimulus occurring.
and rewards; The design of a blocking experiment involves pairing an unconditioned stimulus (e.g., a shock) with
these tokens a conditioned stimulus (e.g., a light) in stage one. In stage two, the same unconditioned stimulus (shock)
are withheld is paired with two different stimuli at the same time: the original conditioned stimulus (light) as well
when the as a new one (e.g., a tone) for the same number of times as the original pairings in stage one. So, the
individual exhibits
unconditioned stimulus has now been paired with two different conditioned stimuli, first the light alone
unwanted
and then the light paired with a tone, for the same number of times. The question is, does the tone elicit
behaviour.
fear of the shock? A strict classical conditioning prediction would be that the tone should elicit fear in
the subject, as the tone has been paired with the shock several times. The results of such experiments,
however, have repeatedly shown that the tone does not elicit fear when presented alone. These findings
can be explained only by invoking unobservable constructs, for example, by arguing that the tone did not
add any new information in predicting occurrence of the shock that was not already conveyed by the light.
As a result of these and similar experimental findings, the field of behaviourism and learning
theory has undergone a conceptual revolution (Lovibond, 1993). Contemporary learning theories now
involve unobservable cognitive constructs, such as information value or expectancies, among their
central notions. Albert Bandura (1977) was one of the primary proponents of contemporary cognitive-
behaviourism, aiming to reconcile traditional learning theories with a need to refer to mental processes
when trying to explain how learning takes place. Bandura was the first to describe and explain the
modelling mechanisms of modelling, an important type of learning that could not be explained by traditional
Process of notions of strict behaviourism. Learning by modelling is extremely common during human development.
learning When children watch another child climb on top of a fence and then do the same, they do so without any
behaviours by
obvious external reinforcer being present. If modelling is not controlled by external reinforcers, then it
imitating others.
must be controlled by processes occurring in the mind. Therefore, learning cannot be explained without
referring to internal, mental processes such as values, beliefs, thoughts or expectations.
CONTRIBUTIONS AND LIMITATIONS OF THE BEHAVIOURAL PERSPECTIVE

Behaviourism can certainly claim to be immune to the major criticism against the psychodynamic
perspective, that its constructs are vague and difficult to test empirically. Behaviourists pride themselves
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on only making claims that are precise, measurable and scientifically testable. Indeed, one of the main
contributions of behaviourism to psychology was its introduction of and insistence upon experimentation
and objective measurement. Psychology as a discipline has now embraced this approach and has applied
it to other theoretical perspectives, such as the currently dominant cognitive perspective.
On the other hand, traditional behaviourism has been criticised for oversimplifying the understanding
of human existence. Traditional, strict behaviourism was unpalatable to many practising clinicians
for excluding anything unobservable from scientific consideration. Using rewards and punishments
in behaviour modification programs without connecting with the person, as recommended by strict
behaviourism, was seen by many as denigrating to the human spirit. Critics argued that thoughts,
values, beliefs, memories, hopes and sorrows are essential to being human and ignoring these was
seen as a major shortcoming of traditional behaviourism.
The cognitive perspective

Can a fledgling psychotherapy challenge the giants in the field—psychoanalysis and behaviour
therapy?
Beck, 1976, p. 333
After the loss of dominance of psychoanalysis during the 1970s, psychiatry as a profession returned to
the biological perspective, while psychology embraced a new revolution: cognitivism. The beginnings
of the cognitive approach in abnormal and clinical psychology are often associated with the names of cognitive
two clinicians: Albert Ellis (1913–2007) and Aaron Beck (b. 1921). Both of these theorists developed approach
their ideas based initially on clinical observations. They share the fundamental premise of the cognitive Theories
perspective that dysfunctional cognitive processes cause emotional and behavioural disturbances. that focus on
Albert Ellis developed rational-emotive therapy, arguing that people do not simply respond to events dysfunctional
ways of thinking
themselves, as behaviourists at the time would have argued, but to their own idiosyncratic interpretations as the causes
of events (Ellis, 1962). Ellis used the ABC model to explain this process: A is the event, B is the person’s of abnormal
interpretation of the event, and C is the person’s reactions to the event (i.e., emotional and behavioural behaviour.
responses), which are dependent upon the interpretation. A simple illustration of the ABC model is given in
Figure 1.1. Ellis explained abnormal behaviour by suggesting that some individuals hold irrational beliefs
which influence their reactions to events in unhelpful ways. These irrational beliefs include such statements
as ‘I must win everybody’s approval, otherwise I
am worthless’ or ‘I should be able to get everything
I want easily and quickly’. The therapist’s aim was
to uncover, confront and adjust such beliefs and
hence alter the individual’s disturbed emotional and
behavioural reactions.
Aaron Beck is perhaps the best-known and most
influential thinker within the cognitive perspective.
Similar to Ellis, during his clinical work as a
psychiatrist Beck noticed that specific psychological
disorders were often associated with certain
specific thinking patterns. He initially made these
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observations while treating depressed patients using

the psychoanalytic technique of free association. He
noted that certain patterns of thoughts repeatedly
emerged and were almost invariably followed by
negative affect. These thoughts usually involved
themes of deprivation, failure and hopelessness. The technique of systematic desensitisation—where the client imagines
In addition to the negative themes in depressed or experiences contact with a feared stimulus such as a spider—can be
individuals’ thought content, Beck noted a number used in the treatment of phobias.
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A: Event
(e.g., a friend didn’t sit next to me in class)
B: Beliefs or interpretations of B: Beliefs or interpretations of

the event the event
(e.g., ‘She didn’t see me because (e.g., ‘I’ve done something to
she was in a hurry’) make her dislike me’)
C: Emotional and behavioural C: Emotional and behavioural

responses responses
(e.g., no emotional distress; go (e.g., feel upset; leave class as
up and talk to friend after soon as it’s over to avoid being
rejected again)
FIGURE 1.1 According to the ABC model, it is the individual’s interpretation of an event (rather than the
event itself) that results in emotional and behavioural responses. As a result, different interpretations of the
same event can result in different emotional and behavioural responses
of errors that these individuals made when interpreting events. He labelled these ‘selective abstraction’,
‘overgeneralisation’, ‘dichotomous thinking’ and ‘exaggeration of the negative’ (Beck, 1976). These and
other cognitive distortions commonly seen in people with psychological disorders are listed in Table 1.3.
In his later work, Beck extended his cognitive theory to other disorders, in addition to depression (Beck,
Emery, & Greenberg, 1985). For example, he proposed that people with anxiety disorders tend to be
preoccupied with thoughts relating to threat and danger, and have an especially sensitive mechanism for
detecting possible cues for danger in the environment.

Much research effort within the cognitive perspective has focused on uncovering ways in which
humans attend to, interpret and remember aspects of the environment. In other words, humans are seen
TABLE 1.3 Examples of cognitive distortions occurring in individuals with psychological disorders
Black and white thinking (all or nothing)
Individuals with this type of thinking see things as being only one extreme or the other, with no middle
ground. For example, ‘My life used to be perfect, now it’s a disaster’, ‘She used to be a wonderful person,
now she’s a monster’, and ‘If I can’t get that job, I’m a total failure’.
Setting unrealistic expectations
Unrealistic expectations occur when the individual attempts to be perfect or faultless at everything s/
he does. Setting such expectations ensures that the individual is doomed to fail. ‘Should’ or ‘must’
statements focus on what the individual is not doing and create unnecessary guilt and disappointment.
Selective thinking (looking on the dark side)
This entails remembering and dwelling on one unpleasant event, or aspect of an event, and dismissing all of
the pleasant experiences one has had. For example, after having a mistake corrected at work, thinking ‘Now
my boss thinks that I’m incompetent’, while ignoring the positive comments that were also given for the work.
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Converting positives into negatives (being a cynic)
Some individuals tend to turn even a positive experience into an unpleasant or neutral event. For example,
after receiving a bonus for good work, thinking ‘It was just good luck, I won’t be able to do as well next year’,
ensures that the individual fails to take credit for his/her achievements and to feel positive about them.
Over-generalising
For some people, one unpleasant occurrence creates an expectation that this is bound to happen in all
future similar situations. For example, a person who fails at a test might think ‘I’m hopeless at everything I do’.
Magnifying or exaggerating unpleasantness (making mountains out of molehills)
Individuals sometimes focus on something unpleasant that has occurred and then exaggerate its
importance and possible consequences. For example, after blushing a little while giving a speech, a
person might think, ‘I’ll never be able to face these people again—they must think I’m an idiot’.
Catastrophising (whatever can go wrong will go wrong in a big way)
This distortion is more extreme than magnifying unpleasantness. Catastrophising turns situations into
life and death issues. For example, a partner arriving home late from work is seen as a sign that s/he has
been in a serious car accident, and a headache is seen as a likely symptom of a brain tumour.
Personalising (it’s all my fault)
Individuals with this thinking habit tend to take the responsibility and blame for anything unpleasant. A
common example is taking responsibility for other people’s feelings and actions, while ignoring the fact that
others are ultimately in control of their own lives.
Mistaking feelings for facts (I feel therefore I am)
People often confuse feelings for facts. Thinking that ‘Because I feel hopeless, I am hopeless’, ‘I feel fat,
therefore I am fat’, and ‘I feel anxious, therefore the situation must be dangerous’ are common examples
of this type of cognitive distortion.
Jumping to negative conclusions

Negative conclusions are often drawn without any supporting evidence or even in spite of obvious
conflicting evidence. This often involves mind-reading of other people. Thinking ‘This is the second time
my friend has looked at the woman at the next table. He is obviously bored with my conversation’ is an
example of such negative conclusions.
Source: Adapted from Burns, D. D. (1980). Feeling good: The new mood therapy. New York: William Morrow & Company.
as engaging in active information processing. The way information is processed then influences the way
individuals react to and interact with the environment. Since it is impossible to attend to all information
that is available in the environment at any given moment, it is necessary to select which aspects of the
environment to attend to and which aspects to filter out. Selective attention, therefore, is an adaptive
process which enables the processing of information that is important and the disregarding of irrelevant
distractions at any given moment. However, biases in selective attention have been shown to be associated
with some psychological disorders. For example, individuals with anxiety disorders tend to attend to
threat-related information more readily than do people without such disorders. Similarly, people who
are depressed show memory patterns that are different from the memory processes of non-depressed
individuals: depression tends to be associated with the recall of negatively biased information. Cognitive
distortions, disturbances in information processing and other cognitive processes have received a large
amount of research attention in the past 30 years (Mathews & MacLeod, 2005). This research will be
discussed more fully in the chapters dealing with specific disorders.
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Finally, it is important to note that while cognitive theorists often use diagnostic labels, the
cognitive model, similar to other psychological models, implies a continuity rather than a categorical
difference between normal and abnormal states. In other words, the cognitive model proposes that
the dysfunctional thoughts, behaviours and emotions found in various psychological disorders are
exaggerations of normal adaptive thoughts, behaviours and emotions (Beck, 1976).
TREATMENT FROM THE COGNITIVE PERSPECTIVE

Given the assumption that distorted cognitions result in emotional distress (e.g., depressed mood)
and behavioural disturbances (e.g., withdrawing from others), clients are guided by the therapist in
discovering their own distorted patterns of thinking and replacing these with more rational thoughts
that are consistent with reality. This process is aided by such techniques as keeping thought diaries to
enable the individual to discover the associations between their thoughts, emotions and behaviour in
everyday life. A careful recording of thoughts then helps the individual to identify negative or biased
cognitive thinking patterns. In the technique of cognitive restructuring, clients are assisted by the therapist to
restructuring change dysfunctional thinking patterns by generating and testing out alternative interpretations and
Cognitive predictions. For example, the client may be asked to conduct a behavioural experiment in which s/he
technique in acts in such a way so as to test the validity of certain beliefs. For instance, the client might ask a friend
which the client
out for a coffee to test the belief ‘people always reject me’.
learns to identify,
challenge and
replace his/her The cognitive-behavioural perspective
dysfunctional
beliefs with more Initially, the new cognitive approach appeared to be inconsistent with the assumptions of behaviourism.
realistic or helpful Cognitive psychologists gave the utmost importance to the internal mental processes that behaviourists
beliefs. were reluctant even to consider to be scientific or meaningful causal processes. However, the 1970s saw
behavioural the beginnings of a conceptual revolution within behaviourism, resulting in the gradual incorporation
experiment of cognitive concepts into behavioural theory and practice. The behavioural and cognitive theories and
Cognitive techniques seemed to complement each other, thus giving rise to the cognitive-behavioural perspective.
technique in The cognitive-behavioural approach incorporates aspects of contemporary behaviourism as well
which the client as cognitivism. It is currently the dominant psychological approach to understanding and treating
participates in a psychological disorders and addressing other types of abnormal behaviour such as excessive anger,
planned activity relationship problems or difficulties adjusting to life change. A large body of research evidence is
in order to test
accumulating in support of cognitive-behavioural theories. In fact, much of this book involves a
the accuracy of
his/her beliefs. discussion of various cognitive-behavioural theories and treatments of mental disorders.
TREATMENT FROM THE COGNITIVE-BEHAVIOURAL PERSPECTIVE
cognitive Cognitive behaviour therapy (CBT) combines both cognitive and behavioural techniques. It has been
behaviour demonstrated in over 400 studies to be effective for many psychological disorders and other abnormal
therapy (CBT) behaviours for children, adolescents and adults. It has been successfully applied to the treatment of
Type of anxiety disorders, mood disorders, alcohol and drug abuse, and eating disorders, among many others
psychological (Australian Psychological Society, 2010; Butler, Chapman, Forman, & Beck, 2006; Chambless &
treatment that Ollendick, 2001; Hofmann, Asnaani, Vonk, Sawyer, & Fang, 2012). CBT has also been shown to have
combines both
cognitive and
more enduring effects than drug therapies for anxiety and mood disorders (Hollon, Stewart, & Strunk,
behavioural 2006). In addition, CBT techniques are currently being evaluated as a preventative approach and as an
concepts and adjunct to medication in the treatment of severe psychological disorders such as schizophrenia (Beck
techniques. & Rector, 2005; Stafford, Jackson, Mayo-Wilson, Morrison, & Kendall, 2013).
CBT is highly compatible with the scientist-practitioner model of clinical psychology. According
to this model, both clinical practice and research need to be informed by a scientific perspective.
Both researchers and clinicians aim for a clear operationalisation of their concepts and emphasise
reliable and valid measurement. CBT therapists set clear, measurable goals at the beginning of
treatment and monitor the attainment of these goals throughout the course of therapy. In addition,
their understandings of the causes of a client’s symptoms and interventions are informed by recent
empirical findings rather than purely theoretical considerations (Baker & Benjamin, 2000).
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CONTRIBUTIONS AND LIMITATIONS OF THE COGNITIVE-BEHAVIOURAL humanistic

PERSPECTIVE approach
Theories based
In spite of its considerable success, the cognitive-behavioural perspective is not without its limitations.
on the view
Most importantly, while the research base for this perspective is impressive, there are still a large that the natural
number of unanswered questions. Most important of these is the limited evidence for the common tendency of
assumption underlying the cognitive perspective: the causal role of cognition. Although specific humans is
cognitive biases are found in many forms of abnormality, as proposed by the theory, these cognitions towards growth
have not yet been clearly shown to have a causal role. That is, negative cognitions may only be a and self-
result, or a symptom, of psychological disorder. Nevertheless, it is likely that negative cognitions actualisation;
abnormality
play a maintaining role in psychological disorders (regardless of the initial cause) and, as such, are
arises as a
appropriate and important targets in therapy (Brewin, 1996; David, 2006). result of societal
pressures to
conform to
The humanistic perspective dictates that clash
In addition to the cognitive approach, another psychological perspective that developed in the 1950s with a person’s
self-actualisation
and 1960s as a reaction to the perceived limitations of both behaviourism and psychoanalysis was the
process.
humanistic approach. The leaders of the humanistic perspective disagreed with what they perceived
as a negative, deterministic view of human existence inherent in the psychoanalytic tradition and a
reductionist, dehumanising approach inherent in behaviourism. They were interested in founding what self-actualisation
In humanistic
became known as a third force in psychology that emphasised the potential for positive human growth,
theory, fulfilment
the uniqueness of individuals, and the freedom and responsibility of humans to make choices rather of one’s potential.
than merely respond to environmental contingencies or be driven by irrational id impulses. Humanistic
psychology aimed to focus on uniquely human issues such as the self, hope, love, creativity and unconditional
individuality. The leading theorists within the humanistic approaches were Carl Rogers (1902–1987) positive regard
and Abraham Maslow (1908–1970). Essential part
of person-
KEY CONCEPTS OF THE HUMANISTIC APPROACH centred therapy;
the therapist
According to Carl Rogers (1961), all human behaviour is motivated by an innate actualising tendency.
expresses full
In other words, humans are born with a tendency to fulfil their potential, develop their talents and acceptance of
live according to their own values. Individuals who achieve these aims are self-actualised. Whether
the client as a
or not individuals achieve self-actualisation depends largely on their childhood experiences and, most person, without
importantly, on the amount of unconditional positive regard they received. All children need positive judgment.
regard, that is, love, affection
and acceptance from their
parents and other important
people in their lives to develop
into healthy adults. Importantly,
this positive regard needs to be
given without conditions—the
child needs to be loved for him/
herself.
In a similar vein, Abraham
Maslow (1970) proposed
that all human behaviour is
motivated by a drive for self-
actualisation. Maslow also
believed that there is a hierarchy
ISTOCK
of needs that must be met in the

process of development before Cognitive therapy for psychological disorders entails the therapist
self-actualisation can occur. helping the client to identify and challenge his or her distorted patterns
At the most basic level are the of thinking.
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conditions of biological needs to satisfy hunger, thirst and sex drives. The second level contains needs to feel safe,
worth secure and free from danger. At the third level is the need for belonging, that is, for warm, loving
Standards relationships with other people. At the fourth level, people need to satisfy their need for esteem,
of behaviour to seek the respect of others as well as to develop a sense of positive self-esteem. Having satisfied
imposed on an
individual by
each of these levels of needs, people can move into the fifth and highest level to fulfil their self-
others that must actualising tendency.
be met in order
to obtain their CLASSIFICATION AND CAUSATION FROM A HUMANISTIC PERSPECTIVE
approval. Unfortunately, positive regard is often received only when certain conditions of worth are satisfied.
That is, children receive affection if they behave according to their parents’ and others’ expectations
psychopathology such as by being polite, doing their homework or achieving their parents’ dreams for them. If parents
Refers to place a large number of conditions of worth upon the child, or if these conditions are not consistent
(a) the study of with the child’s own talents and natural aspirations, the child’s self-actualising tendency will be
psychological thwarted. According to Rogers, a lack of unconditional positive regard and the resulting lack of
abnormality or self-actualisation is the core of all psychopathology. For both Rogers and Maslow, all psychological
(b) manifestations
of psychological
disturbance stems from thwarted self-actualisation.
abnormality. As is clear from the description of the humanistic approach, humanistic psychology holds a non-
pathologising view of the person and does not ascribe to the medical model of psychological disorder.
therapeutic
Humanistic psychologists do not use diagnostic terms, which they see as dehumanising and implying
alliance pathology. Humanistic psychology abandoned the practice of using the label ‘patient’ and began using the
Degree to which label ‘client’ instead to indicate a more equal relationship between those in the therapeutic alliance (i.e.,
the relationship the client and therapist) and to avoid any implication of illness or sickness on the client’s part. Later in
between his career, Rogers took this even further and abandoned the label ‘client-centred’ to describe his therapy
the therapist approach in preference to a person-centred therapy approach, implying an equal, democratic interchange
and client is between persons in the therapeutic relationship.
characterised by
mutual trust and TREATMENT FROM A HUMANISTIC
shared goals.
PERSPECTIVE
person-centred
Rogers’s client-centred therapy aimed to reverse the
therapy psychopathological process by providing the client
Form of with the unconditional positive regard s/he needs to

psychotherapy proceed with self-actualisation. For this therapeutic
within the process to work, a phenomenological approach is
humanistic necessary; that is, the therapist needs to understand the
approach
© EVERETT COLLECTION HISTORICAL/ALAMY STOCK PHOTO

client as if seeing the world through his/her eyes. In
developed by
an influential article in 1957, Rogers outlined what he
Carl Rogers,
which consists
believed to be the necessary and sufficient conditions
of an equal for therapeutic change as follows:
relationship 1. Two persons are in psychological contact.
between the
therapist and
2. The first person, the client, is in a state of
client, and incongruence. Incongruence refers to a state when
in which the a person’s experience is discrepant with his/her
client receives conscious self-image. An example given by Rogers
unconditional is that of a mother who happens to fall ill each time
positive regard her son begins to make plans to leave home. In
and empathy this case, her image of herself as a caring mother
from the therapist
is inconsistent with her underlying desire to hold
in order to attain
self-actualisation on to her son. Thus the incongruity between one’s Carl Rogers was a major proponent of the
(previously called actual and perceived selves results in anxiety or humanistic perspective who conceptualised
client-centred other signs of distress. abnormality as resulting from disruption to the
therapy). 3. The second person, the therapist, is congruent. process of self-actualisation.
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4. The therapist experiences unconditional positive regard for the client—that is, avoids judging the
individual and instead values and respects the individual in all of his/her human facets.
5. The therapist experiences empathy for the client in that s/he is able to understand the client’s
perspectives and emotional experience.
6. The therapist is able to communicate his/her empathic understanding and unconditional positive
regard to the client.
According to Rogers, if these six conditions were met over a period of time, the client would
experience constructive change. No other conditions were deemed necessary. Through such therapeutic
practices, it was hypothesised that the client moves increasingly towards a greater understanding and
acceptance of his/her own goals, wishes, needs and fears and gains the courage to pursue these goals
rather than those that have been imposed by others.
CONTRIBUTIONS AND LIMITATIONS OF THE HUMANISTIC PERSPECTIVE

Rogers’ client-centred therapy and humanistic theories in general have become highly influential
in counselling practice. Humanistic theories, with their emphasis on human growth potential, also
played an important part in the emergence of movements promoting self-exploration and personal
development since the 1960s and continuing to the present day.
Rogers not only developed a new approach to therapy, he was also one of the first psychologists to
empirically investigate the process and outcome of his therapeutic approach. He tape-recorded therapy
sessions, had them transcribed, and used content analytic procedures to investigate the process by
which therapeutic change occurs. He used controlled treatment trials in which people receiving his
therapy were compared with those on a waiting list on various measures of wellbeing.
In general, however, humanistic psychologists preferred qualitative research methods over
experimental or other quantitative research approaches. From a quantitative research perspective,
humanistic theories have often been criticised for involving concepts (e.g., self-actualisation) that
are difficult to measure and to falsify. Consequently, humanistic theories and therapies have received
relatively little research support to date compared to therapeutic approaches (such as behavioural and
cognitive approaches) that are more amenable to measurement and testing via standard experimental
methods (Chambless & Ollendick, 2001; David, 2006).
The sociocultural perspective

An important criticism of both the biological and psychological perspectives is that they neglect the
wider economic, political and social inequality issues that may cause and exacerbate the suffering of
individuals. In some instances, biological and psychological perspectives can be prone to a ‘blaming
the victim’ approach by looking for the cause of suffering in the individual’s biological or psychological
makeup while ignoring pathological features of the social context. The critical psychology movement
has argued that psychiatry and clinical psychology can play a part in the control of social upheaval and
change by diagnosing individuals as having a mental disorder rather than focusing on changing unfair
social structures (Tolman & Maiers, 1991). From this perspective, mental health professions can be
seen as agents of oppression rather than as healing professions.
In general, the sociocultural perspective argues that abnormal behaviours are best understood in
terms of the social environment of the individual. Sociocultural theories focus on the importance of
family functioning, social networks, access to social resources (e.g., education and health services),
cultural values and influences, and religious or spiritual beliefs in influencing individuals’
behaviours, thinking and emotions. For example, the fact that the overwhelming majority of
individuals with eating disorders are female has been hypothesised to be the result of Western
culture’s increasing emphasis on thinness in women since the 1950s (Rubinstein & Caballero,
2000). Professionals working in the fields of community psychology and social work have made
especially important contributions to understanding abnormal behaviours from the sociocultural
perspective.
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biopsychosocial
approach
An integrative approach
View that The biological, psychological and sociocultural perspectives place different emphases on the various
biological, possible causal factors and possible treatment options for mental disorders and abnormal behaviours.
psychological A more fundamental difference among these perspectives lies in their disagreement over the definition
and social factors and conceptualisation of mental disorder and abnormality, particularly over whether a continuum or a
contribute to the
development of
categorical model more accurately describes psychological abnormality.
abnormality. In spite of these differences, most researchers and theorists today would agree that none of
these perspectives on its own is sufficient to explain human behaviour, be it normal or abnormal.
diathesis-stress The biopsychosocial approach holds that human behaviour can best be explained by incorporating a
model variety of biological, psychological and sociocultural factors that interact to influence the development
Originally of psychological disorders. As will be seen in the following chapters, most contemporary theories
developed in of psychological disturbance tend to be variants of the vulnerability-stress model (also known as
the context of the diathesis-stress model) that explain the causation of psychological disorders or other types of
schizophrenia, abnormality in terms of the complex interactions among individuals’ biological and psychological
the view that vulnerabilities and the life events they encounter as they negotiate their roles within their surrounding
abnormality is
caused by the
culture and society.
combination of
a vulnerability or
predisposition
(the diathesis)
LO 1.3 The classification and diagnosis of mental
and life events disorders
(the stressor).
Currently, the two gold standards for classifying mental disorders are the Diagnostic and Statistical
Diagnostic Manual of Mental Disorders (DSM), published by the American Psychiatric Association (APA),
and Statistical and the International Classification of Diseases and Related Health Problems (ICD), published
Manual of Mental by the World Health Organization (WHO). These two publications contain descriptions of various
Disorders (DSM) mental disorders and reflect the consensus of mental health professions regarding the definition and
Manual for classification of mental disorders at the time of their publication. The ICD is primarily used in Europe
diagnosing
and in all projects carried out by the WHO, while the DSM is more widely used in the United States
mental disorders
published by and Australia.

the American The current edition of the latter, the DSM-5, was published in May 2013. It lists more than 300
Psychiatric different mental disorders, some of which are shown in Table 1.4, under a range of categories such as
Association anxiety disorders, depressive disorders and personality disorders. Many of these specific diagnostic
containing a list categories will be described in subsequent chapters.
of specific criteria
for each disorder.
International TABLE 1.4 The categories of mental disorders as contained in Section II: Diagnostic Criteria and Codes
Classification of the DSM-5
of Diseases and
Related Health CLINICAL DISORDER CATEGORIES EXAMPLES OF DISORDERS
Problems (ICD)
System used to Neurodevelopmental disorders Intellectual disability, communication disorders, autism
classify diseases spectrum disorders, attention-deficit/hyperactivity disorder,
and other learning disorders
health problems
Schizophrenia spectrum and other Schizotypal (personality) disorder, schizophrenia, delusional
(including mental
psychotic disorders disorder, schizoaffective disorder
health problems)
published by the Bipolar and related disorders Bipolar I disorder, bipolar II disorder, cyclothymic disorder
World Health
Organization Depressive disorders Disruptive mood dysregulation disorder, major depressive
(WHO). disorder, persistent depressive disorder (dysthymia)
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CLINICAL DISORDER CATEGORIES EXAMPLES OF DISORDERS
Anxiety disorders Separation anxiety disorder, selective mutism, specific

phobia, social anxiety disorder (social phobia), panic
disorder, agoraphobia, generalised anxiety disorder
Obsessive-compulsive and related Obsessive-compulsive disorder, body dysmorphic disorder,

disorders hoarding disorder, trichotillomania, excoriation
Trauma- and stressor-related Reactive attachment disorder, posttraumatic stress disorder,

disorders adjustment disorders
Dissociative disorders Dissociative identity disorder, dissociative amnesia,

depersonalisation/derealisation disorder
Somatic symptom and related Somatic symptom disorder, conversion disorder, factitious
disorders disorder
Feeding and eating disorders Anorexia nervosa, bulimia nervosa, binge eating disorder
Elimination disorders Enuresis, encopresis
Sleep–wake disorders Insomnia disorder, hypersomnolence disorder, nightmare insomnia

disorder Difficulty in
initiating or
Sexual dysfunctions Erectile disorder, female orgasmic disorder maintaining
sleep.
Gender dysphoria Gender dysphoria
Disruptive, impulse-control and Oppositional defiant disorder, conduct disorder, antisocial

conduct disorders personality disorder
Substance-related and addictive Alcohol use disorder, gambling disorder

disorders
Neurocognitive disorders Delirium, major and mild neurocognitive disorders

Personality disorders Antisocial personality disorder, borderline personality

disorder, obsessive-compulsive personality disorder
Paraphilic disorders Exhibitionistic disorder, sexual masochism disorder,

fetishistic disorder
Other mental disorders Other specified/unspecified mental disorder due to . . .

(indicate medical condition)
Medication-induced movement Neuroleptic-induced parkinsonism, tardive dyskinesia,

disorders and other adverse effects antidepressant discontinuation syndrome
of medication
Other conditions that may be a Relational problems, abuse and neglect, educational and
focus of clinical attention occupational problems, housing and economic problems
Source: Adapted from the Diagnostic and Statistical Manual of Mental Disorders (5th ed.), copyright 2013, American Psychiatric Association.
The current list of mental disorders is a relatively recent phenomenon. Mental disorders were
added to the ICD for the first time in 1948, and the first edition of the DSM was published in 1952. The
development of an appropriate classification system for mental disorders is still a work in progress:
progressive editions of both the ICD and the DSM have included revised diagnostic criteria for some
mental disorders, the addition of new disorders and the omission of others.
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Advantages and disadvantages of diagnosis

Since the DSM is a publication of the American Psychiatric Association, its underlying assumptions
diagnosis currently reflect the medical model of mental disorders. The term diagnosis is consistent with the
Label given to a key assumptions of the medical model, according to which (a) an abnormal condition (which is
set of symptoms clearly distinct from normality and from other abnormal conditions) exists and (b) it is driven by
that tend to occur
clearly identifiable underlying pathological processes. Psychological perspectives on the definition
together.
and causation of mental disorders often do not share the categorical assumptions of the medical model.
Nevertheless, the majority of research in abnormal psychology today, irrespective of the theoretical
background of the researchers, investigates abnormal behaviours as defined by DSM diagnostic
categories. In addition, mental health professionals of most theoretical backgrounds, even those who
do not subscribe to the medical model of mental disorders, use diagnostic labels in their clinical
practice. There are several reasons for the current dominance of DSM diagnostic categories in the field
of mental health.
ADVANTAGES OF DIAGNOSIS
In practical terms, a common system of classification and diagnosis improves communication among
mental health professionals. Classification is the description of specific disorders in a way that clarifies
their essential features and their boundaries from other conditions. Diagnosis involves applying these
categories to people to best capture their characteristics (behaviours, thoughts and emotions). When
clinicians apply diagnostic labels, they are saying that the pattern of behaviours, feelings and thoughts
that the person displays is similar to a pattern that has been previously recognised, whose nature and
causes have been studied and for which particular treatments have been found useful. Thus, diagnosis
helps researchers and therapists to communicate with each other regarding the suspected causes
and most effective treatments for individuals experiencing certain patterns of thoughts, feelings and
behaviours.
In addition to communicating with each other, mental health professionals need to collaborate
with other institutions in society. Diagnoses are usually required when mental health professionals are
working with a health insurance company or are involved in a legal matter, workers’ compensation
schemes or government departments. To balance and forecast their budgets, hospitals need to collect
data regarding the numbers of individuals with different diagnoses (e.g., schizophrenia or major
depression) that they treat. Schools receive special funding on the basis of the number of children
with diagnoses such as autism or learning disabilities that they educate. Therefore, the diagnostic
categories of the DSM have become the primary means of communicating about mental health and
illness not only among mental health professionals but also in wider society.
DISADVANTAGES OF DIAGNOSIS
Despite these advantages, the practice of diagnosis is also associated with potential problems. First, the
widespread use of DSM diagnostic labels in society has often resulted in their reification. Both mental
health professionals and others often refer to these diagnostic categories as if they exist in nature the
same way many physical diseases exist. For most mental disorders, however, an underlying biological
disease process has not yet been identified. Mental disorders are simply theoretical constructs and
they are not independent of changing social values and theoretical orientations (as the examples of
homosexuality and drapetomania at the beginning of this chapter have shown).
Related to the above problem, DSM diagnoses are often used in common language and by some
health professionals as if they were explanatory rather than merely descriptive terms. For instance,
when the diagnostic category of ‘schizophrenia’ is applied, it should be taken as simply a description
of a constellation of symptoms including hallucinations or delusions. However, sometimes the
application of this label gives an illusion of explanation, leading to the erroneously attached meaning,
‘he is hallucinating because he has schizophrenia’.
Finally, it is important to keep in mind that applying diagnoses may sometimes be harmful to
people. In some instances, individuals may be stigmatised by others and their opportunities limited
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as a result of having been labelled as mentally ill (Rosenhan, 1973; Szasz, 1961). Diagnostic labels
may also be self-limiting, as in the case of those who take on a sick role (‘I have a mental illness’),
which can lead to increasing beliefs of helplessness regarding their capacity to think, feel and behave
differently. Such beliefs may then interfere with the process of recovery.
Thus, while the vocabulary of the DSM—its diagnostic categories—is the primary means of
communicating about mental health and illness in today’s society, its widespread use is also associated
with risks and limitations. It is crucial for mental health professionals, therefore, to be aware of the
main underlying assumptions that guided the establishment of these diagnostic categories and any
strengths and limitations associated with these assumptions.
The development of the DSM system of classification

and diagnosis
This section will trace the development of the DSM from its inception in 1952 to its most recent, fifth,
edition published in 2013. This historical overview aims to outline the ongoing improvements that
have occurred over time and forecast some of the future directions for diagnostic practice.
THE EARLY YEARS: DSM-I (1952) AND DSM-II (1968)

Given the dominance of psychoanalytic thinking between the 1940s and 1970s, the way mental
disorders were conceptualised in the DSM-I (APA, 1952) and its successor the DSM-II (APA,
1968) was greatly influenced by psychoanalytic theories about the nature and causation of mental
disorders. One important assumption of the time was that some mental disorders were biological
in origin while others were psychological. As a result, both the DSM-I and DSM-II had two main
sections. The first section was titled ‘Diseases of the Psychobiologic Unit’ and contained disorders
known to have a biological causation. These disorders were subclassified according to their presumed
cause, for example, intoxication or a vitamin deficiency. The second section had the self-explanatory
title ‘Disorders of Psychogenic Origin or Without Clearly Defined Physical Cause or Structural
Change in the Brain’. These disorders were referred to as ‘reactions’, implying that the disorder
was a psychological reaction to the individual’s environment or internal processes. Disorders were
presented under several subcategories, the most important of which were ‘Psychotic Disorders’ and
‘Psychoneurotic Disorders’. Consistent with a psychoanalytic approach, the various symptoms of both
psychotic and psychoneurotic disorders were thought to reflect the patient’s unconscious defence
mechanisms. Psychotic disorders were characterised by a ‘varying degree of personality disintegration
and a failure to test and evaluate external reality in various spheres’ (APA, 1952, p. 24). The same
underlying general assumption regarding causation guided the definition of each type of psychotic
reaction: ‘a psychotic reaction may be defined as one in which the personality, in its struggle for
adjustment to internal and external stresses, utilises severe affective disturbance, profound autism
and withdrawal from reality and/or formation of delusions or hallucinations’ (APA, 1952, p. 12). For
example, paranoid schizophrenia was seen as a psychotic reaction where the person uses the defence
mechanism of projection, which ascribes to others characteristics the individual cannot accept in him/
herself. In psychoneurotic reactions, anxiety was the chief characteristic. Such anxiety was either
directly felt or automatically controlled by such defences as depression, phobia formation or repetitive
thoughts and acts. For example, depressive reaction was described in the DSM-I as follows: ‘the
anxiety in this reaction is allayed, and hence partially relieved, by depression and self-deprecation.
The reaction is precipitated by a current situation, frequently by some loss sustained by the patient,
and is often associated with a feeling of guilt for past failures or deeds. The degree of the reaction in
such cases is dependent upon the intensity of the patient’s ambivalent feeling toward his loss (love,
possession) as well as upon the realistic circumstances of the loss’ (APA, 1952, pp. 33–34).
LIMITATIONS OF THE DSM-I AND DSM-II
In general, the constructs involved in psychoanalysis were complex and difficult to measure with precision.
The same problem applied to the diagnostic systems based on psychoanalytic thinking. Foremost among
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reliability the problems was the limited reliability of the diagnostic categories. Reliability refers to the ability of
Degree of a measurement system to yield the same results, no matter when, where and by whom it is used. So, a
consistency in 30-centimetre ruler measures exactly the same length in Sydney or in Perth, whether it is used by one
a measure, that
person or another, and whether it is used today or in six months’ time. Similarly, diagnostic categories
is, the extent
to which it
need to be defined clearly enough to enable different clinicians at different locations and times to arrive
yields accurate at the same diagnosis when assessing the same person. In order to apply modern scientific methods and
measurements empirically investigate the causes of a mental disorder or its treatment, researchers at different sites need to
of a construct be able to apply diagnostic criteria with a high level of agreement between them. At a more fundamental
across different level, the investigators need to be able to agree on whether a person meets the criteria for a disorder or not.
trials, samples, That is, the line between mental health and disorder needs to be clearly identifiable.
raters and forms Psychoanalytic theory, and hence the first two editions of the DSM, were unable to meet these
of the measure.
needs. Returning to the example of the description of depressive reaction in the DSM-I, a number of
obstacles to reliable diagnosis become apparent. First, at the very basic level, the description does
not give the diagnostician any indication as to when a depressive reaction becomes severe enough
to warrant a diagnosis and treatment, that is, when it ceases to be a normal reaction and becomes
‘abnormal’. How much of each of the listed symptoms is required to be considered abnormal? For
example, how much self-deprecation is required? For how long does the self-deprecation need to
continue? These considerations were not important for psychoanalysis, as the theory explicitly
accepted that the dividing line between normality and disorder is blurred.
In addition to not giving any indication regarding the difference between normal and abnormal
levels of the symptoms, it is not known whether all of the symptoms are required or only some of them
to establish a diagnosis. Should a person who feels depressed but does not express self-deprecation be
diagnosed with a depressive reaction or not? Are some of the symptoms more important than others?
Such questions were not explicitly stated in the diagnostic criteria in the first two editions of the DSM
and it was left to individual therapists or researchers to make decisions regarding the answers. This
subjective judgment introduced a great deal of unreliability to the diagnostic process since it allowed
a high level of disagreement to occur between individual therapists making diagnoses.
The other important limitation of the first two editions of the DSM was the lack of evidence for
their assumptions regarding causation. The ultimate aim of medical diagnostic systems is to classify
different disorders according to their underlying causation. The fact that psychoanalytic concepts
were extremely difficult to research empirically meant that the presumed psychodynamic causation
underlying the diagnostic categories in the DSM-I and DSM-II received no empirical support. The
diagnostic system was ultimately based on unproven and untestable assumptions about the aetiology
of the disorders. It was not possible to ascertain whether the disorders really existed as described—
that is, whether the category descriptions were consistent with what occurs in nature. In other words,
the diagnostic system had limited validity.
By the 1970s this state of affairs was no longer acceptable to the medical profession. Psychiatry
needed to introduce a new system for the classification of mental disorders that was more consistent
with the prevailing values of modern medical science. The next edition of the DSM, therefore,
represented a significant departure from the psychoanalytic model.
THE NEO-KRAEPELINIAN APPROACH: DSM-III (1980) AND ITS SUCCESSORS

The publication of the DSM-III has been seen by many as probably the most significant development in
psychiatric classification in the twentieth century. The DSM-III and its successors have attempted to
address the problems of limited reliability and validity that were characteristic of the previous editions by
adopting a neo-Kraepelinian, descriptive approach to classification comparable to Kraepelin’s earlier
work at the end of the nineteenth century. This approach avoided organising a diagnostic system around
hypothetical but unproven theories about aetiology. Instead, the diagnostic categories were defined at the
level of their observable features only, until their underlying causation was identified by further research.
Implicit in this perspective is the assumption that different mental disorders can be categorised and
diagnosed using the same principles that are used to categorise and diagnose physical disorders. These
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principles have also been adopted in the development of the revised third edition (DSM-III-R) (APA,
1987), the fourth edition (DSM-IV) (APA, 1994) and its text-revised version (DSM-IV-TR) (APA, 2000),
as well as the current, fifth, edition (DSM-5) (APA, 2013). The main differences between the first two
and later editions are summarised in Table 1.5.
TABLE 1.5 The main differences between recent editions of the DSM and their predecessors
DSM-III, DSM-III-R, DSM-IV, DSM-IV-TR AND DSM-5 DSM-I AND DSM-II
Specific diagnostic criteria for each category Unspecific, general descriptions of categories
No explicit assumptions about causation Assuming causation from a psychoanalytic

viewpoint
Polythetic format: a set of optional diagnostic Monothetic format: general description of criteria
differential
criteria is provided; only a subset is needed without specifying which ones are necessary and
diagnosis
for diagnosis which ones are optional
Determination of
which of two or
To illustrate the differences between the current and earlier editions, the DSM-5 category of major more possible
depressive disorder can be compared to the description given in the DSM-I. The DSM-5 criteria for major diagnoses is
depressive disorder are shown in Table 1.6. To be diagnosed with the disorder, an individual needs to fulfil appropriate for an
individual.
criteria A, B and C. Unlike the DSM-I, the DSM-5 criteria explicitly specify how many symptoms need to
be present, how long they need to be present for, and which symptoms are necessary or optional. Further, interrater
the DSM-5 gives clear guidelines for differential diagnosis, that is, differentiating the individual’s disorder reliability
Extent to which
from other possible diagnoses, for example, by specifying that a history of manic episodes would qualify
an observational
for a diagnosis of bipolar disorder, rather than major depressive disorder. Similar changes to all diagnostic measure yields
categories resulted in greatly improved levels of interrater reliability for all editions of the DSM following similar results
the introduction of the new approach in DSM-III. That is, the advent of the DSM-III introduced an increased across different
ability for different diagnosticians to agree on when a diagnostic category is applicable and which one it is. raters/judges.
TABLE 1.6 The DSM-5 diagnostic criteria for major depressive disorder
Criterion A At least five of the following symptoms have been present for at least two weeks. At least
one of these symptoms must be either (1) or (2):
1. Depressed mood for most of the day, nearly every day
2. Loss of interest or pleasure in most activities for most of the day, nearly every day
3. Significant weight loss/gain or decrease/increase in appetite nearly every day
4. Insomnia or hypersomnia nearly every day hypersomnia

Being chronically
5. Psychomotor agitation or retardation nearly every day sleepy and
6. Fatigue nearly every day sleeping for long
periods of time.
7. Feelings of worthlessness or excessive guilt
psychomotor
8. Reduced ability to think, concentrate or make decisions nearly every day
agitation
9. Recurrent thoughts of death, which might include suicidal thoughts Excessive
motor activity
Criterion B These symptoms result in significant distress or impaired functioning in an important area (such as pacing
(or areas) of life such as the individual’s ability to function at work/study. and fidgeting)
stemming from
Criterion C These symptoms are not due to the effects of a substance or another medical condition.
mental tension.
Source: Adapted from Diagnostic and Statistical Manual of Mental Disorders (5th ed.), copyright 2013, American Psychiatric Association.
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THE VALIDITY OF THE CURRENT DSM CLASSIFICATION OF DISORDERS
Current classification in psychiatry. . . resembles the medicine of 50–100 years ago, before the
underlying pathophysiology of many disease processes was understood.
Charney et al., 2002, p. 33
The primary strength of the current DSM categorical system is its ability to improve communication
among clinicians and researchers, that is, its increased reliability. However, although it is now possible
to agree on specific diagnoses with a satisfactory level of reliability, it is still unknown whether these
diagnostic categories are at all meaningful, that is, valid disease entities that actually exist. The ultimate
aim of medical diagnostic systems is to classify different disorders according to their underlying
causation. The neo-Kraepelinian approach introduced in the DSM-III aimed to identify symptom clusters
(syndromes) that would eventually be found to share a common causation and to respond to specific
treatments. This aim has not yet been achieved. Indeed, there is now an increasing amount of empirical
evidence questioning the validity of the current classification system. The main problems identified
include diagnostic instability (the finding that individuals often move from one disorder to another over
time), a lack of treatment specificity (the finding that the same treatment—for example, antidepressant
medication—is effective for a variety of different disorders such as depression and anxiety disorders),
comorbidity and a high level of comorbidity (the co-occurrence of two or more disorders in the same person) found
Co-occurrence among psychiatric disorders (Clark, Watson, & Reynolds, 1995; Krueger & Piasecki, 2002). Each of
of two or more these findings questions the assumption that the categories of mental disorder, as implied by the medical
disorders in the
model and currently described in the DSM, are independent of each other.
same person.
Among these problems, the largest amount of research attention has been devoted to comorbidity.
Studies involving large community samples both in the United States and in Australia have found that
it is quite uncommon to have only one psychological disorder. These studies agree that 50–60 per cent
of individuals with one disorder also have at least one other, comorbid disorder (Andrews, Hall,
Teeson, & Henderson, 1999; Kessler et al., 1994). These rates are much higher in clinical samples
(i.e., among individuals who have sought treatment for their condition), where finding individuals
with only one diagnosis is clearly the exception rather than the rule. Moreover, the co-occurrence of
mental disorders often follows a pattern. For example, individuals with major depression often receive
diagnoses of one or more anxiety disorders, and individuals with borderline personality disorder are
often diagnosed with eating disorders and substance use disorders (Clark et al., 1995; Krueger &
Piasecki, 2002; Widiger & Sankis, 2000).
High rates of comorbidity pose two important challenges to researchers and to the classification
system. One problem is that comorbidity complicates any efforts to study the nature, causation and
treatment of individual disorders. If, for example, researchers find that individuals with bulimia
nervosa also have low self-esteem, it is difficult to know whether this finding is associated with the
eating disorder itself or with several other disorders (such as major depression) that individuals with
bulimia nervosa may also have. A possible solution to this problem is to study only pure cases of the
disorder, that is, individuals who do not have any comorbid conditions. However, these cases may
be rare and not representative of the population of individuals with bulimia nervosa. So, given the
problems of extensive comorbidity and the often marked heterogeneity among individuals with the
same diagnosis, research framed by the current putative categories of mental disorder can be very hard
to interpret.
A more fundamental implication of the high comorbidity of mental disorders is that it questions
the validity of separate, independent diagnostic categories. To give an example from physical
illnesses, even though tonsillitis and diabetes are caused by two different disease processes, these
two diseases may nevertheless occasionally co-occur in the same person. However, these two
diseases have not been found to be co-occurring at a rate above chance (i.e., people with tonsillitis
are not more likely to have diabetes than any other disorder). In contrast, increasing amounts of
data suggest a lack of independence among mental disorder categories. Data showing extensive
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comorbidity and a lack of treatment specificity undermine the premise of the medical model that
different mental disorders represent distinct (if unknown) aetiologies: if the disorder categories are
caused by different factors, then they should not regularly co-occur and should not respond to the
same treatment. It is argued, therefore, that the co-occurrence of disorders reflects their common
underlying psychopathology, which would mean that they are not entirely distinct from one another.
DSM-5 AND BEYOND: ALTERNATIVES TO THE CURRENT CLASSIFICATION SYSTEM

Each new edition of the DSM following the publication of the DSM-III in 1980 retained the principal
features of the DSM-III but was more research-based than previous editions and made relatively small,
iterative changes to the list of mental disorders and their diagnostic criteria. For example, the task
force for the DSM-IV conducted literature reviews, analyses of existing data sets and field studies to
collect empirical evidence to guide any decisions for the DSM-IV diagnostic categories. The main
changes introduced in the DSM-IV included the creation of 13 new disorders, the omission of eight
previously described disorders and the revision of the diagnostic criteria for several others.
A similar process occurred during the development of the DSM-5, which involved preparation
in the form of empirical research spanning more than a decade. The planning process for the
revisions that eventually led to the publication of the DSM-5 began in 1999. The initial phase of this
planning process culminated in the publication of a six-chapter volume summarising the American
Psychiatric Association’s research agenda for the DSM-5 (Kupfer, First, & Regier, 2002). This agenda
aimed to provide direction for research that could improve the scientific basis of the DSM-5 and
future classification systems of mental disorders. Topics included developmental issues, disability
and impairment, and cross-cultural issues. In addition, fundamental questions about the nature of
classification and diagnosis were considered in the chapter ‘Basic Nomenclature Issues for DSM-5’
(Rounsaville et al., 2002), including the need to work towards achieving a more valid definition
of mental disorder—a problem that has remained unresolved in spite of many years of effort and
controversy (Broome & Bortolotti, 2010; First & Wakefield, 2010). The authors of the DSM-5 research
agenda also emphasised that one of the main shortcomings of the DSM-IV-TR was its presentation
of various diagnostic categories as if they were equal in validity (Rounsaville et al., 2002), so that
practising clinicians had no way of knowing that certain disorders (e.g., anxiety disorders) listed in the
DSM-IV-TR were better established than others (e.g., most personality disorders). Finally, the authors
emphasised the need to determine whether a dimensional approach should be substituted for the
current categorical approach as a way of improving the validity of the current classification system.
Consequently, the Dimensional Approaches to Psychiatric Classification Work Group was convened
in 2006 to critically appraise the use of dimensional constructs in psychiatric diagnostic systems.
Resultant papers appeared in a special issue of the International Journal of Methods in Psychiatric
Research (Allardyce, Suppes, & van Os, 2007; Andrews et al., 2007; Kraemer, 2007; Lopez, Compton,
Grant, & Breiling, 2007; Regier, 2007; Shear, Bjelland, Beesdo, Gloster, & Wittchen, 2007). The
authors of these papers agreed that psychiatric disorders can be viewed not only in categorical terms
(i.e., as absent or present) but can also be assessed dimensionally via measures such as frequency and
severity. There is now strong evidence suggesting that the symptoms of psychiatric disorders exist on
a continuum of severity and that the cut-off point on this continuum at which a clinical diagnosis is
made and treatment is offered (that is, where ‘normal’ is differentiated from ‘abnormal’) is largely
arbitrary. Nevertheless, the Work Group’s proposal for the DSM-5 was not to substitute dimensional
scales for categorical diagnoses, but to add a dimensional option to the usual categorical diagnoses
(e.g., major depressive disorder of varying degrees of severity including mild, moderate or severe).
The introduction in the DSM-5 of such adjunct dimensional measures is an initial, modest step towards
a dimensional diagnostic system.
Dimensional models of psychopathology not only argue that the boundary between normality
and abnormality (or the presence or absence of disorder) is indistinct, they also challenge the notion
that the hundreds of diagnostic categories contained in the current version of the DSM represent
separate, independent disorders. As explained previously, the pattern and rates of co-occurrence
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among the mental disorders are thought to reflect the existence of a shared underlying dimension of
psychopathology based on a common causation (Kessler et al., 2005; Krueger, 1999; Slade & Watson,
2006). Several research groups have sought to identify underlying dimensions that explain the co-
occurrence of mental disorders. Their ultimate aim is to replace the many categories of mental disorders
in the DSM with a small number of basic dimensions. For example, Watson (2005) has proposed a
model in which the anxiety, depressive and bipolar disorders of the DSM exist along a continuum of
increasing severity (rather than constituting different disorders), which would explain their observed
comorbidity. Similarly, Krueger, Markon, Patrick, and Iacono (2005) proposed a dimensional model
of disorders such as conduct disorder, antisocial personality disorder and substance use disorders.
Although there has been a large amount of research devoted to the issue of a dimensional
understanding of underlying psychopathology, no agreement has yet been reached on what parameters
the dimensions should assess or how many dimensions are necessary to describe the entire domain of
psychopathology. Partly because of this lack of consensus, a dimensional diagnostic system reflecting
common underlying factors was not introduced in the DSM-5. Nevertheless, a tentative step towards a
dimensional approach is reflected in the new organisational structure of the DSM-5: specific disorders
with similar symptom patterns, high levels of comorbidity, shared genetic or environmental risk
factors, or common treatment responses have been placed in the same chapter and disorders thought
to be related to each other have been placed in adjacent chapters. For example, as shown in Table 1.4,
the chapter containing obsessive-compulsive and related disorders is placed adjacent to the chapter
containing anxiety disorders. The adjacent placement emphasises the commonalities between these
two clusters of disorders, both of which, together with depressive disorders, belong to the overarching
internalising group of disorders. Similarly, specific disorders thought to express an underlying
externalising factor (e.g., substance use disorders or conduct disorders) have been clustered together to
emphasise their similarity and possible relatedness. This regrouping of mental disorders in the DSM-5
is intended to stimulate research across the various categories and to enhance the understanding of
underlying commonalities. However, the placement of some specific disorders in larger categories has been
controversial. For example, although attention-deficit/
hyperactivity disorder (ADHD) has been placed within
the ‘Neurodevelopmental Disorders’ chapter in the
DSM-5, empirical findings also support its placement
within the ‘Disruptive, Impulse-control, and Conduct

Disorders’ chapter. Future research might change the
placement of individual disorders in further revisions
of the DSM.
During the development of the DSM-5 it was
predicted that a change towards a dimensional system
was likely to occur first in the field of personality
disorders, where the most research evidence for
common dimensions underlying the current categories
exists (Krueger, Skodol, Livesley, Shrout, & Yueqin,
2007; Samuel & Widiger, 2006). Indeed, the DSM-5
Personality and Personality Disorders Work Group
developed a new dimensional conceptualisation of
personality disorders, characterised by impairments
in various underlying personality traits. However,
despite the well-documented problems posed by the
previous categorical system, the DSM-5 Task Force
decided that it was premature to include this alternative
DAL
conceptualisation of personality disorders in the

The current system for diagnosing mental DSM-5. Instead, the same criteria found in the DSM-IV
disorders has generated much debate. were retained and the alternative conceptualisation of
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personality disorders was included in the section on ‘Conditions for further study’ in the DSM-5. These
diagnostic criteria are expected to stimulate further research in the field of psychiatric classification
(APA, 2013).
Given the usual time lag of 10–15 years between new research findings and their incorporation into
formal diagnostic systems, the DSM-5 is not radically different from previous editions. Nevertheless,
recent developments indicate that the mental health field is now moving towards a re-evaluation of
commonly accepted ideas about the nature of mental disorders. The outcomes of such investigations
will aid in the development of a dimensional approach to diagnosis that is likely to replace the current
categorical approach in coming years. Moreover, these developments illustrate the way in which
the foundation of the DSM mental disorder categories is increasingly moving from expert clinical
consensus to one based on extensive empirical research.
SUMMARY
This chapter aimed to serve as a critical introduction to historical and current conceptualisations of abnormality and mental disorder.
Several different perspectives on the classification, causation and treatment of mental disorders were discussed, highlighting their
strengths and limitations. The development of one of the main systems for diagnosing mental disorders, the DSM, was discussed
in terms of the improvements in its successive editions and the ongoing debates regarding future improvements to this diagnostic
system. It is hoped that an awareness of these issues will enable future researchers and clinicians to be mindful of the fact that the
current diagnostic system is a work in progress and that future diagnostic systems, and the mental disorders contained therein,
may be radically different from the ones currently in use as society’s common vocabulary to communicate about mental health and
disorder.
KEY TERMS
affect. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 differential diagnosis. . . . . . . . . . . . . . . . 33 psychodynamic theories. . . . . . . . . . . . . 16
aversion therapy. . . . . . . . . . . . . . . . . . . . 19 double-blind experiments. . . . . . . . . . . . 17 psychological approaches. . . . . . . . . . . 11
behavioural approach. . . . . . . . . . . . . . . 17 ego. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 psychomotor agitation. . . . . . . . . . . . . . . 33

behavioural experiment . . . . . . . . . . . . . 24 electroconvulsive psychopathology. . . . . . . . . . . . . . . . . . . 26
biological approach. . . . . . . . . . . . . . . . . . 9 therapy (ECT) . . . . . . . . . . . . . . . . . . . . . . . 9 psychopharmacological
biopsychosocial approach. . . . . . . . . . . 28 enlarged ventricles . . . . . . . . . . . . . . . . . 10 treatment. . . . . . . . . . . . . . . . . . . . . . . . . . 10
case study method. . . . . . . . . . . . . . . . . . 17 humanistic approach. . . . . . . . . . . . . . . . 25 psychoses. . . . . . . . . . . . . . . . . . . . . . . . . 15
classical conditioning . . . . . . . . . . . . . . . 18 hypersomnia. . . . . . . . . . . . . . . . . . . . . . . 33 psychosurgery . . . . . . . . . . . . . . . . . . . . . . 9
clinically significant . . . . . . . . . . . . . . . . . . 5 id. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 psychotherapy . . . . . . . . . . . . . . . . . . . . . 11
cognitive approach . . . . . . . . . . . . . . . . . 21 Insomnia . . . . . . . . . . . . . . . . . . . . . . . . . . 29 reality principle. . . . . . . . . . . . . . . . . . . . . 13
cognitive behaviour therapy International Classification of reliability. . . . . . . . . . . . . . . . . . . . . . . . . . . 32
(CBT). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Diseases and Related Health selective serotonin
cognitive restructuring. . . . . . . . . . . . . . 24 Problems (ICD) . . . . . . . . . . . . . . . . . . . . . 28 reuptake inhibitors (SSRIs). . . . . . . . . . . 10
comorbidity. . . . . . . . . . . . . . . . . . . . . . . . 34 interrater reliability. . . . . . . . . . . . . . . . . . 33 self-actualisation. . . . . . . . . . . . . . . . . . . . 25
conditioned responses (CR). . . . . . . . . . 18 libido. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 superego. . . . . . . . . . . . . . . . . . . . . . . . . . 13
conditioned stimulus (CS). . . . . . . . . . . . 18 maladaptive. . . . . . . . . . . . . . . . . . . . . . . . . 4 syndromes. . . . . . . . . . . . . . . . . . . . . . . . . . 7
conditions of worth . . . . . . . . . . . . . . . . . 26 modelling. . . . . . . . . . . . . . . . . . . . . . . . . . 20 systematic desensitisation. . . . . . . . . . . 19
control groups. . . . . . . . . . . . . . . . . . . . . . 17 morality principle. . . . . . . . . . . . . . . . . . . 13 therapeutic alliance. . . . . . . . . . . . . . . . . 26
defence mechanisms. . . . . . . . . . . . . . . 14 neuroses. . . . . . . . . . . . . . . . . . . . . . . . . . 15 token economies. . . . . . . . . . . . . . . . . . . 20
dementia. . . . . . . . . . . . . . . . . . . . . . . . . . . 6 operant conditioning. . . . . . . . . . . . . . . . 18 unconditional positive regard. . . . . . . . 25
diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . 30 person-centred therapy . . . . . . . . . . . . . 26 unconditioned responses (UR). . . . . . . . 18
Diagnostic and Statistical Manual pleasure principle. . . . . . . . . . . . . . . . . . . 13 unconditioned stimuli (US) . . . . . . . . . . . 18
of Mental Disorders (DSM). . . . . . . . . . . 28 pre-frontal cortex. . . . . . . . . . . . . . . . . . . . 9 unconscious . . . . . . . . . . . . . . . . . . . . . . . 12
diathesis-stress model. . . . . . . . . . . . . . . 28 psychoanalysis. . . . . . . . . . . . . . . . . . . . . 11 validity . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
rie66620_ch01_001-040.indd 37 07/31/17 05:14 PM

REVIEW QUESTIONS
LO 1.1
1.1 What are the four main criteria that are used to differentiate abnormal behaviour from normal behaviour?
1.2 How does Wakefield’s notion of ‘harmful dysfunction’ help to differentiate the concept of mental disorder from
the concepts of medical disorder and social deviance?
1.3 In what ways does the classification of psychological disorders (e.g., depression) differ from the classification of
medical disorders (e.g., cancer)?
LO 1.2
1.4 What were the main changes in behaviourism that allowed the development of the cognitive-behavioural
perspective?
1.5 How is the behavioural approach to understanding mental disorders fundamentally different from the
psychoanalytic approach?
1.6 If an individual inherits a biological vulnerability for a mental disorder, does this mean that he/she is destined to
develop a disorder? Explain using the biopsychosocial model of mental disorders.
LO 1.3
1.7 What were the main limitations of the DSM-I and DSM-II?
1.8 How can the reliability of a mental disorder diagnosis be improved?
1.9 In what ways did the DSM-III differ from its predecessors?
1.10 List the main limitations of the categorical system of classification reflected in the DSM-III and beyond.
REFERENCES
Allardyce, J., Suppes, T., & van Os, J. (2007). Dimensions and Andrews, G., Hall, W., Teeson. M., & Henderson, T. (1999).
the psychosis phenotype. International Journal of Methods in The mental health of Australians. Canberra: Commonwealth
Psychiatric Research, 16, S34–S40. Department of Health and Aged Care.
American Psychiatric Association (1952). Diagnostic and statistical Australian Psychological Society (2010). Evidence-based
manual of mental disorders. Washington, DC: Author. psychological interventions in the treatment of mental disorders: A
American Psychiatric Association (1968). Diagnostic and statistical literature review (3rd ed.). Melbourne: Author.
manual of mental disorders (2nd ed.). Washington, DC: Author. Ayllon, T., & Azrin, N. (1968). The token economy: A motivational
American Psychiatric Association (1980). Diagnostic and statistical system for therapy and rehabilitation. East Norwalk: Appleton-
manual of mental disorders (3rd ed.). Washington, DC: Author. Century-Crofts.
American Psychiatric Association (1987). Diagnostic and statistical Baker, D. B., & Benjamin, L. T. (2000). The affirmation of
manual of mental disorders (3rd ed., revised). Washington, DC: the scientist-practitioner: A look back at Boulder. American
Author. Psychologist, 55, 241–247.
American Psychiatric Association (1994). Diagnostic and Bandura, A. (1977). Social learning theory. Oxford: Prentice-Hall.
statistical manual of mental disorders (4th ed.). Washington, DC: Barton, W. E. (1987). The history and influence of the American
Author. Psychiatric Association. Washington, DC: American Psychiatric
American Psychiatric Association (2000). Diagnostic and statistical Press.
manual of mental disorders (4th ed., text revision). Washington, Bech, P. (2002). Pharmacological treatment of depressive disorders:
DC: Author. A review. In M. Maj & N. Sartorius (Eds.), Depressive disorders
American Psychiatric Association (2013). Diagnostic and statistical (pp. 89–129). Chichester: Wiley.
manual of mental disorders (5th ed.). Arlington: Author. Beck, A. T. (1976). Cognitive therapy and the emotional disorders.
Andreasen, N. (2001). Neuroimaging and neurobiology of New York: International Universities Press.
schizophrenia. In K. Miyoshi, C. M. Shapiro, M. Gaviria, & Y. Beck, A. T., Emery, G., & Greenberg, R. L. (1985). Anxiety disorders
Morita (Eds.), Contemporary neuropsychiatry (pp. 265–271). and phobias: A cognitive perspective. New York: Basic Books.
Tokyo: Springer-Verlag. Beck, A. T., & Rector, N. E. (2005). Cognitive approaches to
Andrews, G., Brugha, T., Thase, M. E., Duffy, F. F., Rucci, P., & Slade, schizophrenia: Theory and therapy. Annual Review of Clinical
T. (2007). Dimensionality and the category of major depressive Psychology, 56, 577–606.
episode. International Journal of Methods in Psychiatric Research, Bell, G. (2005). The worried well: The depression epidemic and the
16, S41–S51. medicalisation of our sorrows. Quarterly Essay, 18, 1–75.
rie66620_ch01_001-040.indd 38 07/31/17 05:14 PM

Benjamin, L. T. (2005). A history of clinical psychology as a Horney, K. (1922/1967). Feminine psychology. New York: Norton.
profession in America (and a glimpse at its future). Annual Review Horwitz, A. V. (2003). Creating mental illness. Chicago: The
of Clinical Psychology, 56, 1–30. University of Chicago Press.
Breuer, J., & Freud, S. (1895/1955). Studies on hysteria. In J. Strachey Hyman, S. E. (1998). NIMH during the tenure of Director Steven
(Ed.), The standard edition of the complete psychological works of E. Hyman, M. D. (1996–present): The now and future of NIHM.
Sigmund Freud (Vol. 2). London: Hogarth Press. American Journal of Psychiatry, 155 (Supp.), 36–40.
Brewin, C. R. (1996). Theoretical foundations of cognitive-behavior Kamin, L. J. (1969). Predictability, surprise, attention and
therapy for anxiety and depression. Annual Review of Psychology, conditioning. In R. Church & B. Campbell (Eds.), Punishment and
47, 33–57. aversive behavior (pp. 279–296). New York: Appleton-Century-
Broome, M., & Bortolotti, L. (2010). What’s wrong with ‘mental’ Crofts.
disorders? Psychological Medicine, 40, 1783–1785. Kessler, R. C., Chiu, W. T., Demler, O., & Walters, E. E. (2005).
Brülde, B., & Radovic, F. (2006). What is mental about mental Prevalence, severity, and comorbidity of 12-month DSM-IV
disorder? Philosophy, Psychiatry, & Psychology, 13, 99–116. disorders in the National Comorbidity Survey Replication. Archives
Burns, D. D. (1980). Feeling good: The new mood therapy. New of General Psychiatry, 62, 617–627.
York: William Morrow & Company. Kessler, R. C., McGonagle, K. A., Zhao, S., Nelson, C. B., Hughes,
Butler, A. C., Chapman, J. E., Forman, E. M., & Beck, A. T. (2006). M., Eshleman, S., . . . Kendler, K. S. (1994). Lifetime and
The empirical status of cognitive-behavioral therapy: A review of 12-month prevalence of DSM-III-R psychiatric disorders among
meta-analyses. Clinical Psychology Review, 26, 17–31. persons aged 15–64 in the United States: Results from the National
Chambless, D. L., & Ollendick, T. H. (2001). Empirically supported Comorbidity Survey. Archives of General Psychiatry, 51, 8–19.
psychological interventions: Controversies and evidence. Annual Kraemer, H. C. (2007). DSM categories and dimensions in clinical
Review of Psychology, 52, 685–716. and research contexts. International Journal of Methods in
Charney, D. S., Barlow, D. H., Botteron, K., Cohen, J. D., Goldman, Psychiatric Research, 16, S8–S15.
D., Gur, R. E., . . . Zalcman, S. J. (2002). Neuroscience research Krueger, R. F. (1999). The structure of common mental disorders.
agenda to guide development of a pathophysiologically based Archives of General Psychiatry, 56, 921–926.
classification system. In D. J. Kupfer, M. B. First, & D. A. Regier Krueger, R. F., Markon, K. E., Patrick, C. P., & Iacono, W. G. (2005).
(Eds.), A research agenda for DSM-V (pp. 31–85). Washington, Externalizing psychopathology in adulthood: A dimensional-
DC: American Psychiatric Association. spectrum conceptualization and its implications for DSM–V.
Clark, L. A., Watson, D., & Reynolds, S. (1995). Diagnosis and Journal of Abnormal Psychology, 114, 537–550.
classification of psychopathology. Annual Review of Psychology, Krueger, R. F., & Piasecki, T. M. (2002). Toward a dimensional
46, 121–153. and psychometrically informed approach to conceptualising
David, D. (Ed.) (2006). A critical review of the current trends in psychopathology. Behaviour Research and Therapy, 40,
psychotherapy and clinical psychology. New York: Nova Science 485–499.
Publishers. Krueger, R. F., Skodol, A. E., Livesley, W. J., Shrout, P. E., & Yueqin,
Ellis, A. (1962). Reason and emotion in psychotherapy. New York: H. (2007). Synthesizing dimensional and categorical approaches
Carol Publishing Group. to personality disorders: Refining the research agenda for DSM-V
Eysenck, H. (1952). The effects of psychotherapy: An evaluation. Axis II. International Journal of Methods in Psychiatric Research,
Journal of Consulting and Clinical Psychology, 16, 319–324. 16, S65–S73.
Fink, M. (2001). Convulsive therapy: A review of the first 55 years. Kupfer, D. J., First, M. B., & Regier, D. A. (Eds.) (2002). A research
Journal of Affective Disorders, 63, 1–15. agenda for DSM-V. Washington, DC: American Psychiatric
Firestone, R. W. (2002). The death of psychoanalysis and depth Association.
therapy. Psychotherapy: Theory, Research, Practice, and Training, Lilienfeld, S. O., & Marino, L. (1995). Mental disorder as a Roschian
39, 223–232. concept: A critique of Wakefield’s ‘harmful dysfunction’ analysis.
First, M. B., & Wakefield, J. C. (2010). Defining ‘mental disorder’ in Journal of Abnormal Psychology, 104, 411–420.
DSM-V. Psychological Medicine, 40, 1779–1782. Littlefield, L. (2013). Executive Director’s report: Seven years of
Freud, S. (1900/1997). The interpretation of dreams. Ware: Wordsworth. Better Access. InPsych, 35.
Freud, S. (1923/1960). The ego and the id. London: Norton. Littlefield, L. (2017). Executive Director’s report: Ten years of Better
Freud, S. (1933/1965). New introductory lectures on psychoanalysis. Access. InPsych, 39.
London: Norton. Lopez, M. F., Compton, W. M., Grant, B. F., & Breiling, J. P.
Gilligan, C. (1982). In a different voice: Psychological theory and (2007). Dimensional approaches in diagnostic classification: A
women’s development. Cambridge: Harvard University Press. critical appraisal. International Journal of Methods in Psychiatric
Hecker, E. (1871/2004). On the origin of the clinical standpoint in Research, 16, S6–S7.
psychiatry. History of Psychiatry, 15, 345–360. Lovibond, P. F. (1993). Conditioning and cognitive-behaviour
Hofmann, S. G., Asnaani, A., Vonk, I. J. J., Sawyer, A. T., & Fang, therapy. Behaviour Change, 10, 119–130.
A. (2012). The efficacy of cognitive behavioural therapy: A review Ma, J., Lee, K. V., & Stafford, R. S. (2005). Depression treatment
of meta-analyses. Cognitive Therapy and Research, 36, 427–440. during outpatient visits by U.S. children and adolescents. Journal
Hollon, S. D., Stewart, M. O., & Strunk, D. (2006). Enduring effects of Adolescent Health, 37, 434–442.
for cognitive behavior therapy in the treatment of depression and Mahler, M. S., Pine, F., & Bergman, A. (1975). The psychological
anxiety. Annual Review of Psychology, 57, 285–315. birth of the human infant. New York: Basic Books.
rie66620_ch01_001-040.indd 39 07/31/17 05:14 PM

Maj, M., & Sartorius, N. (Eds.) (2002). Depressive disorders. Samuel, D. B., & Widiger, T. A. (2006). Clinicians’ judgments of
Chichester: Wiley. clinical utility: A comparison of the DSM–IV and five-factor
Maslow, A. H. (1970). Motivation and personality. New York: models. Journal of Abnormal Psychology, 115, 298–308.
Harper & Row. Shear, M. K., Bjelland, I., Beesdo, K., Gloster, A. T., & Wittchen,
Mathews, A., & MacLeod, C. (2005). Cognitive vulnerability to H.-U. (2007). Supplementary dimensional assessment in anxiety
emotional disorders. Annual Review of Clinical Psychology, 56, disorders. International Journal of Methods in Psychiatric
167–195. Research, 16, S52–S64.
McNally, R. J. (2001). On Wakefield’s harmful dysfunction analysis Slade, T., & Watson, D. (2006). The structure of common DSM-IV
of mental disorder. Behaviour Research and Therapy, 39, 309–314. and ICD-10 mental disorders in the Australian general population.
Misbach, J., & Stam, H. J. (2006). Medicalizing melancholia: Psychological Medicine, 36, 1593–1600.
Exploring profiles of psychiatric professionalization. Journal of Stafford, M. R., Jackson, H., Mayo-Wilson, E., Morrison, A. P.,
the History of the Behavioral Sciences, 42, 41–59. & Kendall, T. (2013). Early interventions to prevent psychosis:
Moynihan, R., & Cassels, A. (2005). Selling sickness: How drug Systematic review and meta-analysis. British Medical Journal,
companies are turning us all into patients. Sydney: Allen & Unwin. 346, f185.
O’Neil, W. M. (1987). A century of psychology in Australia. Sydney: Szasz, T. S. (1961). The myth of mental illness. New York: Harper
Sydney University Press. & Row.
Pirkis, J., Harris, M., Hall, W., & Ftanou, M. (2011). Evaluation Szasz, T. (1971). The sane slave. American Journal of Psychotherapy,
of the Better Access to Psychiatrists, Psychologists and General 25, 228–239.
Practitioners through the Medicare Benefits Schedule initiative: Tolman, E. C. (1948). Cognitive maps in rats and man. Psychological
Summative evaluation. Melbourne: Centre for Health Policy Review, 55, 189–208.
Programs and Economics. Tolman, C. W., & Maiers, W. (Eds.) (1991). Critical psychology:
Popper, K. (1968). The logic of scientific discovery. London: Contributions to an historical science of the subject. Cambridge:
Hutchinson. Cambridge University Press.
Regier, D. A. (2007). Dimensional approaches to psychiatric Turtle, A. M. (1995). The forerunners and foundation of the Australian
classification: Refining the research agenda for DSM-V: An Journal of Psychology. Australian Journal of Psychology, 47,
introduction. International Journal of Methods in Psychiatric 123–127.
Research, 16, S1–S5. Valenstein, E. S. (1998). Blaming the brain: The truth about drugs
Rogers, C. R. (1957). The necessary and sufficient conditions of and mental health. New York: Free Press.
therapeutic personality change. Journal of Consulting Psychology, Wakefield, J. C. (1992). The concept of mental disorder: On the
21, 95–103. boundary between biological facts and social values. American
Rogers, C. (1961). On becoming a person: A therapist’s view of Psychologist, 47, 373–388.
psychotherapy. London: Constable. Wakefield, J. C. (1999). Evolutionary versus prototype analyses of
Rosenhan, D. L. (1973). On being sane in insane places. Science, the concept of disorder. Journal of Abnormal Psychology, 108,
179, 250–285. 374–399.
Rounsaville, B. J., Alarcón, R. D., Andrews, G., Jackson, J. S., Watson, D. (2005). Rethinking the mood and anxiety disorders: A
Kendell, R. E., & Kendler, K. (2002). Basic nomenclature issues quantitative hierarchical model for DSM–V. Journal of Abnormal
for DSM-V. In D. J. Kupfer, M. B. First, & D. A. Regier (Eds.), Psychology, 114, 522–536.
A research agenda for DSM-V (pp. 1–31). Washington, DC: Watson, J. B. (1913). Psychology as the behaviorist views it.
American Psychiatric Association. Psychological Review, 20, 158–177.
Routh, D. K. (1998). Hippocrates meets Democritus: A history of Watson, J. B., & Rayner, R. (1920). Conditioned emotional reactions.
psychiatry and clinical psychology. In A. S. Black & M. Herren Journal of Experimental Psychology, 3, 1–14.
(Eds.), Comprehensive Clinical Psychology (pp. 1–48). New York: Widiger, T. A., & Sankis, L. M. (2000). Adult psychopathology:
Pergamon Press. Issues and controversies. Annual Review of Psychology, 51,
Rubinstein, S., & Caballero, B. (2000). Is Miss America an 377–404.
undernourished role model? Journal of the American Medical Wolpe, J. (1958). Psychotherapy by reciprocal inhibition. Stanford:
Association, 283, 1569. Stanford University Press.
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CHAPTER 2
Anxiety disorders
Peter McEvoy
Maree Abbott
CHAPTER OUTLINE
● The nature and types of anxiety disorders
● Specific phobias
● Panic disorder and agoraphobia
● Social anxiety disorder
● Generalised anxiety disorder (GAD)
● Summary

2.1 Describe the nature of anxiety and models regarding the aetiology of anxiety disorders.
2.2 Describe the diagnostic criteria, epidemiology, aetiology and treatments for specific phobias.
2.3 Describe the diagnostic criteria, epidemiology, aetiology and treatments for panic disorder and agoraphobia.
2.4 Describe the diagnostic criteria, epidemiology, aetiology and treatments for social anxiety disorder.
2.5 Describe the diagnostic criteria, epidemiology, aetiology and treatments for generalised anxiety disorder.
ANXIETY DISORDERS: AN AUSTRALASIAN FOCUS

Anxiety is a common and normal emotion that, like all emotions, can provide us with useful information. In fact, anxiety is
so useful that our survival depends on it. When we perceive a threat in our environment, the symptoms of anxiety help
us to respond to the threat in a way that maximises our chances of survival. Anxiety is accompanied by bodily symptoms
(such as muscle tension and increased respiration rate), cognitions (such as thoughts or images of past, present and/
or future danger) and behaviours (freezing to appraise the threat, fighting the threat or fleeing from the threat). Anxiety
disorders arise when the perception of threat, and therefore the persistence or intensity of the anxiety response, is
clearly out of proportion to the actual threat. The threshold for determining whether someone’s anxiety could meet
criteria for an anxiety disorder is if they are debilitated in some important way—for instance, if the anxiety interferes with
their ability to maintain positive social relationships, complete their studies or perform at work.
The most recent National Survey of Mental Health and Wellbeing included Australian adults aged 16–85 years, and
found that 45 per cent of Australians will experience a mental disorder in their lifetime, with anxiety disorders being the
most common (Australian Bureau of Statistics, 2008; Slade, Johnston, Oakley, Andrews, & Whiteford, 2009). In 2016,
Mission Australia conducted a survey of nearly 22 000 young Australians aged 15–19 years (Bailey et al., 2016). While this
survey did not include any questions about anxiety specifically, it did look at the related construct of stress and found
that coping with stress was the most important issue concerning young people. In fact, almost half (44%) of young people
stated that they were either very or extremely concerned about this issue. Thus, coping with stress outranked many
other important issues facing young people such as study problems, body image, depression and family conflict.
Given the high rates of anxiety disorders and stress, these conditions clearly do not discriminate, affecting people
of all genders, ages, professions and socioeconomic circumstances. For example, Australian swimmer and Olympic gold
continued
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medallist Susie O’Neill has spoken and written extensively

about her experiences with severe social anxiety. Despite all
her success, Susie still feared speaking to strangers and being
the centre of attention while standing on the podium after
winning a race. Australian actors Rebecca Gibney and Garry
MacDonald have also spoken about their crippling anxiety and
panic attacks. Although these famous Australians have spoken
out, many others from all walks of life are suffering in silence.
Many assume that they are alone or that their anxiety reflects
negatively on them. Yet many people suffer from anxiety, and
the fact that they continue to achieve their life goals, even with
anxiety, is a sign of considerable strength and fortitude.
DAL
Given this reluctance to seek help, it is perhaps not
surprising that only one in five people with anxiety as their Anxiety disorders are the most common class of
principal complaint consult with a health professional for mental disorders according to the most recent
their mental health problem, and only half of these people National Survey of Mental Health and Wellbeing.
receive treatments known to be effective for anxiety
disorders (Issikadis & Andrews, 2002). Treatments for anxiety
disorders can be highly effective, but recognition and acceptance of the symptoms is the first critical step to seeking
help. The Australian national depression initiative, beyondblue, is one organisation aiming to help people recognise if
they have an anxiety disorder and encouraging them to seek help (www.beyondblue.org.au/the-facts/anxiety).
The present chapter will first describe the nature of fear and anxiety disorders. The range of anxiety disorders will then
be discussed, including specific phobias, panic disorder, agoraphobia, social anxiety disorder and generalised anxiety
disorder. For each disorder, information regarding its diagnosis, epidemiology, aetiology and treatment will be presented.
LO 2.1 Fear and anxiety disorders

The nature of fear and anxiety disorders
Fear is the immediate alarm reaction triggered by a perceived danger. Cannon (1929) described the
fight or flight fear reaction to danger as the fight or flight response. As shown in Figure 2.1, this is an alarm response
response in which the body reacts to prepare itself to deal with danger. The hormone adrenaline (also known
Physiological as epinephrine) is released through the bloodstream to initiate bodily changes. For instance, blood
changes in the pressure increases, with blood flow diverted towards the large muscle groups, and breathing increases
human body that
to provide extra oxygen for both the brain and muscles. Vision becomes more acute as the pupils dilate,
occur in response
to a perceived hearing improves and immediately unnecessary activities, such as digestion and immune responses,
threat, including are inhibited. Together these responses allocate the body’s resources so that it can use the appropriate
elevated heart behaviours of freezing (while the danger is appraised), flight (when the danger is approaching) and
rate, metabolism, fight (if the danger is unavoidable).
blood pressure, Acknowledging the capacity of the fight or flight response to prepare an organism to deal more
breathing and effectively with a threat, Barlow (2002) has described it as a ‘true alarm’. That is, fear occurs in
muscle tension;
response to a direct danger, such as the impending attack of a wild animal. True alarms can be
these changes
prepare the body
contrasted with ‘false alarms’ in which the fight or flight response occurs in situations that do not
for resisting or represent an immediate physical threat. False alarms are the hallmark of anxiety disorders.
fleeing from the Individuals differ in terms of the ease with which the alarm reaction is triggered (Andrews et al.,
source of threat. 2003) and three separate but related vulnerabilities have been identified that increase the sensitivity of
the alarm trigger. This triple vulnerability includes (1) biological factors, (2) generalised psychological
factors and (3) specific psychological factors (Barlow, 2002).
A generalised biological vulnerability comprises the first component of this triple vulnerability.
One example of a biological vulnerability is the fact that individuals seem to inherit a general
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Chapter 2 Anxiety disorders 43
Focus mind
Adrenaline release
Pupils dilate
Breathe faster
Heart rate and Sweat

blood pressure Clotting increases
increase
Digestion decreases
Close bowel
and bladder
Muscles tense
FIGURE 2.1 The fight or flight response
predisposition towards anxiety and depressive disorders (Andrews, Stewart, Morris-Yates, & Holt,
1990). This clustering of emotional disorders around a common genetic vulnerability has been called
‘the general neurotic syndrome’.
The second factor entails a generalised psychological vulnerability. This includes beliefs that the
world is generally a dangerous place combined with broad expectations that events are beyond one’s
control. For example, early life experiences of stress and loss have been found to foster a sense within
the individual that s/he has minimal control over life events (Chorpita, Brown, & Barlow, 1998), and
individuals who worry that life events are beyond their control have been found to be more prone to
anxiety (Craig, Franklin, & Andrews, 1984).
The third component refers to a specific psychological vulnerability. These are psychological factors
that are specific to particular objects or situations and include factors that influence the expectation of a
negative outcome when confronted with a specific object or event. Conditioning is one way to acquire
such an expectation. During the paired occurrence of a conditioned stimulus and an aversive event (the
unconditioned stimulus), an expectation of an aversive outcome develops and fear, as a conditioned
response, occurs (Lovibond & Shanks, 2002). For example, if a person is bitten by a dog, then the
processes of conditioning would result in the individual anticipating injury if confronted by that dog negative
in the future. The individual would be increasingly likely to be afraid in the presence of the dog and reinforcement
would avoid it if possible. The relief from anxiety caused by escape and avoidance would increase the Increasing the
probability that future avoidance would occur through the process of negative reinforcement. In other frequency of
words, the behaviours of escape and avoidance have been negatively reinforced (i.e., rewarded) as a a behaviour
result of the reduction in anxiety. In addition, the process of generalisation would ensure that the fear (e.g., escape
or avoidance)
and avoidance would extend beyond the particular dog to other dogs and signals of the presence of through the
dogs (e.g., parks). The initial response to the dog would be a true alarm, but thereafter many of the removal of
alarms would be false. an aversive
Conditioning is a direct way to learn about potential dangers, but indirect pathways include experience
information and vicarious acquisition (Rachman, 1991). For example, individuals can acquire a fear (e.g., anxiety).
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of wolves and bears even though there is limited opportunity to experience aversive outcomes with
these animals. The informational pathway describes the development of fear following the verbal
transmission of danger-related information from others. In a study by researchers from the University
of Queensland and Macquarie University, New South Wales, Barrett, Rapee, Dadds, and Ryan (1996)
found that anxious children were even more avoidant of feared stimuli after discussing a potentially
threatening situation with a parent. Thus, there is an interaction between the child and the parent, such
that overly protective parental responses (e.g., warnings of danger) can amplify the anxiety reaction.
In vicarious acquisition, fear is acquired through the process of modelling, whereby an individual
observes another responding with fear to a threatening object or situation. The role of modelling
has been demonstrated in the work of Cook and Mineka (1990) with rhesus monkeys. This research
involved an experimental paradigm in which laboratory-reared monkeys (which have no fear of snakes)
observed wild-reared monkeys (which exhibit a fear of snakes) in the presence of a snake. Following
a single training session, the observer monkeys acquired a lasting fear of snakes.
The common thread running through the conditioning, informational and vicarious acquisition
pathways to fear is that, despite their differences, they all contribute to an individual developing
an expectation that, given a particular set of circumstances, an aversive outcome is probable. This
expectation of a negative outcome is, in turn, associated with the fear and avoidance of feared situations
characterising anxiety disorders.
Putting these three independent vulnerabilities together, anxiety disorders are caused by generalised
biological, generalised psychological and specific psychological vulnerabilities that lower the threshold
for the triggering of a false alarm reaction (i.e., a fear reaction to benign environmental occurrences).
Barlow’s (2002) triple vulnerability model is shown in Figure 2.2. It is important to recognise that the
specific vulnerabilities are relative rather than complete. That is, many of the specific psychological
vulnerabilities will be associated with most anxiety disorders because comorbidity is the norm rather
than the exception in clinical samples (i.e., it is likely that individuals will have more than one anxiety
disorder), and the specific vulnerabilities are likely to be correlated with general distress, which is a
common feature across emotional disorders. However, the specific vulnerabilities are thought to be
more strongly associated with, and to play a more important role in maintaining, particular disorders
(Brown & Naragon-Gainey, 2013).
Generalised biological
vulnerability
Specific psychological ANXIETY

vulnerability DISORDER
Generalised psychological
vulnerability
FIGURE 2.2 Characterisation of Barlow’s (2002) triple vulnerability leading to an anxiety disorder
While the triple vulnerability model emphasises similarities between the various anxiety disorders,
other approaches seek to identify areas of both similarity and difference across these conditions. One
such approach is to focus on three dimensions of emotions, namely, negative affectivity, positive
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affectivity and autonomic arousal. Watson and Clark (1984) distinguished the tendency to experience autonomic
negative affect from both positive affect and arousability of the autonomic nervous system (see the nervous system
coloured ovals in Figure 2.3). Negative affectivity is subjective distress involving anxiety, disgust Part of the
and anger. Positive affectivity involves feeling enthusiastic, active and alert. Therefore, low positive peripheral
nervous system
affectivity describes feelings of sadness and lethargy. These dimensions appear important in identifying that regulates
factors that are shared across the anxiety disorders as well as those that are unique. involuntary
functions such
as heart rate,
digestion,
respiration rate
Negative and perspiration;
affectivity includes the
sympathetic and
parasympathetic
nervous systems.
Low
Autonomic
positive
arousal
affectivity
Panic & Social

GAD OCD Depression
agoraphobia phobia
FIGURE 2.3 The relationships between three dimensions of emotion across the anxiety disorders and
depression as found by Brown and Barlow (2009)
One example of this research is described by Brown and Barlow (2009) and the results are
displayed in Figure 2.3. Each of the emotional disorders investigated (i.e., anxiety disorders, OCD
and depression) share a common feature: they are all associated with elevations in negative affectivity
(indicated by the arrows from the oval depicting negative affectivity). Thus, people with these disorders
are high on trait anxiety (one aspect of negative affectivity) and hence are more likely to experience
false alarms. Yet the disorders can also be distinguished from each other in terms of these emotional
dimensions. Specifically, social phobia and depression are distinguished from the other disorders by
the absence of positive affectivity in addition to the elevated negative affectivity (indicated by the
arrows from the oval reflecting low positive affectivity). In addition, agoraphobia and panic disorder
are distinguishable by their association with elevations in autonomic arousal (indicated by an arrow
from the oval depicting autonomic arousal). One important feature of this research is that it shows
both the common and the unique features of psychological disorders by revealing the extent to which
they appear to be extreme variants on three underlying dimensions of emotion.
Types of anxiety disorders

Among the anxiety disorders listed in the current and fifth edition of the Diagnostic and Statistical
Manual of Mental Disorders (DSM-5; American Psychiatric Association [APA], 2013) are specific
phobia, panic disorder, agoraphobia, social anxiety disorder and generalised anxiety disorder. Each of
these conditions is briefly described in Table 2.1. Prior to the DSM-5, obsessive-compulsive disorder
and posttraumatic stress disorder were also classified as anxiety disorders, but each of these conditions
is now contained in a separate category.
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TABLE 2.1 A summary of the anxiety and related disorders from the DSM-5 included in this chapter
DISORDER DESCRIPTION
Specific phobia Marked and persistent fear in response to the presence or
anticipation of a specific object or situation
Panic disorder Recurrent unexpected panic attacks
Agoraphobia Anxiety about being in situations in which escape might be
difficult or help may not be available (e.g., public transport,
open spaces, enclosed spaces, crowds, outside home alone)
in the event of experiencing panic symptoms
Social anxiety disorder (social phobia) Marked fear of social situations where the person is exposed
to possible scrutiny by others (e.g., social interactions, being
observed, performing)
Generalised anxiety disorder Excessive anxiety and worry about a number of events or
activities
Source: Adapted from the Diagnostic and Statistical Manual of Mental Disorders (5th ed.), copyright 2013, American Psychiatric Association.
The tenth edition of the International Statistical Classification of Diseases and Related Health
Problems (ICD-10; World Health Organization, 1992) is an alternative classification system that
contains a chapter for the neurotic, stress-related and somatoform disorders, and includes anxiety
disorders. The ICD-10 distinguishes phobic anxiety disorders (e.g., specific phobias, agoraphobia
and social phobia) from other anxiety disorders (e.g., panic disorder, generalised anxiety disorder,
and mixed anxiety and depressive disorder). ‘Phobic anxiety disorders’ are described as those where
the anxiety is evoked predominantly in specific situations that are not currently dangerous, but which
are nonetheless avoided or endured with dread. For example, someone with social phobia feels extreme
anxiety only when in social situations, and someone with a dog phobia feels extreme anxiety only
when encountering a dog. ‘Other anxiety disorders’ are described as those for which the anxiety is
not restricted to any particular situations. For example, panic attacks within panic disorder may occur
in a variety of situations, and generalised anxiety disorder typically involves worry about all manner
of things rather than any specific situation. The ICD is currently under review and a revised version
(ICD-11) is due to be published in 2018.
LO 2.2 Specific phobias

The diagnosis of specific phobias
specific phobia According to the DSM-5 (APA, 2013), the major feature of a specific phobia is a marked (intense),
Anxiety disorder consistent (almost every time the trigger is encountered) and persistent (over a period of at least six
characterised by months) fear reaction to the presence or anticipation of a specific object or situation. The individual
extreme fear of
attempts to avoid the phobic stimulus or endures it with intense anxiety. The fear must be out of
a specific object
or situation,
proportion to the actual danger of the object or situation with respect to the person’s culture. The fear
which results in and avoidance is severe to the point of causing emotional, social or occupational disruptions. Thus,
the individual although phobic-type fears are common (Agras, Sylvester, & Oliveau, 1969), they become a phobic
avoiding the disorder when the responses are disproportionate to the objective threat and the disruption to the
object or person’s life is excessive.
situation. The DSM-5 specifies four subtypes of phobias according to the primary focus of the fear: animal;
natural environment (e.g., heights, storms and water); blood, injection and injury; and situational
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(e.g., planes, elevators and enclosed places). This subtyping can be useful for treatment. For instance,
for blood, injection and injury phobias there are distinct treatment implications stemming from the
unique properties of this disorder (Marks, 1988; Page, 1994a). Individuals with this disorder may
experience a decrease (rather than the usual increase) in blood pressure when faced with blood and
injury and are thus prone to fainting. Fainting appears to have a separate inherited predisposition
(Page & Martin, 1998) and may involve emotions such as disgust in addition to fear (Page, 2003).
Treatment needs to address the fainting and for this reason additional techniques such as applied tension
have been developed to give individuals greater control over their physiology and make fainting less
likely (Vogele, Coles, Wardle, & Steptoe, 2003). Applied tension involves the deliberate application of
muscle tension to raise blood pressure and therefore prevent fainting (Öst & Sterner, 1987).
CASE STUDY: SPECIFIC PHOBIA

John, a 35-year-old father of two children living in Western Australia, sought treatment for his dog phobia. The reason
for presenting for treatment was that his children desperately wanted a dog and he was embarrassed that his fear would
stop them from owning a pet. John was also very keen for his children to feel more comfortable around animals than he
had been throughout most of his life. He described himself as a relatively social child, but he had been afraid of dogs
since he was around 6 years of age. He remembers playing outside as a young child when he was devastated by seeing
his family’s much-loved dog run over in front of him. His family then got another dog from the local pound, but this dog
bit John on the face. He remembers the red rag used to soak up what seemed like ‘litres of blood’, and that he needed to
go to the hospital to get stitches on his cheek and forehead. From that point on, John was highly distrustful of dogs and
he started to shake whenever he encountered one at the park or in the street. He learnt to live with this fear by avoiding
parks, but he reported becoming extremely anxious and panicky when he took his young children to the park and could
not escape quickly if a dog appeared. He feared that he would not be able to protect his children if a dog approached
them, so he eventually began avoiding taking his children to parks at all. John also actively avoided pursuing friendships
with people who had pets, or insisted on meeting them at restaurants or cafes so that they could not bring their pets.
John’s wife attends fitness classes with a personal trainer at the local park and John would like to start joining her, but he
currently feels that this is impossible. He makes sure that he is locked inside his house when he knows there are going
to be fireworks (e.g., on New Year’s Eve), because he finds the sound of the local dogs barking highly distressing. He
will also listen to music using his sound-attenuating headphones until the fireworks are over and the dogs have settled
down. He relies on his wife to let him know when ‘it’s all over’ and he becomes very angry if he is interrupted while the
fireworks are still on. John also made sure that he bought an apartment after getting married in which neighbours were
not allowed to have pets—this meant that when he eventually had his own family he had a good excuse not to own a dog.
However, as his family grows, they need more space so he would like to buy a house and allow his children to own a pet.
He is ashamed to tell his children that they cannot own a dog as a result of his phobia of dogs.
The epidemiology of specific phobias

As the case study demonstrates, most specific phobias begin in childhood and early adolescence
(Öst, 1987). The prevalence of phobias is greater among children than among adults, suggesting that as
children mature, many phobias tend to remit without treatment. The typical age of onset varies across
the different phobias. For instance, claustrophobia tends to develop after adolescence, whereas animal
phobias develop at about the age of 7 (Öst, 1987). The estimated lifetime prevalence of specific phobias
is 7–9 per cent, with a female-to-male ratio of 2:1 (APA, 2013). Less than 1 per cent of individuals with
a specific phobia seek treatment, even though, in adults, phobias tend to be chronic if untreated.
The aetiology of specific phobias

There is good evidence that phobias have a heritable component (Torgersen, 1979). In terms of
psychological factors, Freud suggested that specific phobias arose from unresolved unconscious sexual
conflict (see Eysenck, 1990, for a critique). However, the contemporary understanding of the origins
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of phobias can be traced back to Watson and Raynor (1920), who reported being able to classically
condition a fear of a white rat (and related objects) in the infant ‘Little Albert’ by contingently pairing
a tame white rat with a loud noise.
While the notion that specific fears are classically conditioned has a strong empirical basis (Bouton,
Mineka, & Barlow, 2001), there are data that call into question its ability to provide a complete
explanation. For example, Di Nardo, Guzy, and Bak (1988) found that while nearly two-thirds of
individuals with a dog phobia reported a conditioning event in which they had experienced a negative
encounter involving a dog, an equivalent number of individuals without such a phobia reported a
similar pairing of dogs with aversive events. Thus, even if the conditioning event is a necessary cause,
it does not appear to be sufficient on its own to produce a phobia. Yet Menzies and Clarke (1995) even
question the necessity of conditioning events, noting that the majority of phobic individuals cannot
recall having experienced the pairing of an aversive event with their phobic object or situation. Thus
indirect (information or vicarious transmission) learning pathways are also likely to be involved in the
development of specific phobias.
A further challenge to the notion that classical conditioning provides a complete account of the
development of specific phobias is Seligman’s (1971) notion of ‘preparedness’. Seligman noted that
prepared phobic fears were not evenly distributed across all possible stimuli. He explained the clustering of
classical phobias around the dark, water, heights, insects or small animals by noting that each of these posed a
conditioning significant biological threat to the ancestors of the species, thus suggesting a biological evolutionary
Theory that
basis for phobic fears. According to prepared classical conditioning, it should be easier to learn
evolution has
prepared people
to associate fear with snakes and spiders rather than flowers and computers (despite some people
to be easily believing they are technophobes!), and more difficult for these fears to be extinguished. Seligman’s
conditioned to account inspired much research, including a study by Öhman, Erixon, and Löfberg (1975) in which
fear objects or an aversive stimulus (electric shock) was contingently paired with pictures of prepared (snakes)
situations that and unprepared (human faces and houses) stimuli. The researchers then examined extinction of
were dangerous fear as indexed by the skin conductance response (SCR). The SCR is a measure of the amount of
in prehistoric moisture on the hands, and the greater the fear, the more moisture should be reflected in a larger
times.
SCR. As expected, they found greater resistance to extinction of responses to the prepared compared
exposure therapy to the unprepared stimuli. Specifically, the SCR demonstrated very little reduction over 10 trials
Behavioural in which shock was no longer paired with snake pictures, whereas the SCR to the faces/houses
technique in pictures disappeared immediately after shock was no longer given. Thus, while individuals may have
which the client conditioning histories that influence the development of phobias, preparedness theory suggests that
confronts the there are biological constraints on the type of stimuli for which phobias can be acquired (Mineka &
feared stimuli that
Zinbarg, 1996).
s/he has avoided
until his/her To summarise, specific phobias are false alarms—that is, instances of the fight or flight response
anxiety reduces; triggered inappropriately or excessively in the presence of specific objects or situations. The fear
there are various may have its origins in an accurate appraisal of a past dangerous event (e.g., a dog bite) that is then
types of exposure inaccurately applied to a current innocuous event. The direct (conditioning) and indirect (information
such as in vivo or vicarious transmission) pathways involve cognitions that certain stimuli will probably result in
versus imaginal. certain negative outcomes. This learning occurs against a backdrop of a biological vulnerability in the
in vivo exposure form of a genetic diathesis. In addition, phobias of certain stimuli may have a biological basis given
Technique their evolutionary significance.
of behaviour
therapy in
which clients The treatment of specific phobias
confront their
If specific phobias represent false alarms in which the fight or flight response is being triggered
feared objects/
situations in real
inappropriately because people have come to expect relatively innocuous objects and situations
life (as opposed to signal danger, then effective treatment must involve procedures that modify these expectations.
to imaginal Exposure-based treatments serve this function. In exposure therapy, the person with a phobia
exposure). gradually faces the phobic stimulus in real life (known as in vivo exposure), by imagining it (known as
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‘imaginal exposure’), or by experiencing computer-generated virtual realities (Pull, 2005). Sometimes flooding
exposure to phobic situations involves confronting the most fearful object or situation and continuing Behavioural
the exposure until the anxiety has decreased, a procedure referred to as flooding. However, since the technique in
which the client
highly anxiety-provoking nature of flooding may not be acceptable to individuals, exposure therapy
is intensively
usually takes place according to a hierarchy, progressing from the least to the most feared objects and exposed to a
situations. During the exposure session, the individual’s experience of anxiety is typically monitored feared object
by the therapist using a Subjective Units of Discomfort Scale (SUDS), ranging from a score of 0 until his/
(no anxiety) to 100 (extreme anxiety). The individual continues to confront the phobic situation until her anxiety
the SUDS scores decrease from the high range (70–100) to the lower range (10–40). Repeated exposure diminishes.
results in reductions in anxiety both within an exposure session and from one exposure session to the extinction
next. Following sufficient anxiety reduction, the person will begin exposure to the next item on the In learning theory,
exposure hierarchy. Sometimes exposure is combined with anxiety management techniques such as elimination of
relaxation training. a classically
Reviews of treatment studies continue to find that in vivo exposure is the most effective treatment conditioned
for specific phobias (Wolitzky-Taylor, Horowitz, Powers, & Telch, 2008). Moreover, treatment gains response by
removal of the
are generally maintained over the following year and can improve further if exposure continues after unconditioned
treatment. While the effectiveness of exposure therapy for phobias is not disputed, the mechanisms stimulus or the
responsible for anxiety reduction during exposure are the focus of much research, with the debate elimination of
focusing on whether exposure works through behavioural and/or cognitive processes. A behavioural an operantly
mechanism that may account for the effectiveness of exposure therapy is extinction. That is, through conditioned
confronting conditioned feared stimuli (e.g., a dog) in the absence of any unconditioned stimuli (e.g., response by
being bitten by the dog), the conditioned fear response gradually decreases. removal of the
reinforcement.
Habituation, whereby the intensity of fearful responding reduces upon repeated exposures to the
feared stimulus, is one proposed mechanism of exposure therapy. According to the habituation model habituation
of treatment, reductions in fear during and across exposure trials are necessary for treatment to be Lessening of
effective. However, an important challenge to the habituation model is that the level of fear reduction an organism’s
during exposure therapy does not predict fear responding in the long term. This suggests that other response with
repetition of the
factors are more important in consolidating new, non-fearful learning.
stimulus.
Contemporary behavioural accounts suggest that during exposure therapy the original association
learnt between the conditioned stimulus (dog) and unconditioned stimulus (dog bite) is not erased, inhibitory
but rather new inhibitory learning about the conditioned and unconditioned stimuli occurs (Craske, learning
Treanor, Conway, Zbozinek, & Vervliet, 2014). Specifically, the new learning is that a conditioned Learning that
stimulus no longer predicts an unconditioned stimulus. Rather than habituation, inhibitory learning occurs when
new associations
approaches emphasise the need to maximise expectancy violations during exposure. Expectancy
between
violation refers to the difference (i.e., prediction error) between an individual’s expectations of a conditioned
situation (‘I will be bitten by the dog’) and the actual outcome (‘Wow! The dog was friendly and just stimuli (CS) and
wanted a pat’). The greater the prediction error (the ‘wow factor’), the stronger the new inhibitory unconditioned
learning. The implication of the inhibitory learning approach is that exposure therapy is guided by stimuli (US) are
what the individual needs to learn about the feared stimulus based on their fear expectancies, rather developed during
than whether anxiety reduces during that learning (as in the habituation model). From the case study exposure therapy.
The original
of John with a dog phobia, this would mean exposing him to dogs he believes will bite him, in a
associations
way that will maximally violate this expectation— dogs of different sizes, breeds, familiarity and between the CS
apparent friendliness (within reason). The therapist would be less concerned about whether John’s and US are not
anxiety reduces within or across exposure sessions, but would instead design exposure sessions that erased.
will maximise his surprise when his feared outcome does not eventuate.
self-efficacy
Possible cognitive processes accounting for the effectiveness of exposure therapy include
Person’s belief
challenging expectations that danger will occur when confronted with the phobic stimulus. This that s/he has the
increases self-efficacy (i.e., the level of confidence that the individual can cope in the phobic ability to succeed
situation) by increasing perceptions of control over the phobic stimulus and the anxiety (Johnstone & in a specific
Page, 2004). situation.
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LO 2.3 Panic disorder and agoraphobia

The diagnosis of panic disorder and agoraphobia
Earlier editions of the DSM grouped all disorders that involved escape or avoidance of particular feared
objects or situations together and distinguished the ‘simple’ phobias, now called specific phobias,
agoraphobia from the ‘complex’ phobia called agoraphobia. From the Greek, meaning ‘fear of the marketplace’,
Anxiety disorder agoraphobia is frequently misunderstood as a fear of open spaces. However, agoraphobia is anxiety
characterised about being in places where escape might be difficult or embarrassing, or in which help may not
by a fear of
be available, in the event of having a panic attack or panic symptoms (APA, 2013). As a result of
situations in
which it would
anxiety, these situations are avoided, endured with extreme distress or require the presence of a
be difficult to companion. Typical agoraphobic situations include being outside the home alone, travelling alone,
escape or in tunnels, bridges, crowds and open spaces. Given the seemingly random clustering of feared situations,
which help may it was understandable that agoraphobia was deemed to be a ‘complex phobia’. However, the apparent
not be readily complexity became understandable once the unifying principle had been identified. This unifying
available (such as principle was that the focus of the fear in agoraphobia was not the external environment, but rather the
enclosed places fear of panic and its consequences in these environments.
and crowds)
A panic attack is defined as an episode of intense fear or discomfort in which there is a rapid increase
in the event of
experiencing in symptoms such as a pounding or racing heart; sweating; trembling; dizziness or faintness; choking/
panic symptoms. smothering sensations or shortness of breath; chills or heat sensations; and fears of dying, going crazy
or losing control (APA, 2013). Panic disorder is diagnosed when the sufferer is plagued by recurrent
panic attack
unexpected panic attacks, with at least one month of (a) persistent concern or worry about additional
Episode
during which panic attacks or their consequences (e.g., the individual fearing that s/he is at risk of a heart attack) and/
an individual or (b) significant changes in behaviour related to the attack (e.g., avoiding any exercise because it may
experiences a increase heart rate) (APA, 2013). Earlier versions of the DSM described diagnoses of ‘panic disorder
rapid increase in with agoraphobia’ or ‘panic disorder without agoraphobia’, but the DSM-5 (APA, 2013) has separated
the physiological panic disorder and agoraphobia so that they can be given together or on their own. Agoraphobia is
and cognitive diagnosed when the sufferer experiences marked fear or anxiety about at least two of the following five
symptoms of
situations: (1) using public transport, such as buses and trains, (2) being in open spaces, such as car
intense fear and

discomfort.
parks, (3) being in enclosed spaces, such as theatres and cinemas, (4) standing in queues or being in a
crowd, and (5) being outside of home alone. The agoraphobic situations almost always trigger fear and
panic disorder anxiety; they are actively avoided or are endured with intense fear or anxiety for at least a period of six
Anxiety disorder months; and the fear or anxiety is out of proportion with the situation and cultural context.
characterised
by recurrent,
unexpected panic
The epidemiology of panic disorder and agoraphobia
attacks. In the American National Comorbidity Survey, the lifetime prevalence of panic disorder was 4.7 per
cent (Kessler et al., 2005). In the Australian National Survey of Mental Health and Wellbeing, the
lifetime prevalence was 3.5 per cent for panic disorder and 2.3 per cent for agoraphobia (McEvoy,
Grove, & Slade, 2011). One of the limitations of retrospective epidemiological surveys is that not
everyone has passed through the risk period when they complete the survey. That is, a 20-year-old
who completes the survey may not have developed the disorder as yet, but s/he may develop one later
in life. When McEvoy and colleagues (2011) accounted for this statistically, the projected lifetime risk
(i.e., the proportion of people likely to experience the disorder in their lifetime), the proportions were
5.0 per cent for panic disorder and 2.9 per cent for agoraphobia. The median ages of onset are 30 years
and 22 years for panic disorder and agoraphobia, respectively.
As with most other anxiety disorders, panic disorder occurs somewhat more often among females,
with the proportion of females to males increasing as the severity of agoraphobia increases. Although
the course of panic disorder tends to be chronic, its severity waxes and wanes over time. Given that
most individuals with panic disorder do not seek treatment immediately (with the average duration
until seeking treatment being 10 years), it is important for psychologists to become more proactive
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in encouraging the prevention, early detection and treatment of panic disorder. Agoraphobia is also
typically a chronic disorder unless it is actively treated, with only around 10 per cent of cases remitting
on their own (APA, 2013).
CASE STUDY: PANIC DISORDER AND AGORAPHOBIA

Suzanne is a 24-year-old office worker who arrived at the clinic presenting as quiet and shaky. During her assessment
by a psychologist, she reported an eight-year history of panic attacks, which she now experiences several times a week.
The attacks interfere with virtually all aspects of her life, including her ability to leave the house, attend work and socialise
with family and friends. She stated that she feels very depressed and hopeless about her future.
Suzanne reported being a quiet child and adolescent who was somewhat wary of new situations, but she managed
her uneasiness by focusing her attention on her studies and by reading books. She reported experiencing her first panic
attack at the age of 16 when she was on a bus and was late for work. The first thing she noticed was that her heart was
beating very fast and she had a sharp pain in her chest. The more she focused on these symptoms the more intense they
felt, to the point where she thought she was having a heart attack. Suzanne immediately got off the bus and asked her
father to pick her up and take her to the emergency department of the local hospital. The doctors ran a range of tests but
could not find any medical reason for Suzanne’s symptoms, which led them to diagnose her as having had a panic attack.
Despite the doctor’s reassurance, Suzanne was not so sure and she continued to keep a close eye on her symptoms.
From that point on, she started noticing more symptoms, such as shortness of breath, a hastened pulse rate and dizziness.
Suzanne started visiting her GP more and more regularly for checkups as the panic attacks became more frequent. She
now understands that she is experiencing anxiety, but she fears having more panic attacks because they are such
terrifying experiences, and when the symptoms are intense she still worries that her heart will ‘explode’. Suzanne’s panic
attacks are now triggered by using public transport, being in places where help might not be available if she has another
panic attack and, more recently, just by leaving the house. She also experiences panic attacks without warning that seem
to come ‘out of the blue’. Suzanne has tried to use drugs and alcohol to manage her anxiety, but she now knows that the
relief is temporary and that the next day her anxiety is worse. So after a long struggle, she has finally sought help from a
psychologist to manage her anxiety.
The aetiology of panic disorder and agoraphobia

As displayed in Figure 2.4, the origins of panic disorder involve all three aspects of the triple
vulnerability model (Barlow, 2002). It is theorised that individuals with a generalised biological
vulnerability react more strongly to everyday stressors. As a consequence, the alarm reaction is
Generalised
psychological Anxious
vulnerability PANIC ATTACK
apprehension
(e.g., anxiety
sensitivity)
Specific
psychological
Stressful life Flight or fight vulnerability:
event alarm catastrophic
misinterpretation
of sensations
Generalised
biological
vulnerability
(e.g., neuroticism)
FIGURE 2.4 The interaction of vulnerabilities giving rise to panic disorder

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neuroticism triggered at lower intensities of stress. Similar to other anxiety disorders, it has been proposed that the
Personality inherited factor includes anxiety proneness, which is evident in constructs such as neuroticism (trait
trait entailing anxiety).
a tendency to
However, the experience of false alarms is not sufficient to cause panic disorder. In fact,
experience
negative approximately 10 per cent of the general population experience occasional panic attacks, but only
emotional states. about 3 per cent go on to develop panic disorder (Mattis & Ollendick, 2002). The psychological
vulnerabilities account for the progression from having a panic attack to developing panic disorder.
A generalised psychological vulnerability exacerbates the experience of a false alarm, and one such
anxiety vulnerability is anxiety sensitivity (Reiss, Peterson, Gursky, & McNally, 1986). Individuals who are
sensitivity high in anxiety sensitivity have a fear of arousal-related sensations in their body stemming from their
Belief that the belief that these bodily sensations are dangerous.
bodily symptoms The final element is a specific psychological vulnerability in which the individual specifically fears
of anxiety
the sensations of panic. According to Clark’s (1986) cognitive model of panic disorder, individuals
have harmful
consequences. misinterpret the physical sensations accompanying panic in a catastrophic manner (e.g., ‘I am going
to have a heart attack’ or ‘I am going crazy’). These catastrophic misinterpretations will elicit the
fight or flight response, which generates additional physical sensations. These physical sensations in
turn become a focus of further misinterpretation. In short, the panic escalates in a spiral of arousal,
tricyclic misinterpretation of the arousal as an indication of danger, and hence further arousal. Finally, the
antidepressants psychological vulnerabilities increase further as the person worries about the possible occurrence
(TCAs) of more panic attacks in the future. Such beliefs increase the likelihood of further arousal, which
Class of is misinterpreted as a sign of impending catastrophe. Thus, the individual moves beyond a single
antidepressant isolated panic attack to frequent panic attacks.
drugs such as A study by Sanderson, Rapee, and Barlow (1989) tested the cognitive model of panic disorder by
imipramine and examining the role of one particular catastrophic thought in producing panic attacks, namely, thoughts
amitriptyline.
regarding loss of control. In this study, individuals with panic disorder inhaled carbon dioxide, which
selective induces body sensations similar to those occurring during a panic attack. Participants were told that
serotonin when a light was on, they could reduce the amount of carbon dioxide they inhaled by turning a dial and
reuptake thereby control the intensity of their bodily sensations. The light was on throughout the experiment
inhibitors (SSRIs) for half of the participants but was never on for the remaining participants. However, unknown to the
Class of participants was the fact that the dial was inoperative—that is, they had no actual control over the
antidepressant amount of carbon dioxide they inhaled and hence the intensity of their bodily sensations. Of those
drugs (such participants with the illusion of control, only 20 per cent panicked, whereas 80 per cent of participants
as fluoxetine)
who believed they had no control panicked. This study supports the role of a particular catastrophic
that inhibit the
reuptake of thought (the thought that one has no control over his/her experience) in producing panic attacks.
serotonin. Agoraphobia can develop as a complication of panic disorder. Around 30 per cent of community
samples and over 50 per cent of clinical samples report a history of panic attacks or panic disorder
benzodiazepines
prior to developing agoraphobia. People with panic attacks come to fear situations in which panic may
Drugs (such
as Valium and
occur. Situations feared with phobic intensity include confined spaces such as lifts and trains (because
Xanax) that escape may be difficult or help may not be available in case of panic) or crowded places such as movie
reduce anxiety theatres and supermarkets (because escape may be difficult or embarrassing in case of panic).
and insomnia.
cognitive
behaviour
The treatment of panic disorder and agoraphobia
therapy (CBT) Effective pharmacological treatments for panic disorder include tricyclic antidepressants (TCAs),
Type of selective serotonin reuptake inhibitors (SSRIs) and high-potency benzodiazepines. These medications
psychological can have various disadvantages that must be weighed up against their benefits. For instance, the
treatment that
benzodiazepines are dependence producing, the tricyclics can produce unpleasant side effects such as
combines both
cognitive and
dizziness and a dry mouth, and the SSRIs may lead to sexual dysfunctions.
behavioural Cognitive behaviour therapy (CBT) is an effective psychological treatment for panic disorder and
concepts and agoraphobia (Andrews et al., 2003). A major aim of CBT is to address phobic avoidances, which can
techniques. be external or internal. External phobic avoidances (e.g., supermarkets) are treated with graded in
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vivo exposure, in which people first confront less fear-provoking shopping situations (such as a local
newsagent) until only minimal fear is produced. They then proceed through a hierarchy of phobic
situations until they are able to confront the most fear-provoking situation (such as waiting in a lengthy
queue at a crowded supermarket). An example of a hierarchy is shown in Table 2.2.
TABLE 2.2 Graded exposure hierarchy
James feared travelling on public transport. He developed the following steps to achieve his goal, which
was to travel to and from work on the bus.
Step 1: Stand at the bus stop and watch buses come and go for 1 hour.
Step 2: Travel one stop on a bus at a quiet time of day (10 am)
Step 3: Travel two stops on a bus at a quiet time of day (10 am)
Step 4: Travel two stops on a bus at a busy time of day (9 am)
Step 5: Travel three stops on a bus at a quiet time of day (10 am)
Step 6: Travel three stops on a bus at a busy time of day (9 am)
Step 7: Travel 30 minutes on a bus at a busy time of day (9 am)
Step 8: Travel 30 minutes on a bus at busy times of the day in the morning (9 am) and afternoon (5 pm)
Step 9: Travel on the bus to and from work
From an inhibitory learning perspective, it is less important whether an individual’s anxiety reduces
during the exposure task or if the exposure is graded, although grading might help the individual
tolerate treatment. Instead, the emphasis would be on maximising prediction errors by creating a
situation that directly violates the individual’s expectations of the feared situation (e.g., ‘If I travel
on a bus, I will panic and I will have to jump off or I will go crazy’). If Suzanne, from the case study
on panic disorder, takes the risk of riding on a bus during therapy and discovers that (a) she is far
less likely to panic than she thought, and/or (b) even if she does panic she can cope with this without
having to jump off the bus or her heart exploding, this new learning will be most important for helping
to reduce her anxiety in the longer term.
Phobic avoidance can also be internal, in which the person is overly afraid of and avoids bodily
sensations that may signal panic. This fear and avoidance can be treated using behavioural or cognitive
techniques. As an example of the behavioural technique of interoceptive exposure, a person may fear interoceptive
the sensations of hyperventilation (overbreathing) since hyperventilation paradoxically produces a exposure
sensation of being short of breath. To confront these sensations in exposure therapy, the person is Behavioural
asked to deliberately and repeatedly generate the feelings of hyperventilation by overbreathing until technique that
entails exposing
the fear of the sensations decreases. From an inhibitory learning perspective, the client is learning
the individual
to decouple physical sensations (shortness of breath) from feared expectancies (these symptoms will to the physical
definitely lead to panic or death). To maximise the prediction error, the therapist might encourage sensations of a
the client to intensely and repeatedly hyperventilate until the client is convinced that the physical panic attack.
sensation is extremely unlikely (e.g., less than 5% likely) to lead to panic or death. Clients might
also believe that even if the symptoms do not lead to panic or death, they are intolerable. This belief
can also be tested through repeated exposure, with the therapist guiding the client to continually
test their expectancies about what they can and cannot tolerate. Prediction errors can be maximised
by encouraging the client to push themselves well beyond what they think they can tolerate (e.g.,
hyperventilate more intensely, more frequently and for longer durations). The degree to which clients
are willing to take these risks will determine the rate of improvement and the likelihood of long-term
improvement.
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The fear of panic can also be addressed with cognitive techniques that aim to change the false
beliefs a person has about panic and its sensations. Common beliefs associated with panic are that the
symptoms signal that the person is about to die, go crazy or lose control. In cognitive restructuring,
the person learns to challenge false beliefs by examining the evidence supporting and disconfirming
these beliefs. Psychoeducation is one way of achieving this aim, whereby the psychologist provides
corrective information about the true basis of panic attacks. For instance, as shown in Table 2.3,
information may be given to teach the person about the nature of panic attacks as false alarms rather
than being a sign of a real danger. Psychoeducation is usually the first step in effective treatments. If
the client understands the alternate, more benign explanation for their symptoms, and believes the
explanation is plausible, then they will be much more willing to start confronting their fears in order
to learn to manage their symptoms in more helpful ways.
TABLE 2.3 An example of psychoeducation for panic disorder
Some alarms are false alarms. You may have seen a shop alarm go off. Although you weren’t trying
to steal anything, the alarm still reacts as though you’re a burglar. The problem is that the alarm is too
sensitive. In the same way, anxiety problems start when the fight or flight response is too sensitive. When
the alarm is too sensitive, the fight or flight response is triggered at the wrong times. If your anxiety alarm
goes off too easily, you will be more likely to become anxious in situations where other people would not
feel anxious.
Source: Adapted from Page, A. C., & Stritzke, W. G. K. (2006). Clinical psychology for trainees: Foundations of science-informed practice.
Cambridge: Cambridge University Press.
These cognitive-behavioural treatments for panic and agoraphobia have been found to be highly
effective. For instance, Craske, Brown, and Barlow (1991) found that over 80 per cent of the
participants treated with CBT remained panic-free up to two years after treatment. Effective treatment
of panic disorder has been found to involve a combination of exposure, relaxation training, breathing
retraining (i.e., teaching clients to slow their breathing to stop hyperventilation from intensifying their
anxiety symptoms), homework assignments to consolidate positive changes and to generalise these
changes to new situations, and a follow-up program to ensure that improvements are maintained over
time (Sanchez-Meca, Rosa-Alcazar, Marin-Martinez, & Gomez-Conesa, 2010). In order to find out
which components of CBT are most effective, one study compared four treatments: (1) interoceptive
exposure alone, (2) interoceptive exposure with cognitive restructuring (i.e., learning how to
challenge the catastrophic misinterpretations of the physical sensations), (3) interoceptive exposure
plus diaphragmatic breathing (i.e., learning how to reverse the uncomfortable physical sensations
of hyperventilation by actively slowing one’s breathing rate) and (4) a control condition involving
expressive writing (Deacon et al., 2012). Interoceptive exposure alone was superior to the control
condition in reducing anxiety sensitivity and symptoms. Somewhat surprisingly, adding cognitive
restructuring or diaphragmatic breathing did not provide additional benefits to interoceptive exposure
alone. This study suggests that gradual and regular exposure to panic-like physical sensations is a
powerful technique to reduce vulnerability to panic attacks and anxiety symptoms. Thus, regularly
experiencing the uncomfortable physical sensations during interoceptive exposure, in the absence
of a catastrophic consequence (e.g., having a heart attack, panic attack or going crazy), may be a
powerful strategy for disconfirming the individual’s catastrophic misinterpretations of benign physical
sensations that lead to full-blown panic attacks.
Inhibitory learning approaches suggest that using coping strategies such as diaphragmatic breathing
can actually undermine the effectiveness of exposure because they reduce the magnitude of the prediction
error. For example, clients might believe that as long as they are controlling their breathing they are safe,
and therefore they may not be as surprised that they could cope with their symptoms. If clients learn that
they are unlikely to panic even without coping strategies, and even if they do, nothing terrible happens,
this is likely to generate a larger prediction error and therefore better long-term outcomes.
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LO 2.4 Social anxiety disorder

The diagnosis of social anxiety disorder
Humans are social beings, with social interactions being central to human activity. Therefore,
problems with social anxiety have a far-reaching impact. According to the DSM-5 (APA, 2013), the
key features of social anxiety disorder (also known as social phobia) involve marked fear or anxiety in social anxiety
social situations in which the person faces potential scrutiny by others, including social interactions, disorder (social
being observed and performing in front of others. The key fear is that the individual will act in a phobia)
humiliating or embarrassing manner (e.g., his/her anxiety symptoms will be obvious to others), which Anxiety disorder
will lead to negative evaluation and rejection. Entering situations such as initiating or maintaining characterised by
an extreme fear
conversations, being observed eating, writing, using public toilets or public speaking provoke anxiety
of being judged
and panic that is excessive given the level of actual threat. As a result, social situations may be avoided or embarrassed
entirely. The anxiety or avoidance interferes with the individual’s functioning (e.g., the ability to form in front of
relationships or give presentations at work) and/or causes considerable distress. The DSM-5 specifies others, causing
‘performance only’ social anxiety disorder, where the fear is restricted to speaking or performing the individual
in public. Individuals are more likely to present with this subtype when their work performance is to avoid social
significantly impaired, such as musicians, athletes or public speakers (APA, 2013). situations.
Even though the symptoms of the fight or flight response are similar among people with social
phobia to those with other anxiety disorders, the sensations that are most troubling to individuals
are those that are visible to others (e.g., sweating, blushing, shaking) since they may elicit negative
evaluation from others (Page, 1994b). Likewise, even though the situations avoided (e.g., crowded
shopping malls) may be similar to other anxiety disorders, the reasons for avoidance revolve around a
fear of negative evaluation from others.
The epidemiology of social anxiety disorder

The most recent Australian National Survey of Mental Health and Wellbeing found that the diagnostic
criteria for social anxiety disorder were met for over 8 per cent of Australian adults across their
lifetime, which translated to over 1.3 million people (McEvoy, Grove, & Slade, 2011). In the general
population, around 1.5 as many women meet criteria for social anxiety disorder compared to men
(ABS, 2008), but the gender rates are approximately equal in clinical samples (APA, 2013). Apart
from specific phobias, social anxiety disorder is one of the most common and earliest onset anxiety
disorders, with half of sufferers reporting the onset prior to 12 years of age (McEvoy et al., 2011).
CASE STUDY: SOCIAL ANXIETY DISORDER

Jason is a 28-year-old single man. He works as an accountant and lives at home with his parents. He presented to
the clinic for assistance with his nervousness when meeting people. Jason reported being shy for ‘as long as I can
remember’ and as a child he recalls hiding behind his parents when meeting strangers or visiting family friends. He was
able to form a small group of friends at school, but he always felt ‘on the outer’ because he avoided getting too involved
in their conversations. He was known as the ‘quiet one’ and teachers would sometimes refer to him as ‘Mr Chatty’ as a
joke. After leaving school, Jason made no effort to remain in contact with his schoolfriends and they eventually stopped
calling him after he kept making excuses for why he could not go out with them. He found it difficult to form friendships
at university and, although he played soccer, he avoided attending any soccer-related social events other than training
and the games. When Jason could not avoid social events he would make sure he had a few alcoholic drinks before
going. Although he believed this helped him to relax, he tended to feel more anxious the next day. He also started to
rely heavily on alcohol and he began to worry that he would he make a fool of himself by being drunk. In the lead-up
to social situations, Jason would worry about what he would say, how anxious he would look and whether the other
continued
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people would be critical of him, so he felt highly anxious even before he arrived. When he was in the social situation,
he became very self-focused and aware that his heart was racing, he was sweating, his mouth was dry and his cheeks
were blushing. He described a vivid self-image in which he imagines his cheeks are glowing bright red, sweat is pouring
from his face, he is stammering over his words, and others are looking at him with a confused expression on their face.
Jason is aware that this image is probably exaggerated, but whenever he notices these physical symptoms within social
situations, he expects that others will also notice them, think he is a fool and reject him. At this point, he usually looks for
a way to escape the situation and heads straight home. Afterwards, Jason undergoes a ‘cognitive post-mortem’, where
he reviews the situation in his mind, criticises himself for how he behaved and feels really down. At work, he isolates
himself and, whenever possible, will email colleagues rather than speak to them. He is frustrated that he is stuck at a
lower level than that for which he is qualified because he thinks he could not cope with a job interview. He would like to
have a relationship and a family in the future, but he cannot see how this is possible if he cannot even speak to women
without breaking into a drenching sweat.
In the absence of effective treatment, the course of social anxiety disorder tends to be chronic,
with one study finding a median duration of 25 years without treatment (DeWit, Ogborne, Offord, &
MacDonald, 1999). Unfortunately, the average delay between the onset of social anxiety disorder and
attendance for therapy has been found to be as long as 14 years (Dingemans, van Vliet, Couvee, &
Westenberg, 2001). Part of the reluctance to seek treatment stems from the disorder itself, with
individuals being embarrassed about their condition.
The delay in seeking treatment is cause for concern, given that social anxiety disorder tends to be
comorbid with other anxiety disorders, depression and substance abuse. The comorbidity between
social anxiety disorder and depression appears to be particularly strong (Mineka, Watson, &
Clark, 1998). Those individuals with more comorbid conditions tend to be more severely afflicted,
with a ‘cascade of comorbidity’ increasing the level of disability across various aspects of their
lives (Brunello et al., 2000, p. 61). Perhaps because most people feel anxious in social situations,
the severity of the disorder in terms of its impact on functioning tends to be under-acknowledged.
Yet 9 out of 10 individuals with social anxiety disorder indicate that the problem has significantly
interfered with their academic, occupational and interpersonal functioning (Beidel, Turner, &
Dancu, 1985). People with social anxiety disorder often perform below predicted levels of
achievement in education and occupation and they are less likely to marry (reflecting their dearth
of close personal relationships).
The aetiology of social anxiety disorder

A range of biological, psychological and social factors has been implicated in the aetiology of social
anxiety disorder. Supporting a genetic vulnerability, there is a two- to three-fold increased risk of
social anxiety disorder among the relatives of people with the disorder (Tillfors, Furmark, Ekselius, &
Fredrikson, 2001). The results of twin studies are consistent with these findings, estimating that a
third of the variability in the familial transmission of social phobia is due to genetic factors (Kendler,
Neale, Kessler, Heath, & Eaves, 1992).
Among the psychosocial factors, excessive parental criticism may reduce the child’s self-
confidence. In addition, the child may learn from his/her parents to be overly concerned with
the opinions of others. The social withdrawal associated with lacking self-confidence and being
concerned with the opinions of others may in turn elicit dislike and rejection from others during
adolescence (Neal & Edelmann, 2003). Cognitive dysfunctions will also increase the likelihood of
experiencing anxiety in social situations. For example, an excessive self-focus, in which attention
is disproportionately focused on real or imagined failures of the self during social interactions, not
only increases anxiety but also diverts attention away from engaging in the prosocial behaviours
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(e.g., smiling) necessary for successful social encounters (Woody, 1996). Rapee and Heimberg
(1997) argue that the core psychological vulnerabilities for social phobia involve the distorted way in
which people perceive how they are evaluated by an audience. Specifically, they propose that people
with social phobia assume that others are inherently critical and likely to form negative evaluations
of them. For example, people with social anxiety disorder require fewer facial cues to identify a face
as threatening (Coles, Heimberg, & Schofield, 2008) and they make less optimistic assessments
about their ability to communicate effectively (Fay, Page, Serfaty, Tai, & Winkler, 2008). Moreover,
individuals with social phobia attach considerable importance to the evaluations of others. These
cognitive factors increase the probability that performance in social situations will trigger a false
alarm, which is perceived by the individual as evidence of his/her social ineptness and contributes
to the intensification of anxiety in social situations. The aversive nature of the social anxiety
drives future avoidance of these situations. Unfortunately, this avoidance deprives the individual of
opportunities to develop confidence in his/her social skills and to challenge dysfunctional beliefs
regarding social situations, thus maintaining the disorder.
Spence, Donovan, and Brechman Toussaint (1999) found that children with social anxiety disorder
initiate fewer interactions, speak less, interact for shorter durations, and are rated by themselves and
others as being less socially competent compared to non-anxious controls, suggesting that they have
a social skills deficit. However, contrary to what people with social anxiety disorder often believe
about themselves, adults with this disorder are not always assessed as being less socially skilled than
non-clinical controls, suggesting that they do not necessarily have a social skills deficit but rather
that their social skills are inhibited by the anxiety (Rapee & Lim, 1992). Therefore, if the social
anxiety is effectively treated, people with social anxiety disorder can usually interact skilfully. In other
words, a large part of the problem is that they believe they are socially incompetent, not that they are
necessarily socially incompetent.
The treatment of social anxiety disorder

Psychological treatments for social anxiety disorder specifically target the cognitive vulnerabilities
and the behavioural avoidances. The most common and evidence-supported treatment for social
phobia is cognitive behaviour therapy, either in groups or individually. Group treatment has the
advantage of providing a social context within which clients can practise their skills, and around two-
thirds of patients achieve substantial improvement (McEvoy, Erceg-Hurn, Saulsman, & Thibodeau,
2015; McEvoy, Nathan, Rapee, & Campbell, 2012). Treatment involves psychoeducation about the
factors maintaining social phobia, skills for challenging negative thoughts and images, behavioural
experiments designed to directly challenge the negative cognitions (e.g., providing a tutorial
presentation to test the belief that the individual will faint during the presentation), reducing reliance
on safety behaviours (i.e., subtle avoidance behaviours such as averting eye gaze, not contributing to
conversations or using alcohol), video-feedback to challenge negative self-images, attention training
(to distract attention from a negative focus on the self) and challenging entrenched negative core
beliefs about one’s self (e.g., ‘I am inadequate’) and others (e.g., ‘People are highly critical’). There
is evidence that adding a cognitive rationale for exposure tasks (i.e., that the individual confronts
the feared social situation in order to challenge the reality of his/her fear-based thoughts) increases
the effectiveness compared to exposure alone (Mattick, Peters, & Clarke, 1989). Researchers
have recently started to investigate imagery-based techniques for social anxiety disorder, such as
imagery rescripting, which may further enhance treatment outcomes (Lee & Kwon, 2013). Imagery
rescripting involves identifying recurrent negative images, which may have formed during early
socially traumatic experiences (e.g., bullying at school), and working to modify the meaning of the
images so that they no longer negatively influence the person’s cognitions, emotions and behaviour
in the here-and-now.
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LO 2.5 Generalised anxiety disorder (GAD)

The diagnosis of generalised anxiety disorder
generalised According to the DSM-5 (APA, 2013), the main feature of generalised anxiety disorder (GAD) is
anxiety disorder excessive anxiety and worry (anxious expectation) about a number of events or activities such as
(GAD) work, health, finances, relationships or educational performance. The anxiety and worry must have
Anxiety disorder been present on most days for a period of at least six months. These worries must be difficult to
characterised control, meaning that the individual finds it difficult to stop and cannot easily dismiss these thoughts
by chronic worry
from his/her mind.
in daily life
accompanied Unlike other anxiety disorders where worries are contained in a few closely related themes (e.g.,
by physical the fear of having a panic attack in panic disorder), the worries that characterise GAD include a
symptoms of more diverse range of future-focused fears. Core worries in GAD are broadly categorised into those
tension. that relate to social threat and physical threat, with sufferers typically experiencing worries that fall
into both categories. Social threat fears centre on work performance (e.g., worrying about making
mistakes) and interpersonal relationships (e.g., worrying about not pleasing or being liked by others).
Physical threat fears typically involve health problems (e.g., worrying about developing cancer) and
fears about the impact of world events (e.g., worrying about being a victim of a terrorist attack).
Irrespective of whether worry scenarios focus on perceived social or physical threat, individuals
with GAD tend to engage in a catastrophising style of thinking that typically ends in imagining
‘worst-case scenarios’, causing considerable anxiety. The process of catastrophising seems to occur
automatically, such that fears of being reprimanded for arriving slightly late at work, for example,
can quickly transform into a scenario of experiencing criticism from colleagues, losing one’s job,
becoming destitute and not being able to support one’s family. This type of worry scenario, which
activates significant anxiety, is not uncommon in those with GAD and may be triggered by seemingly
benign events (such as when an individual with GAD is stuck in traffic on the way to work).
Those with GAD also believe that if their fears were to eventuate, they would lack the necessary
resources and capacity to cope. In short, individuals with GAD tend to over-estimate the likelihood
of catastrophic events happening while under-estimating their ability to cope with negative events
should they occur.

In addition, the DSM-5 criteria specify that the individual experiences a range of associated
symptoms in relation to his/her worries such as feelings of irritability, fatigue, difficulties concentrating,
sleep problems, restlessness/agitation and muscle tension. The anxiety and these associated symptoms
also cause the individual high levels of distress and interfere with his/her ability to function in
important areas of life such as relationships and work. At a personal level, GAD interferes with the
sufferer’s social, work and interpersonal functioning. Some GAD sufferers become rigidly focused
on over-achievement to the exclusion of other pursuits to avoid fears of inadequacy being confirmed
by themselves or others. In contrast, others with GAD tend to avoid perceived challenges due to fears
of failure and poor confidence in being able to complete the task to a high standard. The chronic
worrying and autonomic arousal experienced by people with GAD impacts strongly on their enjoyment
and quality of life and interpersonal functioning, with close relationships characterised by stress and
dependence (Stein & Heimberg, 2004).
The DSM-5 diagnostic criteria for GAD remain unchanged from the previous edition of the
DSM (DSM-IV-TR; APA, 2000). This is despite the fact that several changes to the criteria had been
recommended on the basis of empirical data, cognitive models and clinical expertise. The proposed
changes included (1) identifying excessive worry about two life areas and removing the criterion
that worry should be difficult to control, (2) suggesting that excessive worry be present for three,
rather than six, months, (3) retaining fewer associated symptoms and (4) including the presence of
behavioural symptoms such as time spent avoiding or planning for potential threat, procrastinating or
seeking reassurance because of worrying (Andrews et al., 2010).
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CASE STUDY: GENERALISED ANXIETY DISORDER

The case of Lisa illustrates the DSM-5 criteria for GAD. Lisa recently made an appointment to see a clinical psychologist.
She described being a worrier for as long as she can remember, ever since childhood. Her worries became more difficult
to control during adolescence and were accompanied by periods of low mood where she found it difficult to summon the
energy and motivation to complete her schoolwork. Lisa sought help for depression in her teens, which was very helpful,
and is now keen to address her worrying, which she feels is intensifying to the point that it places undue stress on her
body and is likely to cause her some serious illness. She reported a number of stressors over the past year that have
intensified her stress levels. She says she’s now ‘worrying all the time’.
Lisa has worked for the past 10 years as a secretary in a local school office. She is friendly and polite and always
makes an effort to get on well with the other office staff and teachers. However, of late, there has been tension in the
workplace between senior office staff, and Lisa feels that she is being forced to take sides and worries about the effect
this will have on her work relationships. She is also struggling at home, where she has been taking time off work to care
for her mother who is undergoing treatment for cancer. Her husband has been supportive, but Lisa’s stress levels and
increased irritability have placed pressure on their relationship. Lisa and her husband had wanted to start a family but
have put these plans on hold until her mother’s health improves. Lisa worries that the amount of tension and stress she
is experiencing would make it difficult to conceive and worries that she will never have a normal family life like others.
She had always tried to plan her future and achieve her goals, but she says she is finding it difficult to cope with ‘all of
this uncertainty about her future’.
Lisa finds herself worrying about worst-case scenarios while she is at work and when she is trying to sleep at night. She
worries that her frustration with the situation at work will result in her having a public ‘outburst’ in the office, jeopardising
her job and relationships with her colleagues. She also worries about losing her mother and that her stress and worry will
have a negative effect on her own physical and psychological wellbeing. She is terrified that her husband will not be able
to cope with her stress and leave her.
Whenever Lisa finds it difficult to remove these worries from her mind, she speaks with her husband or mother to seek
reassurance that she has their support, that she can cope and that things will be okay. She does not want her stress and
worry to impact her work performance and, as a result, she has started repeatedly checking her work (such as emails) for
mistakes. At home or on lunch breaks she monitors her stress levels and scans her body for signs of stress and tension
as well as for worrying thoughts. She reports feeling tense all of the time and feeling fatigued and overwhelmed from
worry and stress. Lisa recently bought a blood pressure monitor so that she can check her stress levels. She believes
that it is only a matter of time before she develops a serious health problem such as cancer, and she has made more
frequent visits to her doctor of late. She also worries about the effect that her stress and imminent ill-health will have on
her husband and her capacity to care for her mother.
Lisa feels that her stress and worry are out of control. She is finding it hard to sleep and is more irritable with her
family. She repeatedly asks her friends and family for reassurance about her work situation and her health, which has
placed a burden on these relationships, and she is in a constant state of nervous tension, unable to relax or enjoy time
with friends and family. She is sure she will not be able to cope for much longer. Lisa would like help to worry less, to
enjoy her relationships, to view the future more positively, and to be able to relax and not feel stressed all of the time.
The epidemiology of generalised anxiety disorder

GAD is one of the most commonly experienced anxiety disorders, with a lifetime prevalence of
6.1 per cent in Australia (McEvoy et al., 2011). GAD occurs more frequently in women compared to
men. Research has shown that most sufferers do not seek help from mental health professionals and of
those that do, the delay in seeking help is often more than a decade (Olfson, Kessler, Berglund, & Lin,
1998). This delay in seeking treatment is particularly concerning given that GAD has an early age of
onset and a chronic course that is unlikely to improve without treatment (Kessler et al., 2005). Adults
with GAD often report a long history of the disorder that dates back to childhood (Noyes et al., 1992).
Several studies have also shown that GAD is costly to the community, representing a significant
financial burden by reducing the work productivity and increasing the use of healthcare services by
those with the disorder (Wittchen, 2002). On the psychological front, GAD has been found to be as
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disabling as major depression (Kessler, Dupont, Berglund, & Wittchen, 1999). It is associated with
substantial comorbidity, particularly with other anxiety disorders (most notably panic disorder and
social phobia), depressive disorders and personality disorders (such as dependent personality disorder)
(Yonkers, Dyck, Warshaw, Massion, & Keller, 1996).
The aetiology of generalised anxiety disorder

Models of the factors involved in causing GAD have emerged over the past two decades. Biological
factors are believed to play a role in causing GAD, including a moderate genetic predisposition
(Craske & Waters, 2005). However, cognitive models dominate current thinking about GAD, including
the information processing model, meta-cognitive model, avoidance theory of worry, and intolerance
of uncertainty model.
THE INFORMATION PROCESSING MODEL

Ronald Rapee from Macquarie University in Sydney, an expert in the field of anxiety disorders, has
developed an information processing model of the factors that contribute to GAD (Rapee, 1991).
This model starts with the premise that people with GAD are vigilant or on the lookout for potential
threats in their environment—that is, they selectively attend to cues of danger. Triggers occur in the
environment that create an expectation of threat, which in turn activates symptoms of anxiety, including
behavioural responses such as avoidance. The anxiety reduces only once a perception of control over
the threat has occurred. For example, people with GAD may monitor others’ reactions towards them
for signs of disapproval and feel anxious if they perceive that the other person is not pleased with
them. This in turn triggers attempts to please the person more (e.g., being more agreeable). The model
argues that people with GAD over-estimate both the probability (likelihood) of negative events and
their consequences (how bad it would be if the negative event were to occur). In addition, individuals
with GAD under-estimate their own abilities to cope with negative events.
There is now a large body of evidence supporting biased information processing towards threat
in GAD. People with GAD selectively attend to threatening information and interpret ambiguous
scenarios as threatening (Butler & Mathews, 1983). For instance, one study sought to investigate
selective attention in individuals with GAD through the use of the Stroop task (Mogg, Bradley,
Williams, & Mathews, 1993). In this task, participants are asked to name the colour in which words
are printed. It is argued that individuals will be slower to name the colour of a word if they are unable
to ignore the meaning of the word. Thus, if individuals with GAD have an attentional bias towards
threat-related information, they should be slower to colour-name words that have a negative meaning
(e.g., danger) compared to those without the disorder. As shown in Figure 2.5, this is precisely what
the researchers found: negative words interfered more with the colour-naming responses of GAD
patients than of those who were depressed or normal controls.
THE META-COGNITIVE MODEL

The meta-cognitive model developed by Wells (1995) highlights the importance of a number of
interacting systems that maintain and promote worry, such as the use of worry as a coping strategy,
negative appraisals or beliefs about worry, and control strategies aimed at stopping the worry process.
Wells’s model describes two types of worry. Type 1 is characterised as ‘normal’ worry about everyday
meta-beliefs events (e.g., ‘What if I fail my exam?’). Type 2 involves beliefs about worry itself, termed meta-beliefs.
Beliefs about Specifically, these meta-beliefs entail negative appraisals or interpretations of the worry process
one’s own beliefs that focus on the idea that one’s worry is dangerous. For example, meta-beliefs such as ‘worrying is
and those of
uncontrollable’ or ‘I’ll go crazy with worrying’ increase the frequency of worry by triggering worrying
others.
about worry. Negative meta-beliefs have indeed been found to be elevated in people with GAD and to
successfully discriminate GAD sufferers from those with other anxiety disorders and those without an
anxiety disorder (Wells & Carter, 2001).
Wells’s model argues that people with GAD also hold positive beliefs about worry such as ‘worry
helps me prepare for danger’, ‘worry stops bad things from happening’ and ‘worrying about others
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20
15
10
Interference score (ms) Anxious
5
Depressed
0
Control
–5
–10
–15
–20
Mood group
FIGURE 2.5 Mean interference scores (in milliseconds) for colour-naming negative words in the anxious,
depressed and control groups
Source: From Mogg, K., Bradley, B., Williams, R., & Mathews, A. (1993). Subliminal processing of emotional information in anxiety and
depression. Journal of Abnormal Psychology, 102, 304–311, © 1993 The American Psychological Association. Used with permission.
means I am a caring person’. These positive meta-beliefs maintain the worry process by promoting
worry as a seemingly helpful coping strategy. However, research has not found that positive beliefs
about worry are specific to those with GAD. As such, these beliefs may represent a vulnerability factor
for anxiety disorders in general rather than GAD specifically (Dugas, Marchand, & Ladouceur, 2005).
Wells’s model further proposes that the process of worry in turn activates a range of other unhelpful
coping strategies aimed at controlling worry and preventing threat, such as avoidance (e.g., avoiding
leaving work on time to ensure that no mistakes have been made) and seeking reassurance from others
(e.g., obtaining repeated medical tests to ensure that there is no serious medical condition). While
these strategies help to reduce anxiety in the short term (and are thereby negatively reinforced), they
prevent the individual from learning that nothing bad was going to happen, even if they had not used
the strategy.
THE AVOIDANCE THEORY OF WORRY

Borkovec, Alcaine, and Behar (2004) argue that excessive worry is a strategy used by individuals
to avoid the anxiety associated with (a) distressing images and (b) underlying fears or concerns.
Beginning with the former, Borkovec and colleagues (2004) propose that worry is a verbal-linguistic
activity that acts to avoid the occurrence of distressing images and hence lessen the negative
physiological arousal of the fear response triggered by these images. Worrying in thoughts is less
distressing than processing feared scenarios as emotional images. For example, thoughts about having
cancer produce fewer physiological symptoms than emotional images of having cancer. Processing
fears as thought-based worries instead of images becomes reinforced as a strategy to help deal
with distressing emotions since the process of worrying helps people with GAD to avoid some of
the physiological arousal associated with the image. In relation to the second aspect of avoidance,
the everyday content of worry is hypothesised to also serve as a means of avoiding more distressing
and emotional topics or core underlying fears (e.g., ‘The world is dangerous and I am inadequate and
unable to cope’) that developed as a consequence of past traumatic events (e.g., childhood abuse),
early negative experiences with primary caregivers or poor current interpersonal relationships.
Certainly, the vast evidence suggests that worry is characterised more by thought-based than by
image-based cognitive activity, which is consistent with the notion that worrying helps to reduce the
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occurrence of distressing images (Borkovec & Inz, 1990). In addition, several studies have suggested
that worrying prior to recalling a past trauma or engaging in feared imagery serves to reduce heart
rate and anxious and depressive affect (Behar, Zuellig, & Borkovec, 2005). These data support the
function of worry as cognitive avoidance of physiological activity and negative affect.
Few studies have directly assessed Borkovec’s hypotheses, suggesting that the content of worry
serves to avoid underlying emotional issues and relationship problems. Nonetheless, consistent with
these hypotheses, people with GAD report higher rates of past traumatic experiences (Roemer, Molina,
Litz, & Borkovec, 1997) and histories of difficulties with primary caregivers (Turk, Heimberg, &
Mennin, 2004). In addition, individuals with GAD who have the highest levels of interpersonal
problems tend to have the worst treatment outcomes (Borkovec, Newman, Pincus, & Lytle, 2002).
THE INTOLERANCE OF UNCERTAINTY MODEL

The intolerance of uncertainty model regarding the aetiology of GAD proposed by Ladouceur, Talbert,
and Dugas (1997) argues that situations and events that involve uncertain outcomes (i.e., carry the
risk of a negative outcome) trigger negative emotional (anxious feelings), cognitive (threat beliefs)
and behavioural (avoidance) responses in people with GAD. Uncertainty is something that cannot be
controlled or avoided and hence people with GAD find this distressing as it signals the possibility of
threat. This model argues that people with GAD are intolerant of even mild amounts of uncertainty
and will attempt to control situations that are associated with uncertain outcomes (e.g., doing things
perfectly so that nothing can possibly go wrong).
Intolerance of uncertainty is argued to interact with three other key processes to maintain GAD
symptoms. First, similar to the meta-cognitive model, it is proposed that individuals with GAD have
positive beliefs about the use of worry as a coping strategy. Second, the model posits that people with
GAD possess a ‘poor problem orientation’ such that they selectively focus on the uncertain aspects
of problems and have low levels of confidence regarding their capacity to solve problems. Third, this
model adopts the hypothesis of Borkovec and colleagues (2004) that worry is a process that functions
as a means of inhibiting distressing mental images and accompanying physiological arousal. Thus, the
process of worry is negatively reinforced in the short term (since it reduces fear) but it prevents
the processing of feared scenarios and habituation processes over the longer term.
There is evidence to suggest that the construct of intolerance of uncertainty is significantly and
uniquely associated with GAD symptoms rather than anxiety disorders generally. In addition, the
other key processes in the model (i.e., positive beliefs about worry, poor problem-solving efficacy
and emotional avoidance) have shown significant correlations with intolerance of uncertainty (Dugas
et al., 2005). Moreover, clinical treatment studies suggest that reductions in intolerance of uncertainty
precede reductions in GAD symptoms (Ladouceur, Gosselin, & Dugas, 2000).
The treatment of generalised anxiety disorder

PHARMACOLOGICAL TREATMENTS FOR GAD
azapirones The main classes of medications for the treatment of GAD are benzodiazepines, azapirones (primarily
Class of drugs buspirone), tricyclic antidepressants (such as imipramine), selective serotonin reuptake inhibitors
(such as (SSRIs such as fluoxetine) and serotonin-norepinephrine reuptake inhibitors (SNRIs such as
buspirone) that
venlafaxine). While the benzodiazepines produce quick relief from anxiety and have been frequently
may be used in
the treatment
prescribed, they are now thought to be associated with difficulties in producing tolerance and
of generalised dependence (Mahe & Balogh, 2000). The SSRIs and SNRIs are more commonly prescribed nowadays
anxiety disorder. and are thought to have reduced side effects than older medications while producing similar reductions
in symptoms. A primary limitation with this approach is the return of symptoms once medication is
discontinued. As a result, current treatment recommendations suggest that medications be used, when
necessary, only as an adjunct to psychological interventions, rather than as a treatment on their own,
and in cases that are resistant to psychological treatment (Mahe & Balogh, 2000).
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PSYCHOLOGICAL TREATMENTS FOR GAD

Cognitive behaviour therapy (CBT) is the psychological intervention that has received the most
empirical attention in assessing treatment outcome for GAD. CBT programs aim to treat the primary
factors thought to maintain the client’s symptoms. Most CBT programs include psychoeducation
about worry and teach realistic thinking skills to help clients reappraise negative predictions about
threat, beliefs about worry and negative self-beliefs (e.g., ‘I am inadequate’).
In the technique of cognitive restructuring, the client is assisted by the therapist to identify worry-
related beliefs and then to evaluate the accuracy of these beliefs with the aim of replacing unrealistic
beliefs with realistic ones. The following dialogue between a therapist and client illustrates the process of
cognitive restructuring regarding a specific meta-belief, namely, the belief that worry is uncontrollable.
Therapist: You mentioned that you fear that once you start worrying, you’ll never be able to stop.
Client: Yes, that’s right. I’ve been worrying all morning. It feels out of control.
Therapist: Was the worry there all morning? Did anything else take your attention?
Client: I was distracted for a little while by my book.
Therapist: And then did you start worrying again?
Client: No, I was cleaning the house.
Therapist: So given that you stopped worrying at least for a short time while you were
distracted by reading and cleaning the house, how does that fit with the idea that
you can’t control your worry?
Client: I guess it isn’t completely uncontrollable.
In addition to these cognitive strategies, CBT programs use behavioural techniques to further
challenge the helpfulness and accuracy of worry-related beliefs. The use of behavioural experiments
is one strategy that is particularly helpful for challenging meta-cognitive beliefs about worry, such as
‘My worry is uncontrollable’ or ‘I’ll go crazy with worry’. The therapist and client collaboratively
design an ‘experiment’ to test one of the client’s negative predictions. In the following dialogue, the
therapist and client discuss a behavioural experiment designed to test the belief that the client will ‘go
crazy from worry’.
Client: Whenever I start worrying, I think it will never stop.

Therapist: What would happen if you kept worrying?
Client: I feel like it would get so out of control that I’d go crazy.
Therapist: What would losing control and ‘going crazy’ look like?
Client: Well, I’m sure I’d lose my mind. I guess I would run around not in control of what I
think or my behaviour. I’d say and do odd things.
Therapist: We can test this belief by deliberately worrying for five minutes to see whether you
lose control of your faculties and start running around the room, behaving in ways
that are not normal for you.
Client: I’m scared it will be true.
Therapist: Shall we start by worrying as much as we can for five minutes together? Let’s see
whether your prediction is true.
Therapist: Now that you’ve worried as much as you could for five minutes, what did you
notice happened?
Client: Well, it’s strange, but I found it hard to worry at first, then I started thinking of all
the negative things that could happen. I was scared that I would lose my mind. But
in the end I just kept worrying, I stayed sitting down, and nothing really happened.
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This behavioural experiment taught the client that worrying does not cause them to go crazy or
wait-list control to behave irrationally. CBT programs often include a range of other behavioural techniques to help
group clients better control their worry, such as teaching relaxation skills to help reduce anxious arousal,
In a treatment and helping clients to face their fears without using unhelpful coping strategies (such as seeking
outcome reassurance from others). Behavioural approaches also include graded exposure to help clients face
study, group of feared situations and feelings.
participants that Because many of the fears held by people with GAD are unlikely to occur but would be objectively
functions as a no-
distressing (e.g., contracting a serious illness), programs include a technique called ‘worry exposure’
treatment control
group while the that helps clients face their fears imaginally (i.e., imagining in detail the worst-case scenario, such as
experimental dying from cancer). CBT programs ask clients to practise these skills and strategies repeatedly both in
group receives therapy sessions and as part of agreed homework exercises.
the intervention. CBT for GAD results in significant improvement in symptoms relative to other psychological
interpersonal interventions (e.g., psychodynamic therapy) and wait-list control conditions (i.e., those waiting to
psychotherapy receive treatment that controls for any symptom improvement that may simply occur as a result of the
(IPT) passage of time). Research using meta-analysis (i.e., research that collates the data from all available
Short-term studies) comparing cognitive therapy for GAD with control conditions (e.g., a wait-list control
psychological group) have demonstrated large effect sizes across both self-report symptom measures and clinician-
treatment administered measures. Importantly, these gains are maintained over the longer term and also extend
originally to significantly improving self-reported levels of depression (Borkovec, 2002; Cuijpers et al., 2014;
developed by Gould, Safren, Washington, & Otto, 2004; Hanrahan, Field, Jones, & Davey, 2013).
Gerald Klerman,
Nevertheless, there have been calls to further improve treatments for GAD since even our best CBT
Myrna Weissman
and their interventions leave only 57 per cent of sufferers with scores in the non-clinical range on symptom
colleagues for measures (Borkovec, 2002; Hanrahan et al., 2013). These results indicate that there is considerable
the treatment scope for the development and evaluation of enhanced or new approaches to help people with GAD.
of depression; For instance, increased understanding of the processes underlying and maintaining worry has led
addresses to the development of enhanced CBT programs that include addressing meta-worries, impaired
the client’s interpersonal styles and problems coping with emotions (Leahy, 2005). New approaches for the
interpersonal
treatment of GAD include interpersonal psychotherapy (IPT) and mindfulness meditation approaches.
problems
as a way of IPT focuses on addressing interpersonal problems that are believed to be maintaining the symptoms.
improving his/ Mindfulness meditation is an approach in which patients learn to be more present-focused (rather than
her psychological future-focused) and learn to simply observe (rather than react) to their worries. An example of one
symptoms.
TABLE 2.4 A summary of the ‘mindfulness of the breath’ exercise used in mindfulness-based
cognitive therapy
1. Settle into a comfortable sitting position.

2. Bring your awareness to the physical sensations in the lower abdomen as the breath moves in and
out of your body.
3. Focus your awareness on the sensations of slight stretching as the abdominal wall rises with each
in-breath, and of gentle deflation as it falls with each out-breath.
4. There is no need to try to control the breathing in any way.
5. Sooner or later your mind will wander away from the focus on the breath in the lower abdomen. This
is perfectly okay—it’s simply what minds do. It is not a mistake or a failure. When you notice that your
awareness is no longer on the breath, gently congratulate yourself—you are once more aware of your
experience. Then gently escort the awareness back to a focus on the changing pattern of physical
sensations in the lower abdomen. Repeat this step each time you notice that your mind has wandered.
6. Continue with the practice for 15 minutes, reminding yourself from time to time that the intention is
simply to be aware of your experience in each moment, as best you can.
Source: From Segal, Z. V., Williams, J. M. G., & Teasdale, J. D. (2002). Mindfulness-based cognitive therapy for depression. New York: Guilford Press.
Adapted with permission of Guilford Press.
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mindfulness exercise—‘mindfulness of the breath’—is described in Table 2.4. Research suggests that
integrating mindfulness techniques with CBT programs for GAD are beneficial (Roemer & Orsillo,
2007; Roemer, Orsillo, & Salters-Pedneault, 2008). Moreover, mindfulness meditation programs
alone result in improved outcomes compared to CBT and wait-list control groups, with patients who
take part in mindfulness meditation programs being more likely to no longer meet criteria for GAD at
the end of treatment (Abbott, 2007).
SUMMARY
This chapter addressed a range of anxiety and related disorders that are summarised in Table 2.5. Anxiety is characterised by
distressing emotions (such as fear), physical symptoms (such as increased blood pressure), cognitions (typically, thoughts of danger
and misfortune) and the behaviours of escape or avoidance. Anxiety disorders arise when the frequency or intensity of anxiety
interferes with the individual’s capacity to function in everyday life. They essentially entail the frequent occurrence of false alarms
in which the fight or flight response is inappropriately activated. The triple vulnerability—consisting of generalised biological,
generalised psychological and specific psychological vulnerabilities—is believed to drive the experience of false alarms.
The main anxiety disorders identified in the current DSM-5 (APA, 2013) classification system are specific phobias, panic disorder,
agoraphobia, social anxiety disorder and generalised anxiety disorder. The essential feature of specific phobia is a marked and
TABLE 2.5 Examples of common triggers, cognitions (thoughts/images), behaviours, emotions and physiological responses
associated with each of the anxiety and related disorders described in this chapter
TRIGGERS COGNITIONS BEHAVIOURS EMOTIONS PHYSIOLOGY
Specific Animals ‘I will be bitten’, ‘I will Avoidance Fear, anxiety Increased heart
phobias Natural fall’, ‘I will faint’ Safety behaviours rate, sweating,
environment (e.g., holding an object trembling, increased
Blood, injection, that the individual respiration rate
injury thinks will keep him/
Situational her safe)
Panic Bodily sensations ‘I will have a heart Avoidance of activities Fear, anxiety Increased heart
disorder (e.g., changes attack’, ‘I am going that trigger panic, such rate, sweating,
in heart rate, crazy’ as bodily sensations trembling, increased
breathlessness, (e.g., walking up stairs) respiration rate
dizziness) Safety behaviours (e.g.,
carrying medication)
Agoraphobia Shopping centres, ‘I can’t cope if I can’t Avoidance (e.g., Fear, anxiety Increased heart
parks, being alone escape or someone avoiding trains, rate, sweating,
isn’t there to help crowded buses, trembling, increased
me’ shopping centres) respiration rate
Safety behaviours
(e.g., only leaving the
house with a family
member)
Social Social interactions, Fear of negative Avoidance (e.g., not Fear, anxiety, Increased heart
anxiety being the focus evaluation (e.g., giving presentations shame rate, sweating,
disorder of attention, ‘Others will see how at work, avoiding eye trembling, increased
performing anxious I am and I contact with others) respiration rate
will be rejected’) Safety behaviours
(e.g., using alcohol)
continued
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TABLE 2.5 (continued)
TRIGGERS COGNITIONS BEHAVIOURS EMOTIONS PHYSIOLOGY
Generalised A large variety ‘Bad things will Avoidance and safety Fear, anxiety, Increased heart rate,
anxiety of internal happen, they will behaviours such worry respiration rate,
disorder and external be catastrophic and as avoiding feared sweaty, trembling,
triggers, such I won’t be able to situations, negative hypervigilance,
as news stories, cope’. ‘Uncertainty thoughts and feelings, agitation,
noticing thoughts is threatening; worry worry triggers restlessness,
or feelings, will make me crazy’, Reassurance seeking irritability, muscle
noticing worries, ‘My feelings are Being overly pleasing tension, sleep
interpersonal dangerous’, ‘Worry Perfectionism problems
situations makes me a good Busyness
person—it shows I Controlling behaviour
care for others’
persistent fear that is excessive and unreasonable in response to the presence or anticipation of a specific object or situation.
Learning accounts have dominated theories regarding the aetiology of specific phobias, whereby, through classical conditioning,
information from others or modelling of others, the individual learns to expect that confrontation with the phobic object or situation
will result in a negative outcome. In vivo exposure is a highly effective treatment for specific phobias, perhaps due to the fact that it
disconfirms the individual’s belief that confronting the feared object or situation results in an aversive outcome. Inhibitory learning
approaches emphasise the need to design exposure tasks that maximise prediction errors (i.e., the discrepancy between the
expected and actual outcomes) to optimise the violation of fear expectancies and hence the long-term improvement in anxiety.
The main characteristic of panic disorder is the presence of recurrent, unexpected panic attacks, which are defined as episodes
of intense and rapid fear entailing symptoms such as increased heart rate, sweating, trembling, shortness of breath, sensations
of choking, chest pain, dizziness or faintness and tingling or numbness. A substantial proportion of individuals with panic disorder
also have agoraphobia, the defining feature of which is anxiety about being in situations from which escape might be difficult
(or embarrassing) or in which help may not be available in the event of having a panic attack. The cognitive model emphasises the
role of catastrophic misinterpretations of bodily symptoms (e.g., interpreting rapid heart rate as a sign that the individual is having
a heart attack) in triggering panic attacks. Cognitive-behavioural approaches to treating panic disorder seek to overcome this
misinterpretation of bodily symptoms. Agoraphobic avoidance is targeted through exposure to feared situations.
The primary feature of social anxiety disorder is a marked and persistent fear of social and performance situations, with the
individual fearing that s/he will act in a way that is humiliating or embarrassing and subsequently avoiding such situations or
enduring them with intense distress. Once again, cognitive models are the dominant approach to understanding the aetiology of
social phobia, emphasising the role of thoughts (such as the belief that others are likely to be critical) in triggering anxiety in social
situations. Cognitive behaviour therapy, delivered individually or within a group context, is the dominant approach for the treatment
of social phobia.
Individuals with generalised anxiety disorder (GAD) experience pervasive patterns of worry about a range of everyday topics
that are experienced as uncontrollable. They also report associated symptoms, including feelings of irritability, sleep problems,
muscle tension and fatigue, associated with worry. GAD is a common, chronic, costly and disabling disorder with an early age of
onset and a low likelihood of improvement without treatment. Cognitive models of GAD are particularly prominent in understanding
the disorder’s aetiology. CBT has been shown to produce reasonably good outcomes, although there is a need to further improve
the outcomes for those with GAD.
KEY TERMS
agoraphobia. . . . . . . . . . . . . . . . . . . . . . 50 azapirones. . . . . . . . . . . . . . . . . . . . . . . . 63 exposure therapy. . . . . . . . . . . . . . . . . . 48
anxiety sensitivity. . . . . . . . . . . . . . . . . . 52 benzodiazepines . . . . . . . . . . . . . . . . . . 52 extinction. . . . . . . . . . . . . . . . . . . . . . . . . 49
autonomic nervous system. . . . . . . . . . 45 cognitive behaviour therapy (CBT). . . 52 fight or flight response . . . . . . . . . . . . . 42
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flooding. . . . . . . . . . . . . . . . . . . . . . . . . . 49 negative reinforcement. . . . . . . . . . . . . 43 social anxiety disorder (social

generalised anxiety disorder (GAD) . . 58 neuroticism. . . . . . . . . . . . . . . . . . . . . . . 52 phobia). . . . . . . . . . . . . . . . . . . . . . . . . . . 55
habituation. . . . . . . . . . . . . . . . . . . . . . . . 49 panic attack. . . . . . . . . . . . . . . . . . . . . . . 50 specific phobia. . . . . . . . . . . . . . . . . . . . 46
inhibitory learning. . . . . . . . . . . . . . . . . . 49 panic disorder. . . . . . . . . . . . . . . . . . . . . 50 tricyclic antidepressants (TCAs). . . . . . 52
interoceptive exposure. . . . . . . . . . . . . 53 prepared classical conditioning. . . . . . 48 wait-list control group. . . . . . . . . . . . . . 65
interpersonal psychotherapy (IPT). . . . 64 selective serotonin reuptake
in vivo exposure. . . . . . . . . . . . . . . . . . . 48 inhibitors (SSRIs). . . . . . . . . . . . . . . . . . . 52
meta-beliefs. . . . . . . . . . . . . . . . . . . . . . . 61 self-efficacy. . . . . . . . . . . . . . . . . . . . . . . 49
REVIEW QUESTIONS
LO 2.1
2.1 What are the characteristic features of the fight or flight response?
2.2 Explain the distinction between a true alarm and a false alarm.
LO 2.2
2.3 Define classical conditioning and outline three lines of evidence as to why this is an incomplete explanation for
the development of specific phobias.
2.4 What are some of the behavioural and cognitive mechanisms by which exposure therapy can have its effect?
LO 2.3
2.5 Explain the psychological vulnerabilities that are important in determining whether individuals who experience
panic attacks go on to develop panic disorder.
2.6 From a cognitive perspective, describe how repeated and graded exposure to physical sensations similar to
anxiety (i.e., interoceptive exposure) can be therapeutic for someone with panic disorder.
LO 2.4
2.7 Safety behaviours are common in anxiety disorders. Define what is meant by safety behaviours. How could
safety behaviours serve to maintain an anxiety disorder? Describe using an example of an individual with social
anxiety disorder.
2.8 Why would video feedback be helpful for someone with social anxiety disorder?
LO 2.5
2.9 How do the results on the Stroop task provide evidence of an attentional bias towards threat in individuals with
generalised anxiety disorder (GAD)?
2.10 Compare and contrast cognitive-behavioural and mindfulness-based treatments for generalised anxiety
disorder (GAD).
REFERENCES
Abbott, M. J. (2007). Enhancing outcomes in the treatment of Andrews, G., Creamer, M., Crino, R., Hunt, C., Lampe, L., & Page, A.
generalised anxiety disorder. In D. Eistein (Ed.), Innovations and (2003). The treatment of anxiety disorders: Clinician guides and
advances in cognitive behaviour therapy (pp. 157–170). Bowen patient manuals (2nd ed.). New York: Cambridge University
Hills: Australian Academic Press. Press.
Agras, S., Sylvester, D., & Oliveau, D. (1969). The epidemiology of Andrews, G., Hobbs, M. J., Borkovec, T. D., Beesdo, K., Craske, M.
common fears and phobia. Comprehensive Psychiatry, 10, 151–156. G., Heimberg, R. G., . . . Stanley, M. A. (2010). Generalized worry
American Psychiatric Association (2000). Diagnostic and statistical disorder: A review of DSM-IV generalized anxiety disorder and
manual of mental disorders (4th ed., text revision). Washington, options for DSM-V. Depression and Anxiety, 27, 134–147.
DC: Author. Andrews, G., Stewart, G., Morris-Yates, A., & Holt, P. (1990).
American Psychiatric Association (2013). Diagnostic and statistical Evidence for a general neurotic syndrome. British Journal of
manual of mental disorders (5th ed.). Washington, DC: Author. Psychiatry, 157, 6–12.
rie66620_ch02_041-072.indd 67 08/02/17 06:48 AM

Australian Bureau of Statistics (2008). National Survey of Mental Cook, M., & Mineka, S. (1990). Selective associations in the
Health and Wellbeing: Summary of results (cat. No. 4326.0). observational conditioning of fear in rhesus monkeys. Journal
Canberra: Author. of Experimental Psychology: Animal Behaviour Processes, 16,
Bailey, V., Baker, A.-M., Cave, L., Fildes, J., Perrens, B., Plummer, J., & 372–389.
Wearring, A. (2016). Mission Australia’s 2016 Youth Survey Craig, A. R., Franklin, J., & Andrews, G. (1984). A scale to measure
Report. Mission Australia. locus of control of behaviour. British Journal of Medical Psychology,
Barlow, D. H. (2002). Anxiety and its disorders: The nature and 57, 173–180.
treatment of anxiety and panic (2nd ed.). New York: Guilford Press. Craske, M. G., Brown, T. A., & Barlow, D. H. (1991). Behavioral
Barrett, P. M., Rapee, R. M., Dadds, M. M., & Ryan, S. M. (1996). treatment of panic disorder: A two-year follow-up. Behavior
Family enhancement of cognitive style in anxious and aggressive Therapy, 22, 289–304.
children. Journal of Abnormal Child Psychology, 24, 187–203. Craske, M. G., Treanor, M., Conway, C. C., Zbozinek, T., & Vervliet,
Behar, E., Zuellig, A. R., & Borkovec, T. D. (2005). Thought and B. (2014). Maximizing exposure therapy: An inhibitory learning
imaginal activity during worry and trauma recall. Behavior approach. Behaviour Research and Therapy, 58, 10–23.
Therapy, 36, 157–168. Craske, M., & Waters, A. M. (2005). Panic disorder, phobias
Beidel, D. C., Turner, S. M., & Dancu, C. V. (1985). Physiological, and generalised anxiety disorder. Annual Review of Clinical
cognitive and behavioural aspects of social anxiety. Behaviour Psychology, 1, 197–226.
Research and Therapy, 23, 109–117. Cuijpers, P., Sijbrandij, M., Koole, S., Huibers, M., Berking, M., &
Borkovec, T. D. (2002). Life in the future versus life in the present. Andersson, G. (2014). Psychological treatment for generalized
Clinical Psychology: Science and Practice, 9, 76–80. anxiety disorder: A meta-analysis. Clinical Psychology Review, 34,
Borkovec, T. D., Alcaine, O., & Behar, E. (2004). Avoidance theory 130–140.
of worry and generalized anxiety disorder. In R. G. Heimberg, C. Deacon, B. J., Lickel, J. J., Possis, E. A., Abramowitz, J. S., Mahaffey,
L. Turk, & D. S. Mennin (Eds.), Generalized anxiety disorder: B., & Wolitzky-Taylor, K. (2012). Do cognitive reappraisal and
Advances in research and practice (pp. 77–108). New York: diaphragmatic breathing augment interoceptive exposure for
Guilford Press. anxiety sensitivity? Journal of Cognitive Psychotherapy, 26,
Borkovec, T. D., & Inz, J. (1990). The nature of worry in generalized 257–269.
anxiety disorder: A predominance of thought activity. Behaviour DeWit, D. J., Ogborne, A., Offord, D. R., & MacDonald, K. (1999).
Research and Therapy, 28, 153–158. Antecedents of the risk of recovery from DSM-III-R social phobia.
Borkovec, T., Newman, M., Pincus, A., & Lytle, R., (2002). A Psychological Medicine, 29, 569–582.
component analysis of cognitive-behavioral therapy for generalized Di Nardo, P. A., Guzy, L. T., & Bak, R. M. (1988). Anxiety response
anxiety disorder and the role of interpersonal problems. Journal of patterns and aetiological factors in dog-fearful and non-fearful
Consulting and Clinical Psychology, 70, 288–298. subjects. Behaviour Research and Therapy, 26, 245–251.
Bouton, M. E., Mineka, S., & Barlow, D. H. (2001). A modern Dingemans, A., van Vliet, I., Couvee, J., & Westenberg, H. (2001).
learning theory perspective on the aetiology of panic disorder. Characteristics of patients with social phobia and their treatment in
Psychological Review, 108, 4–32. specialised clinics for anxiety disorders in the Netherlands. Journal
Brown, T. A., & Barlow, D. H. (2009). A proposal for a dimensional of Affective Disorders, 65, 123–129.
classification system based on the shared features of the DSM-IV Dugas, M., Marchand, A., & Ladouceur, R. (2005). Further validation
anxiety and mood disorders: Implications for assessment and of a cognitive-behavioural model of generalized anxiety disorder:
treatment. Psychological Assessment, 21, 256–271. Diagnostic and symptom specificity. Journal of Anxiety Disorders,
Brown, T. A., & Naragon-Gainey, K. (2013). Evaluation of the unique 19, 329–343.
and specific contributions of dimensions of the triple vulnerability Eysenck, H. J. (1990). The decline and fall of the Freudian empire.
model to the prediction of DSM-IV anxiety and mood disorder Washington, DC: Scott-Townsend Publishers.
constructs. Behavior Therapy, 44, 277–292. Fay, N., Page, A. C., Serfaty, C., Tai, V., & Winkler, C. (2008).
Brunello, N., den Boer, J., Judd, L., Kasper, S., Kelsey, J., Lader, Speaker overestimation of communication effectiveness and fear
M.,  . 
. 
. Wittchen, H. (2000). Social phobia: Diagnosis and of negative evaluation: Being realistic is unrealistic. Psychonomic
epidemiology, neurobiology and pharmacology, comorbidity and Bulletin & Review, 15, 1160–1165.
treatment. Journal of Affective Disorders, 60, 61–74. Gould, R. M., Safren, S., Washington, D., & Otto, M. (2004).
Butler, G., & Mathews, A. (1983). Cognitive processes in anxiety. A meta-analytic review of cognitive-behavioural treatments. In
Advances in Behaviour Research and Therapy, 5, 51–62. R. G. Heimberg, C. L. Turk, & D. S. Mennin (Eds.), Generalized
Cannon, W. B. (1929). Bodily changes in pain, hunger, fear and rage anxiety disorder: Advances in research and practice (pp. 248–264).
(2nd ed.). New York: Appleton-Century-Crofts. New York: Guilford Press.
Chorpita, B. F., Brown, T. A., & Barlow, D. H. (1998). Perceived Hanrahan, F., Field, A. P., Jones, F. W., & Davey, G. C. L. (2013). A
control as a mediator of family environment in etiological models meta-analysis of cognitive therapy for worry in generalized anxiety
of childhood anxiety. Behavior Therapy, 29, 457–476. disorder. Clinical Psychology Review, 33, 120–132.
Clark, D. M. (1986). A cognitive approach to panic. Behaviour Issikadis, C., & Andrews, G. (2002). Service utilisation for anxiety
Research and Therapy, 24, 461–470. in an Australian community sample. Social Psychiatry and
Coles, M. E., Heimberg, R. G., & Schofield, C. A. (2008). Psychiatric Epidemiology, 37, 153–163.
Interpretation of facial expressions and social anxiety: Specificity Johnstone, K. A., & Page, A. C. (2004). Attention to phobic stimuli
and source of biases. Cognition & Emotion, 22, 1159–1173. during exposure: The effect of distraction on anxiety reduction,
rie66620_ch02_041-072.indd 68 08/02/17 06:48 AM

self-efficacy and perceived control. Behaviour Research and 1995: Perspectives on anxiety, panic, and fear (pp. 135–210).
Therapy, 42, 249–275. Lincoln: University of Nebraska Press.
Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas, K. R., & Mogg, K., Bradley, B., Williams, R., & Mathews, A. (1993). Subliminal
Walters, E. E. (2005). Lifetime prevalence and age-of-onset processing of emotional information in anxiety and depression.
distributions of DSM-IV disorders in the National Comorbidity Journal of Abnormal Psychology, 102, 304–311.
Survey Replication. Archives of General Psychiatry, 62, 593–602. Neal, J. A., & Edelmann, R. J. (2003). The aetiology of social phobia:
Kessler, R. C., Dupont, R. L., Berglund, P., & Wittchen, H. (1999). Toward a developmental profile. Clinical Psychology Review, 23,
Impairments in pure and comorbid generalized anxiety disorder and 761–786.
major depression at 12 months in two national surveys. American Noyes, R., Woodman, C., Garvey, M. J., Cook, B. L., Suelzer, M.,
Journal of Psychiatry, 156, 1915–1923. Clancy, J., & Anderson, D. J. (1992). Generalized anxiety disorder
Ladouceur, R., Gosselin, P., & Dugas, M. J. (2000). Experimental versus panic disorder: Distinguishing characteristics and patterns
manipulation of intolerance of uncertainty: A study of a theoretical of comorbidity. Journal of Nervous and Mental Disease, 180,
model of worry. Behaviour Research and Therapy, 38, 933–941. 369–370.
Ladouceur, R., Talbert, F., & Dugas, M. J. (1997). Behavioral Öhman, A., Erixon, G., & Löfberg, I. (1975). Phobias and
expressions of intolerance of uncertainty in worry. Behavior preparedness: Phobic versus neutral pictures as conditioned stimuli
Modification, 21, 355–371. for human autonomic responses. Journal of Abnormal Psychology,
Leahy, R. L. (2005). The worry cure: Seven steps to stop worry from 84, 41–45.
stopping you. New York: Harmony Books. Olfson, M., Kessler, R. C., Berglund, P. A., & Lin, E. (1998).
Lee, S. W., & Kwon, J. (2013). The efficacy of imagery rescripting Psychiatric disorder onset and first treatment contact in the
(IR) for social phobia: A randomized controlled trial. Journal of United States and Ontario. American Journal of Psychiatry, 155,
Behavior Therapy and Experimental Psychiatry, 44, 351–360. 1415–1422.
Lovibond, P. F., & Shanks, D. R. (2002). The role of awareness Öst, L.-G. (1987). Age of onset in different phobias. Journal of
in Pavlovian conditioning: Empirical evidence and theoretical Abnormal Psychology, 96, 223–229.
implications. Journal of Experimental Psychology: Animal Öst, L.-G., & Sterner, U. (1987). Applied tension: A specific
Behaviour Processes, 28, 3–26. behavioural method for treatment of blood phobia. Behaviour
Mahe, V., & Balogh, A. (2000). Long-term pharmacological Research and Therapy, 25, 25–29.
treatment of generalized anxiety disorder. International Clinical Page, A. C. (1994a). Blood-injury phobia. Clinical Psychology
Psychopharmacology, 15, 99–105. Review, 14, 443–461.
Marks, I. M. (1988). Blood-injury phobia: A review. American Page, A. C. (1994b). Distinguishing panic disorder and agoraphobia
Journal of Psychiatry, 145, 1207–1213. from social phobia. Journal of Nervous and Mental Disease, 182,
Mattick, R. P., Peters, L., & Clarke, J. (1989). Exposure and cognitive 611–617.
restructuring for social phobia: A controlled study. Behavior Page, A. C. (2003). The role of disgust in faintness elicited by blood
Therapy, 20, 3–23. and injection stimuli. Journal of Anxiety Disorders, 17, 45–58.
Mattis, S. G., & Ollendick, T. H. (2002). School refusal and separation Page, A. C., & Martin, N. G. (1998). Testing a genetic structure of
anxiety. In M. Hersen (Ed.), Clinical behavior therapy: Adults and blood-injury-injection phobias. American Journal of Medical
children (pp. 304–325). Hoboken: John Wiley & Sons. Genetics, 81, 377–384.
McEvoy, P. M., Erceg-Hurn, D. M., Saulsman, L. M., & Thibodeau, Page, A. C., & Stritzke, W. G. K. (2006). Clinical psychology for
M. A. (2015). Imagery enhancements increase the effectiveness trainees: Foundations of science-informed practice. Cambridge:
of cognitive behavioural group therapy for social anxiety disorder: Cambridge University Press.
A benchmarking study. Behaviour Research and Therapy, 65, Pull, C. B. (2005). Current status of virtual reality exposure therapy in
42–51. anxiety disorders: Editorial review. Current Opinion in Psychiatry,
McEvoy, P. M., Grove, R., & Slade, T. (2011). Epidemiology of 18, 7–14.
anxiety disorders in the Australian general population: Findings Rachman, S. (1991). Neo-conditioning and the classical theory of
from the 2007 Australian National Survey of Mental Health and fear acquisition. Clinical Psychology Review, 11, 155–173.
Wellbeing. Australian and New Zealand Journal of Psychiatry, 46, Rapee, R. M. (1991). Generalized anxiety disorder: A review of
957–967. clinical features and theoretical concepts. Clinical Psychology
McEvoy, P. M., Nathan, P., Rapee, R. M., & Campbell, B. N. C. Review, 11, 419–440.
(2012). Cognitive behavioural group therapy for social phobia: Rapee, R. M., & Heimberg, R. G. (1997). A cognitive-behavioural
Evidence of transportability to community clinics. Behaviour model of anxiety in social phobia. Behaviour Research and
Research and Therapy, 50, 258–265. Therapy, 35, 741–756.
Menzies, R. G., & Clarke, J. (1995). The aetiology of phobias: A Rapee, R. M., & Lim, L. (1992). Discrepancy between self- and
nonassociative account. Clinical Psychology Review, 15, 23–48. observer ratings of performance in social phobics. Journal of
Mineka, S., Watson, D., & Clark, L. A. (1998). Comorbidity of anxiety Abnormal Psychology, 101, 728–731.
and unipolar mood disorders. Annual Review of Psychology, 49, Reiss, S., Peterson, R. A., Gursky, D. M., & McNally, R. J. (1986).
377–412. Anxiety sensitivity, anxiety frequency and the predictions of
Mineka, S., & Zinbarg, R. (1996). Conditioning and ethnological fearfulness. Behaviour Research and Therapy, 24, 1–8.
models of anxiety disorders: Stress-in-dynamic-context anxiety Roemer, L., Molina, S., Litz, B. T., & Borkovec, T. D. (1997).
models. In D. A. Hope (Ed.), Nebraska Symposium on Motivation, Preliminary investigation of the role of previous exposure to
rie66620_ch02_041-072.indd 69 08/02/17 06:48 AM

potentially traumatizing events in generalized anxiety disorder. Torgersen, S. (1979). The nature and origin of common phobic fears.
Depression and Anxiety, 4, 134–138. British Journal of Psychiatry, 134, 343–351.
Roemer, L., & Orsillo, S. M. (2007). An open trial of an acceptance- Turk, C., Heimberg, R., & Mennin, D. (2004). Assessment. In
based behavior therapy for generalized anxiety disorder. Behavior R. G. Heimberg, C. L. Turk, & D. S. Mennin (Eds.), Generalized
Therapy, 38, 72–85. anxiety disorder: Advances in research and practice (pp. 219–247).
Roemer, L., Orsillo, S. M., & Salters-Pedneault, K. (2008). Efficacy New York: Guilford Press.
of an acceptance-based behavior therapy for generalized anxiety Vogele, C., Coles, J., Wardle, J., & Steptoe, A. (2003).
disorder: Evaluation in a randomised controlled trial. Journal of Psychophysiologic effects of applied tension on the emotional
Consulting and Clinical Psychology, 76, 1083–1089. fainting response to blood and injury. Behaviour Research and
Sanchez-Meca, J., Rosa-Alcazar, A. I., Marin-Martinez, F., & Therapy, 41, 139–155.
Gomez-Conesa, A. (2010). Psychological treatment of panic Watson, D., & Clark, L. A. (1984). Negative affectivity: The
disorder with or without agoraphobia: A meta-analysis. Clinical disposition to experience negative aversive emotional states.
Psychology Review, 30, 37–50. Psychological Bulletin, 96, 465–490.
Sanderson, W. C., Rapee, R. M., & Barlow, D. H. (1989). The Watson, J. B., & Raynor, R. (1920). Conditioned emotional reactions.
influence of an illusion of control on panic attacks induced via Journal of General Psychology, 37, 394–419.
inhalation of 5.5% carbon dioxide-enriched air. Archives of General Wells, A. (1995). Meta-cognition and worry: A cognitive model
Psychiatry, 46, 157–162. of generalized anxiety disorder. Behavioural and Cognitive
Segal, Z. V., Williams, J. M. G., & Teasdale, J. D. (2002). Psychotherapy, 23, 301–320.
Mindfulness-based cognitive therapy for depression: A new Wells, A., & Carter, K. (2001). Further tests of a cognitive model
approach to preventing relapse. New York: Guilford Press. of generalized anxiety disorder: Metacognitions and worry in
Seligman, M. E. (1971). Phobias and preparedness. Behavior GAD, panic disorder, social phobia, depression and nonpatients.
Therapy, 2, 307–320. Behavior Therapy, 32, 85–102.
Slade, T., Johnston, A., Oakley, B. M., Andrews, G., & Whiteford, Wittchen, H. U. (2002). Generalized anxiety disorder: Prevalence,
H. (2009). 2007 National Survey of Mental Health and Wellbeing: burden, and cost to society. Depression and Anxiety, 16, 162–171.
Methods and key findings. Australian and New Zealand Journal of Wolitzky-Taylor, K. B., Horowitz, J. D., Powers, M. B., & Telch, M. J.
Psychiatry, 43, 594–605. (2008). Psychological approaches in the treatment of specific
Spence, S. H., Donovan, C., & Brechman Toussaint, M. (1999). phobias: A meta-analysis. Clinical Psychology Review, 28,
Social skills, social outcomes, and cognitive features of childhood 1021–1037.
social phobia. Journal of Abnormal Psychology, 108, 211–221. Woody, S. R. (1996). Effects of focus of attention on anxiety levels
Stein, M. B., & Heimberg, R. G. (2004). Well-being and life and social performance of individuals with social phobia. Journal
satisfaction in generalized anxiety disorder: Comparison to major of Abnormal Psychology, 105, 61–69.
depressive disorder in a community sample. Journal of Affective World Health Organization (2010). International statistical
Disorder, 79, 161–166. classification of diseases and related health problems. Retrieved
Tillfors, M., Furmark, T., Ekselius, L., & Fredrikson, M. (2001). from http://apps.who.int/classifications/icd10/browse/2010/en.
Social phobia and avoidant personality disorder as related to Yonkers, K. A., Dyck, I. R., Warshaw, M. G., Massion, A. O., &
parental history of social anxiety: A general population study. Keller, M. B. (1996). Phenomenology and course of generalized
Behaviour Research and Therapy, 39, 289–298. anxiety disorder. British Journal of Psychiatry, 168, 308–313.
rie66620_ch02_041-072.indd 70 08/02/17 06:48 AM

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72
GRADUATE SPOTLIGHT
NAME: SOFIA ROBLEDA
Degree studied: Bachelor of Psychological Science &

Doctor of Clinical Psychology
University: University of Queensland
Current position: Clinical Psychologist
Employer: Walters Green Clinical Psychology Practice
What interested you about working in/studying psychology?

I grew up in a few different countries, including Mexico, Saudi Arabia and Singapore. Living with so many
people from different cultural backgrounds fascinated me, and I became interested in what makes us so
distinct, and so similar, at the same time. I wanted to study psychology to better understand people.
What have you been up to since graduation?

After completing my Honours degree, I worked as a research assistant and contributed to some scientific
publications. I then realised my passion lay in clinical practice. I was accepted into a clinical doctorate
program, and through one of my university placements I was able to get a job upon my second graduation.
I worked at Alzheimer’s Australia as a behaviour consultant, until I began to consult privately.
What does your job/position involve?

In a nutshell, when a patient first comes in to see me, an initial assessment is completed. From that
assessment, the patient and I work out how and why they are having difficulties, and what is keeping them
going. We then apply evidence-based therapies to treat those difficulties. I mainly work with adults and
older adults who are experiencing mental health issues, particularly depression and anxiety. I also work
with couples experiencing relationship distress.
What do you enjoy most about your work?

I really enjoy it when my patients apply the skills we discuss and notice improvements. It can be very
rewarding in that sense. Clinical psychology is also great because there are many things to learn, depending
on what populations, disorders or therapies you’re interested in.
What advice would you give to students wanting to work in psychology?

I would say, first try to figure out as early as possible what area in psychology you’d like to work in. If you’re
hoping to become a clinical psychologist, know that it’s a long, hard road, and it’s very competitive. It’s
important to practise what you preach. Prioritise your self-care, be kind to yourself as well as others, and
look out for different pathways towards accreditation, as there are a few!
rie66620_ch02_041-072.indd 72 08/02/17 06:48 AM

CHAPTER 3
Obsessive-compulsive
and related disorders
Ross G. Menzies
CHAPTER OUTLINE
● The diagnosis and presentation of obsessive-compulsive disorder (OCD)
● The epidemiology and aetiology of obsessive-compulsive disorder
● The treatment of obsessive-compulsive disorder
● obsessive-compulsive disorder-related disorders
● Summary

3.1 Describe the nature and diagnostic criteria for obsessive-compulsive disorder (OCD).
3.2 Describe the epidemiology and aetiological accounts of OCD.
3.3 Describe the essential elements of contemporary treatment approaches to OCD.
3.4 Describe the nature and diagnostic criteria for hoarding disorder, body dysmorphic disorder, trichotillomania and
excoriation disorder.
OBSESSIVE-COMPULSIVE AND RELATED DISORDERS: AN AUSTRALASIAN FOCUS

Obsessive-compulsive disorder gained a high profile in Australia when Scott Draper, a national sporting hero, revealed
his struggle with the condition.
Scott had emerged as a huge talent in the tennis world after winning the Wimbledon Junior Doubles title in 1992. The
following year he turned professional and began rising up the world rankings. He would go on to many impressive victories
in the sport before making the stunning decision to leave tennis and take up professional golf. On 11 February 2007, he
won the New South Wales PGA Championship, giving him the rare achievement of titles in two professional sports.
Despite his outward success, Scott had privately been facing a series of personal tragedies and mental health issues.
Among these, he has now revealed that he developed religious and contamination obsessions, which resulted in crippling
compulsive rituals at the age of 19. At that time, as he began his assault on the professional tennis world, he formed
the obsessive belief that God would punish him for minor and trivial ‘wrongdoings’. Given a fear of germs and vomiting,
Scott believed that if all of his daily tasks were not completed ‘correctly’, God would inflict vomiting upon him. Beginning
rapidly, as is often the case in OCD, he engaged in ever more complicated compulsive behaviours to prevent this outcome
from happening. These behaviours included making his bed perfectly, fastidiously straightening and rearranging items,
checking, and cleaning and wiping down surfaces.
Of all of his rituals, repetitive touching behaviours became the most debilitating element of his disorder. This involved
touching dozens of items in particular number patterns, or until ‘they felt right’. At his worst, Scott took over three hours
to perform his rituals each evening before he could go to bed.
Scott has spoken about his OCD on several occasions over recent years, providing a salient example of how the condition
can suddenly grip otherwise highly functioning individuals. The present chapter will examine this complex disorder, beginning
continued
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with an outline of its diagnostic criteria and a description of

the astonishing range of its possible presentations. Following
this, the epidemiology and aetiology of OCD will be examined.
Particular emphasis will be given to Australasian research in
the investigation and refinement of cognitive models of the
disorder. Attention will then turn to the treatment of OCD.
Emphasis will be given to exposure-based procedures that
have dominated treatment programs for OCD for nearly
40 years. However, it will be shown that OCD does not always
respond to such treatment and the Australasian development of
alternatives to exposure will be detailed. Finally, an introduction
to additional ‘OCD-related’ conditions will be given, including
DAL
hoarding disorder, body dysmorphic disorder, trichotillomania
and excoriation disorder.
LO 3.1 Obsessive-compulsive disorder: diagnosis
and presentation
The diagnosis of obsessive-compulsive disorder
Historically, obsessive-compulsive disorder (OCD) was conceptualised as an anxiety disorder. Yet
with the introduction of the current, fifth edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-5; American Psychiatric Association [APA], 2013), OCD was included in a separate
chapter entitled ‘Obsessive-Compulsive and Related Disorders’. The DSM-5 chapters on anxiety
disorders and obsessive-compulsive disorders have been placed adjacent to each other in order to
obsessive-
reflect the close relationships between these conditions.
compulsive
disorder (OCD)
The DSM-5 describes OCD according to four diagnostic criteria. The first criterion is the presence
of obsessions and/or compulsions. Obsessions are defined as recurrent and persistent thoughts,
Anxiety disorder
characterised by impulses or images that are experienced as intrusive and inappropriate or distressing. The thoughts
obsessions and/ are not simply excessive worries about real-life problems (such as mortgage interest rates or difficult
or compulsions. interpersonal relationships). In addition, to be defined as an obsession, the person must attempt to
ignore the thoughts, impulses or images or to neutralise them by engaging in some other mental
obsessions
Uncontrollable, routine or behaviour. Finally, in order to distinguish obsessions from some aspects of psychotic illness,
persistent the person must recognise that the obsessional thoughts are the product of his/her own mind.
thoughts, images, Compulsions are defined as repetitive behaviours (including mental routines) that the person
ideas or impulses feels compelled to perform in response to an obsession or according to strict rules. To be termed a
that an individual compulsion, the behaviours must be aimed at reducing anxiety (usually triggered by an obsession) or
feels intrude preventing a threatening outcome.
upon his/her
As in many other conditions, the second criterion of the DSM-5 states that the disorder must cause
consciousness
and that cause marked distress, be time-consuming (i.e., take more than one hour a day) or significantly interfere with
significant anxiety the sufferer’s occupational or social functioning. The third criterion states that the symptoms are not
or distress. attributable to a substance (i.e., a drug of abuse or medication) or another medical condition. Finally, in
a related fourth criterion, the DSM-5 emphasises that the content of obsessions or compulsions cannot
compulsions be restricted to another disorder that is present. For example, excessive concern about appearance in
Repetitive
an individual with body dysmorphic disorder would not warrant the additional diagnosis of OCD.
behaviours or
mental acts that In addition to meeting these criteria, the DSM-5 requires that the individual’s level of insight is
an individual specified. ‘Good or fair insight’ is defined as the individual recognising that his/her OCD beliefs
feels s/he must are probably not true. ‘Poor insight’ is noted in cases where the sufferer argues that his/her OCD
perform. beliefs are probably true. ‘Absent insight’ (or ‘delusional beliefs’) refers to individuals who appear
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Chapter 3 Obsessive-compulsive and related disorders 75
to be completely convinced that their OCD beliefs are true. It should be noted that the inclusion of
an ‘absent insight’ specifier is somewhat controversial as it makes the distinction between OCD and
psychotic conditions more difficult. Finally, given the frequent experience of tic-related problems in
OCD, a current or past history of tic disorder (e.g., Tourette’s disorder, in which sufferers experience
motor tics such as repeated eye blinking and vocal tics such as repeating one’s own words), should
also be specified in a complete DSM-5 assessment of OCD.
As mentioned, the most notable change from the DSM-IV-TR (APA, 2000) to the DSM-5 was the
removal of OCD from the chapter on anxiety disorders. In its new category of ‘Obsessive-Compulsive
and Related Disorders’, OCD is now grouped with body dysmorphic disorder, hoarding disorder,
trichotillomania (hair-pulling) and excoriation (skin-picking) disorder. The American Psychiatric
Association (2013) states that this regrouping reflects ‘increasing evidence of these disorders’ relatedness
to one another in terms of a range of diagnostic validators as well as the clinical utility of grouping these
disorders in the same chapter’ (p. 235). In other words, the commonalities in the diagnostic features and
treatment approaches for these various disorders have led to their being classified together in the DSM-
5. However, separating OCD from the anxiety disorders is a contentious decision given the substantial
commonalities in the cognitive models used to understand the aetiology of OCD and anxiety disorders.
The presentation of obsessive-compulsive disorder

While the DSM-5 does a good job of describing the limits of OCD, it does little to indicate the
breadth of possible presentations of this disorder. Perhaps more than any other psychiatric condition,
OCD varies considerably from case to case. A seemingly endless list of possible topics can become
the source of an obsession. Australian researchers have noted that the content of many obsessions
seem linked to broader theses related to death (Menzies & Dar-Nimrod, in press). Among common
obsessions are fears of contamination and germs; of fire, robbery, rape and assault; of losing one’s
mind or becoming insane; of insulting others; of impulsive swearing; of harming others by acting
on a sudden impulse (e.g., stabbing a friend); of engaging in a homosexual act; of engaging in a
paedophilic act; of offending a higher power through blasphemy; or of driving into an individual
without knowing it (Einstein & Menzies, 2003).
Further, almost any behaviour can become a compulsion, even when there is no obvious or logical
link between the behaviour and the prevention of harm. For example, in order to prevent fire, a sufferer
may repeatedly engage in any of the following: checking power points and electrical appliances;
touching the knobs on the gas stove; blinking one’s eyes a set amount of times; counting objects;
saying a mantra in one’s head or out loud; tapping a surface; touching an object; hopping; climbing
onto a chair; getting into and out of a chair; re-entering a room; or arranging objects on a desk.
Thus, given the possible combinations of obsessions and compulsions, an almost infinite variety of
presentations of the disorder are possible.
CASE STUDY: OBSESSION WITH HARMING OTHERS

Mary is a 48-year-old woman who developed OCD in adolescence. After being a victim of bullying for many years at
school, she lashed out at another girl one day, striking her to the ground in the schoolyard. Following this, she began to
slowly develop the fear that she would enter an uncontrollable rage and harm others.
Mary’s obsession waxed and waned throughout her 20s and 30s. She reported that, at her best, she was relatively
untroubled by her fears, often for months at a time. Inevitably, however, the fear of harming others would return.
Typically, its reappearance would follow news reports or media coverage of apparently random acts of violence.
In the past five years, with increasing terrorist activities targeting innocent civilians, Mary became overwhelmed
with her obsessions. When she finally sought treatment, she revealed that she was also suffering with repetitive
nightmares in which she stabbed people in her home or random people in the street, or drove over pedestrians in
continued
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her car. In terror, she had stopped driving several months earlier. Her insight into the irrational nature of her fears
was poor, with Mary stating that:
One day, I think I’ll end up in jail. I think I’ve just been lucky so far. Sometimes I feel such a strong urge to strike or
stab someone—one day I think it could happen. I worry when I have to walk down the street. I’m sure I’m going
to strike a young child or baby in a pram. Dinner parties, and cooking in general, are even harder. If I have to do
anything in the kitchen when other people are near me, I get strong fears that I’ll pick up a knife and stab them. It’s
worse if I really care for the person. I can’t have my husband help me cook and I keep all the largest knives in the
highest cupboard in the kitchen, out of easy reach. Part of me knows the thoughts are just my OCD, but a larger part
is petrified that I really will carry out the thoughts. I think the urges are probably genuine.
Mary’s treatment centred on exposure and response prevention. She was encouraged to confront her fears by sitting
near large knives while watching television with her family. She also engaged in purposeful exposure to thoughts and
images of harming others while walking down busy streets. All reassurance-seeking (e.g., asking family members to
confirm that she had not lashed out) was prevented in treatment. She was also prevented from compulsively turning
around on the street to see if she had harmed anyone. As her treatment continued, Mary grew increasingly confident
that her aggressive thoughts and images were insignificant. After struggling with OCD for more than 30 years, she was
finally able to realise that she was not a danger to anyone.
Though there are many diverse manifestations of OCD, some types of the disorder are more
common than others. For example, it has been suggested that the majority of individuals with OCD have
performed excessive, compulsive washing at some point (Jones & Krochmalik, 2003; Rapoport, 1989).
Summerfeldt, Antony, Downie, Richter, and Swinson (1997) reported that of nearly 200 patients with
OCD, 63.7 per cent had current washing compulsions. Compulsive washing typically entails excessive
handwashing, showering or toilet routines, although cleaning of kitchen and bathroom surfaces is not
uncommon. The following case illustrates one individual’s experience of compulsive washing:
It takes me at least two hours to shower properly, so I avoid it whenever I can. I’d rather stay in
my pyjamas and not leave the house than have to shower and dress. First I have to strip off my
pyjamas and lay out my new clothes. If my clean clothes touch my pyjamas, or anything I think is
dirty, I have to put them in the wash. Then I have to clean the bathroom. I use bleach on all the
taps in the bathroom before I shower, and I also clean the shower door. When I’m in the shower
I work on one body part at a time. I use an antibacterial soap and wash each part of my body until
I count to 50 in my head. I do this five times and then I move to a different body part. Before I start,
I also mix up a bottle of face cleanser, bleach
and water—I use this mix on my genitals.
Sometimes it makes my skin go red, but it’s
the only way I can be sure I’m clean.
In addition to washing/cleaning, compulsive

checking is another common feature of OCD.
Checking behaviours can include a seemingly
endless range of objects and activities, although
the most common involve the checking of taps,
power points, stoves, electrical appliances
and door and window locks. Rachman (2003)
argues that compulsive checking is the most
common and prominent feature of OCD and
DAL
some research supports this claim. For instance,

Compulsive washing is a common symptom of obsessive-compulsive Antony, Downie, and Swinson (1998) found the
disorder. Compulsive washing typically entails excessive handwashing, ratio of checkers to washers to be about 4:3.
showering or toilet routines. Certainly, together with washing, compulsive
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checking accounts for much of the behaviour seen in OCD clinics around the world. The following
case describes an individual’s compulsive checking ritual:
I check so many things—I really don’t know where to start. Stuff around the house is the worst.
Before I leave the house I have to check that every tap and power point is turned off, all the
downstairs windows are locked and all the knobs on the gas stove are off. The taps and the stove
are the most difficult. I find it very hard to trust my eyes. I look at the bottom of each tap and
stare, sometimes for 5 or 10 minutes, looking for water. Often I have to put my hands under each
tap repeatedly to see if they get wet, even though I see that no water is coming out. With the stove,
I’m terrified that I will knock a gas knob on while I do my checks. To help me, I’ve marked the
‘off’ symbol in bright red paint so I can do a final check from the other side of the room. That way
I know I can’t have accidentally knocked the knobs on, because I’m too far away to touch them.
CASE STUDY: CONTAMINATION OBSESSIONS AND COMPULSIONS

Peter is a 32-year-old man who has suffered with OCD since early childhood. His anxiety began at age 8 when his
uncle died suddenly of a heart attack. Peter became obsessed with the idea that his mother would suddenly die
and he began a counting ritual each night to prevent any harm from occurring. At first, this simply involved counting
backwards by 3s from 90. However, over time, the ritual became more elaborate, involving a series of movements
and mantras that had to be performed in order to prevent his mother’s death. These behaviours were kept secret
from his family for several years because he feared that his parents would stop him from completing the rituals if they
were discovered.
During adolescence, Peter’s fears transferred to the nature of his identity. Most notably, he became obsessed with
the fear of becoming someone else. He believed that physical contact with boys that he did not like might magically lead
him to take on some of their properties, including their personality, interests and expressions. He engaged in washing to
remove this risk, but eventually the fear intensified and produced a significant school refusal problem. Peter would not
attend school on days involving sport (in which contact with others was inevitable), and increasingly attempted to isolate
himself at school. He would sit in the library at lunch on his own rather than join in ball games with the other boys. At age
15, he transferred to a distance education program because school attendance had become too difficult for him.
Over the decade that followed, Peter’s fears slowly changed to more general contamination concerns. He was
no longer afraid of losing his identity, but he became fearful of illness and disease through contact with others. He
managed to complete several IT courses at TAFE and now works for himself running a small web-design business. At
32, Peter lives a quiet life on his own. He has few friendships and has not had a sexual relationship. Not surprisingly,
Peter has suffered with significant and recurrent depressive episodes across his life. He had not sought treatment for
his OCD previously.
Given that contamination concerns were now the central feature of his OCD, Peter was trialled on the Australian
‘DIRT’ treatment program. Therapy focused on psychoeducation about the nature of bacteria and disease, corrective
information about illness, and rational restructuring of his erroneous beliefs. Given his varied history of OCD symptoms,
the treatment was provided within a broader context in which Peter came to learn that he was giving too much significance
or importance to his doubt thoughts.
LO 3.2 The epidemiology and aetiology

of obsessive-compulsive disorder
The epidemiology of obsessive-compulsive disorder
In the early 1980s, the Epidemiology Catchment Area program was undertaken to examine the
prevalence of mental disorders in five communities across the United States (Karno, Golding,
Sorenson, & Burman, 1988). It represented the first large-scale epidemiological investigation of
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mental disorders, with over 30 000 individuals surveyed. Results from this survey suggested that OCD
was a more common disorder than had previously been thought. Across the five communities, lifetime
prevalence rates ranged from 1.9 to 3.3 per cent. These findings suggested that OCD was twice as
common as schizophrenia or panic disorder, and the fourth most common psychiatric condition
(Pigott, 1988).
Later research has essentially replicated these findings in other communities. For example, the Cross-
National OCD Collaborative Group study found comparable prevalence rates to the Epidemiology
Catchment Area study in six countries: Canada, Germany, Korea, New Zealand, Puerto Rico and
Taiwan (Weissman, Bland, Canino, & Greenwald, 1994). In sum, there is now a general consensus
that OCD is a relatively common disorder, with a prevalence rate in the 2–3 per cent range.
In addition to its high prevalence, OCD is regarded as a particularly serious condition because it can
be associated with a lifetime of impairment. Obsessive-compulsive disorder occurring in childhood
is common, with an average age of onset for the disorder of 10.3 years (Geller et al., 1998). As many
as 80 per cent of adults with OCD recall that the onset of their symptoms was before 18 years of age
(Shafran, 2003). Hence, it is argued that OCD will often begin in early childhood and, left untreated,
remain throughout adulthood. While the condition may wax and wane across the lifetime, varying in
intensity and form at various points, it will rarely spontaneously remit.
The aetiology of obsessive-compulsive disorder

The question of aetiology or cause remains the most controversial topic among leading OCD
researchers. Two divergent models, the neuropsychological and the cognitive, have strong advocates.
THE NEUROPSYCHOLOGICAL MODEL

In support of the neuropsychological model, Baxter and colleagues (2000) present a large body
neuroimaging of neuroimaging and neuropsychological findings that suggest that OCD results from a failure of
Range of inhibitory pathways in the basal ganglia of the brain to stop ‘behavioural macros’ being triggered in
techniques used response to internal or external stimuli. Behavioural macros are defined as complex sets of behaviours
to image the choreographed for specific situations, such as grooming and checking. Many studies have found
structure and/
differences between OCD sufferers and controls in aspects of functioning in the caudate nucleus and
or function of
the brain such other areas of the basal ganglia (Frampton, 2003). To date, however, research has not been able to
as computerised establish that these differences have a causal role in triggering OCD symptoms.
tomography (CT),
positron emission THE COGNITIVE MODEL
tomography (PET) The relevance of the neuroimaging and neuropsychological findings has been questioned by
and magnetic advocates of the cognitive model of OCD. Salkovskis (1996a) points out that most of the observed
resonance differences in brain function could be a consequence of having OCD, rather than a cause of it.
imaging (MRI)
In addition, there have been no replicated demonstrations of any specific neural dysfunction in
scans.
individuals with OCD (Macdonald, 2003). Further, the enormous variety of OCD presentations
does not seem to be covered by the notion of behavioural macros. That is, OCD sufferers do more
basal ganglia than check and groom. They engage in compulsions as diverse as tapping, hopping, blinking,
Group of large counting, arranging, getting into and out of chairs and so on. Finally, several researchers have
nuclei in the shown that the obsessions experienced in OCD are not qualitatively different from the intrusive
forebrain; thoughts experienced by the general population (Rachman & de Silva, 1978; Salkovskis &
involved in the Harrison, 1984). What appears to be different is the way in which OCD sufferers appraise or
control of motor
interpret their intrusive thoughts.
behaviour and
may be relevant The cognitive model emphasises that OCD results from the misinterpretation of intrusive
to obsessive- thoughts. Salkovskis and McGuire (2003) argue that OCD sufferers give the intrusive thoughts
compulsive significance, rather than simply ignoring them as do the rest of the general population. OCD
disorder. sufferers interpret an intrusive thought to indicate that danger may occur to themselves and others,
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and that they could be personally responsible for bringing about or

preventing this danger. Behavioural responses (such as compulsions) are
driven by the desire to reduce these threat appraisals and seek safety.
Salkovskis (1996b) argues that the appraisal ‘I will be responsible for
harm’ (or responsible for the prevention of harm if action is taken) is a
crucial motivating factor in driving repetitive behaviour in OCD. The
cognitive model of OCD remains the only theoretical position that is
consistent with the full range of phenomenology of OCD. It is also
supported by the effectiveness of cognitive-behavioural approaches to
treatment that are based on the cognitive model.
A study by the Australian team of Jones and Menzies (1997a)
investigated the cognitive model of OCD among individuals who engaged
in compulsive washing. Specifically, they explored the role of expectations
of threat (particularly disease and death) in driving compulsive washing
in 27 participants with OCD. Participants were required to place their
hands in a receptacle containing a mixture of soil, animal hair, raw meat
and household food scraps. During the task, ratings of participants’ threat
appraisals (i.e., the perceived likelihood of catching a disease and estimates
of the severity of the diseases on a ‘death’ scale) were taken. It was found
that threat appraisals were strongly related to participants’ anxiety during
the task, avoidance of the task and the amount of time spent washing after
the task. The results are thus consistent with the notion that threat appraisals
DAL
trigger compulsive washing and the related symptoms of anxiety and
avoidance. However, since this is a correlational study, the causal role of Fear of death may mediate some compulsive
threat appraisals has not been definitively established. Causal claims need to behaviours.
be supported by experimental studies.
correlational study
Experimental research does indeed support the notion that perceptions of threat trigger OCD Type of study in
symptoms. One type of threat appraisal relates to death anxiety, which has been proposed as playing which researchers
a role in OCD (Iverach, Menzies, & Menzies, 2014; Menzies & Iverach, 2016; Menzies, Menzies, assess only the
& Iverach, 2015). An Australian team was the first in the world to demonstrate that death priming relationship
in the laboratory may increase compulsive behaviour. Specifically, Rachel Menzies and Ilan Dar- between two
Nimrod examined whether death priming could selectively exacerbate compulsive cleaning behaviours variables and do
among OCD washers (Menzies & Dar-Nimrod, in press). In this study, 132 participants with OCD not manipulate
one variable to
(66 washers and 66 non-washers) were randomly allocated to either a death or dental pain priming determine its
condition. In the death priming condition, participants were asked to answer two questions about the effect on another
moment of death, namely: (1) ‘Please briefly describe the emotions that the thought of your own variable (as in
death arouses in you’; and (2) ‘Jot down, as specifically as you can, what you think will happen to an experimental
you as you physically die and once you are physically dead’. Participants allocated to the dental pain study).
priming condition were asked similar questions relating to the experience of dental pain. Following experimental
priming, participants completed a series of tasks that involved taking skin conductance recordings, study
with these recordings requiring the application of conductive gel. They were then allowed to wash Type of study that
the conductive gel off their hands. As hypothesised, death priming among compulsive washers led can address the
to greater efforts in cleaning (as measured by washing duration, soap use and paper towel use) than issue of causality
dental priming. given that the
In a second study in the same report, Menzies and Dar-Nimrod (in press) investigated the independent
relationships between death anxiety and a variety of markers of psychopathology in 171 OCD variable is directly
manipulated so
participants. Large, positive correlations were obtained between measures of fear of death and OCD that its effect on
severity, the number of hospitalisations, the number of medications and the total number of lifetime the dependent
anxiety-related diagnoses identified. In sum, death anxiety was shown to potentially underlie many of variable can be
the mental health difficulties experienced across the life-course by individuals with OCD. examined.
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cognitive
behaviour LO 3.3 The treatment of obsessive-compulsive
therapy (CBT)
Type of disorder
psychological
treatment that Cognitive behaviour therapy (CBT) remains the treatment of choice for OCD, with approximately
combines both 75 per cent of patients treated with CBT procedures improving significantly and remaining
cognitive and improved over time (Kyrios, 2003). Cognitive behavioural procedures include exposure-based tasks,
behavioural
behavioural experiments and other tasks designed to challenge the irrational threat-related beliefs of
concepts and
techniques. OCD sufferers.
The CBT procedure that has received the strongest support for OCD is known as exposure and
exposure response prevention. Here, the individual is asked to confront the feared stimuli and the typical
and response compulsive response is prevented or reduced. For instance, compulsive washers may be asked to
prevention reduce the duration of their washing rituals after touching feared stimuli (e.g., light switches or door
Behavioural handles believed to be contaminated) or may be prevented from washing entirely after such encounters,
technique in
thereby disconfirming their belief that harm will occur unless they engage in the compulsive behaviour.
which the client
is: (a) exposed Clinical judgment determines the extent of fear that can be tolerated by the patient and thus the level
to feared of difficulty of the exposure and response prevention tasks.
stimuli (such The related concept of the behavioural experiment is also widely applied in the treatment of OCD.
as obsessions The individual is asked to engage in tasks that test the validity of his/her OCD threat-related beliefs.
in obsessive- For example, a woman with aggressive obsessions was asked to predict the outcome of walking
compulsive through a busy city street in peak hour when she would be forced to bump into others. Her threat
disorder), and
appraisal (‘I will lash out and slap someone’) was tested by carrying out the behaviour of walking
(b) prevented
from utilising any down the street, which was filmed to prove to the sufferer that no harm occurred during this activity.
responses (such Various forms of cognitive restructuring have also been successfully used in OCD. Cognitive
as compulsions restructuring involves challenging the appraisals that individuals with OCD give to their intrusive
in obsessive- thoughts. This often involves modifying the inflated risk estimates of OCD sufferers. For example,
compulsive one patient believed that she was 95 per cent certain of contracting a serious illness from an incident
disorder) aimed in which her hand might have brushed against a rubbish bin in the street. The therapist and patient
at escaping from
broke the feared outcome into a sequence of steps that would have to occur for the feared outcome
his/her anxiety.
(i.e., serious illness) to actually happen. The patient was then asked to estimate the likelihood or
behavioural probability of each step occurring. A cumulative probability was then calculated, showing the
experiment individual that, even by her own estimates, the chance that she would contract a serious illness from
Cognitive the incident was only 1 in 200 000. The probability estimates for each of the steps occurring separately
technique in and together as a cumulative probability are shown in Table 3.1
which the client
participates in a
planned activity
in order to test
the accuracy of TABLE 3.1 The probability of each event occurring separately and cumulatively in the case of a patient
his/her beliefs. with OCD who feared catching a disease after possibly touching a rubbish bin
cognitive STEP CHANCE (CUMULATIVE CHANCE)

restructuring
Hand actually brushed against bin 1:2 (1:2)
Cognitive
technique in Germs present where hand touched 1:2 (1:4)
which the client
learns to identify, Particular germs present capable of producing serious illness 1:100 (1:400)
challenge and (i.e., not simply minor gastrointestinal upset)
replace his/her
dysfunctional Germs transferred to hand 1:5 (1:2000)
beliefs with more Germs enter body before next wash occurred 1:10 (1:20 000)
realistic or helpful
beliefs. Immune system fails to defend against germs 1:10 (1:200 000)
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In some cases, cognitive techniques alone, without the need for exposure, can be successfully
applied to treat OCD. This is important, because many individuals with OCD refuse to engage
in exposure tasks because of the high levels of anxiety and agitation associated with this form of
treatment. In an Australian development, Jones and Menzies (1997b) introduced Danger Ideation
Reduction Therapy (DIRT) for compulsive washers. The program focuses on psychoeducation about
disease and immune function, and includes a variety of cognitive therapy strategies to lower patients’
risk estimates of illness. The treatment has been shown to eliminate OCD in individuals who have
failed to benefit from exposure and response prevention and medication. In addition, DIRT can
result in rapid recovery, sometimes in as few as eight one-hour sessions (Jones & Krochmalik, 2003;
St Clare, Menzies, & Jones, 2008). The DIRT program has been extended to address compulsive
checking (Viccaro, St Clare, Menzies, & Jones, 2010).
The other treatment modality with established efficacy in OCD is pharmacological therapy. By the
1960s, some evidence was already available suggesting that drugs which increase the availability
of the neurotransmitter serotonin, such as clomipramine, could play a role in OCD treatment. To
date, studies comparing the effectiveness of drugs in treating OCD have suggested that clomipramine
produces the largest treatment effect (McDonough, 2003). Having said that, it should be noted that
only 40–60 per cent of sufferers seem to benefit from medication.
LO 3.4 OCD-related disorders

Hoarding disorder
Closely related to OCD is hoarding disorder. The DSM-5 defines this condition as a persistent difficulty hoarding
in discarding possessions (even those of useless or limited value), with a high level of distress associated disorder
with removing the items. This accumulation of possessions results in significant congestion of living Persistent
areas, which are cleared only through the actions of others. Not surprisingly, this can lead to significant difficulty in
discarding
interpersonal difficulties. It has been suggested that the point prevalence of clinically significant
possessions,
hoarding is approximately 2–6 per cent (APA, 2013). At present, little is known about the gender ratio with a high
of this disorder, although most clinical studies report slightly more female than male sufferers.
level of distress
Frost, Steketee, and Williams (2000) reported that hoarding is associated with substantial risk to associated with
health and safety. In a five-year study of complaints made about hoarding to local health departments removing the
in the state of Massachusetts in the United States, several deaths were directly attributed to hoarding items.
(e.g., house fires stemming from hoarded newspapers). Frost and Hartl (2003) provide several anecdotes
that point to the severity and impact of compulsive hoarding, including a description of an 80-year-old
hoarder who could not walk anywhere in her house, but instead had to ‘swim’ through the waist-high
debris. The following illustrates a case of compulsive hoarding:
I simply can’t throw out sections of newspapers that could be
useful in the future. At last count I had over 125 cardboard
boxes of newspaper clippings and other papers. I have them
stacked in the hall of my home and in two bedrooms. I have most
trouble with the travel sections, and with food and restaurant
reviews. I could miss out on something important if I simply
throw them out—when I do travel, I want to know that I have
collected everything that could guide me. It would be a disaster
SHUTTER STOCK
to miss something, and it would be all my own fault.
As can been seen in the above case, unhelpful thoughts about

imagined costs arising from the removal of items dominate in
hoarding disorder. However, the costs do not always relate to Hoarding may be so extreme as to severely restrict
‘missing out’ on possibilities. The costs can also be emotional people’s ability to move about their home.
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(e.g., ‘I just can’t cope with parting with those dolls’) or existential (e.g., ‘If I throw out my primary
school assignments it’s like they never existed’).
Body dysmorphic disorder

body dysmorphic Also included within the DSM-5 chapter on ‘Obsessive-Compulsive and Related Disorders’ is body
disorder dysmorphic disorder, which entails a preoccupation with an imagined defect of appearance. The
Disorder involving individual believes that a part of his/her body is deformed or of the wrong size (too big or too small).
obsessive Even if there is a slight defect in appearance, the individual’s level of concern is markedly excessive.
concern
Women with the disorder tend to have unhelpful thoughts about their nose, breasts, hips and weight;
regarding a
part of the body with men the thoughts are about their genitals, body hair, baldness and general body build. The point
the individual prevalence of the disorder is estimated at approximately 2.5 per cent, with similar numbers of male
believes is and female sufferers in most reports (APA, 2013).
defective. The preoccupation causes compulsive mirror checking, excessive grooming or reassurance-seeking
from others. As with most DSM-5 conditions, to be considered a disorder it must be associated
clinically with clinically significant distress or impairment in social, occupational or other important areas
significant of functioning (e.g., avoidance of public situations) and is not better accounted for by another
Meaning the psychological disorder (e.g., dissatisfaction with body shape and weight in anorexia nervosa). Those
disorder causes with the disorder may seek cosmetic surgery, but unfortunately this is not always successful in
substantial
eliminating the individual’s concerns. Evidence suggests that up to 15 per cent of people seeking
impairment
in social, cosmetic surgery meet criteria for body dysmorphic disorder (Crerand, Franklin, & Sarwer, 2006).
occupational or Although surgery may have only limited success in reducing the patient’s concerns, psychological
other areas of therapies can be of benefit (Cororve & Gleaves, 2001).
functioning.
Trichotillomania (hair-pulling disorder)
trichotillomania Trichotillomania involves the recurrent pulling out of one’s own hair, resulting in hair loss. While many
Condition that body regions can be involved, hair from the scalp, eyelashes and eyebrows are the most common targets.
involves the In severe cases, virtually all of the hair on the head may be removed, causing obvious distress and
recurrent pulling
impairment in social functioning. Individuals with trichotillomania report that the impulse to remove hair
out of one’s own
hair.
may arise when anxious and worried, but also when bored. To satisfy the DSM-5 criteria, the person must
have engaged in repeated attempts to decrease or stop hair pulling. Importantly, hair removal for cosmetic
reasons (i.e., to improve the appearance in some way) does not qualify for a diagnosis of the disorder.
The 12-month prevalence of the disorder is approximately 1–2 per cent (APA, 2013). While
more large-scale community studies are needed to clarify the gender ratio in the disorder, the DSM-5
estimates a female:male ratio of 10:1 among adult sufferers. However, this figure is largely based
on individuals seeking treatment for the condition, which may reflect differing attitudes to hair loss
between the genders. It has been suggested that since hair loss is more common in males, men might
be less distressed by trichotillomania and therefore less likely to seek treatment for the disorder.
Individuals with trichotillomania often search for bent, thick, split or otherwise imperfect hairs to
remove. They may experience unhelpful perfectionistic thoughts (e.g., ‘It’s right to remove bad hairs’)
that play a role in maintaining the disorder. Alternatively, they may have positive beliefs about the
role of hair pulling in their lives (e.g., ‘It reduces stress to pull my hairs’, ‘It’s better than smoking or
drinking’). Often, the sufferer does not believe s/he will be able to stop pulling (e.g., ‘I can’t imagine
ever stopping completely—the impulse is just too strong at times’).
Excoriation (skin-picking) disorder

excoriation
disorder Excoriation disorder is often seen as a comorbid condition in those with OCD or trichotillomania.
Condition that It involves recurrent skin picking resulting in lesions. As in trichotillomania, the essential DSM-5
involves recurrent criteria include repeated attempts to decrease or stop picking, and significant distress or impairment in
skin picking. social or occupational functioning as a result of the skin picking.
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The most commonly picked sites are hands, face and arms, although any body part may be involved.
Many individuals with the condition report that they scan the surface of their skin (typically by touch)
for imperfections, bumps or unevenness. These sites become the target for picking. Similarities can
be drawn to trichotillomania in which bent, thick or otherwise imperfect hairs become the target for
pulling. In both conditions, boredom can become triggers for the behaviour.
The lifetime prevalence of excoriation disorder is approximately 1.5 per cent (APA, 2013).
This relatively low prevalence figure probably reflects the low level of interference in functioning
associated with mild cases of the condition. Up to 75 per cent of sufferers are female. The higher
prevalence for women may reflect greater concerns about appearance among females compared
to males.
The treatment of OCD-related disorders

Compared to OCD itself, far fewer clinical trials exist for the OCD-related disorders. In fact, in some
cases, there is not a single well-controlled and adequately powered (i.e., a large enough sample)
randomised controlled trial. Accordingly, detailed descriptions of the specific treatment packages
currently used for the OCD-related conditions would be premature and more research is needed to
establish the effectiveness of the various treatment procedures on offer.
Having said this, some broad comments can be made about the treatment of these conditions. Not
surprisingly, given their similarity to OCD, CBT procedures based on exposure and the prevention
of escape or avoidance behaviours are becoming central in the management of these problems. This
can involve exposure to unpleasant emotions and states (e.g., urges, impulses, anxiety and boredom)
without engaging in corrective behaviours (e.g., hair pulling in the case of trichotillomania or mirror
checking in the case of body dysmorphic disorder). Similarly, some form of cognitive restructuring
to target unhelpful thoughts, beliefs and attitudes is a component of most contemporary treatment
approaches for the OCD-related disorders. Finally, as in OCD, medications that increase the availability
of the neurotransmitter serotonin are also widely used. The relative effectiveness of these treatments
remains unknown.
SUMMARY
With the introduction of the DSM-5 (APA, 2013), OCD was controversially removed from the anxiety disorders and included in a
new section of the manual entitled ‘Obsessive-Compulsive and Related Disorders’. The present chapter explored the nature,
aetiology, maintenance and treatment of OCD, and introduced the additional disorders that are now grouped together in
this section.
The chapter highlighted the extensive range of clinical presentations that can be seen in these conditions. It was shown
that almost any behaviour can become a compulsion. Further, given that no logical link between obsessions and compulsions is
needed, the possible combination of symptoms seen in clinical practice is virtually endless. When it comes to OCD and the related
disorders, it can truly be said that no two cases are precisely the same.
Despite this, the cognitive model of Salkovskis provides a basis for understanding the similarities across OCD presentations.
In general, individuals with obsessions have been shown to place great significance on their thoughts and beliefs. They interpret
their thoughts as signals to danger, and feel an overwhelming responsibility to act to reduce this threat and anxiety. This feeling of
responsibility typically leads to the development of corrective behaviours or compulsions.
The contribution of Australian researchers was highlighted throughout the chapter. These researchers have advanced our
understanding of additional variables driving OCD symptoms, with a focus on death anxiety. They have also clarified critical
components in cognitive models of the conditions (such as threat expectancy) and developed novel treatment approaches (such
as DIRT). More research is needed to establish the relative effectiveness of all of these treatment options, particularly in the case
of the OCD-related disorders.
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KEY TERMS
basal ganglia. . . . . . . . . . . . . . . . . . . . . . . 78 compulsions . . . . . . . . . . . . . . . . . . . . . . . 74 hoarding disorder. . . . . . . . . . . . . . . . . . . 81
behavioural experiment . . . . . . . . . . . . . 80 correlational study. . . . . . . . . . . . . . . . . . 79 neuroimaging. . . . . . . . . . . . . . . . . . . . . . 78
body dysmorphic disorder. . . . . . . . . . . 82 excoriation disorder. . . . . . . . . . . . . . . . . 82 obsessions . . . . . . . . . . . . . . . . . . . . . . . . 74
clinically significant . . . . . . . . . . . . . . . . . 82 experimental studies. . . . . . . . . . . . . . . . 79 obsessive-compulsive
cognitive behaviour therapy (CBT). . . . 80 exposure and response disorder (OCD). . . . . . . . . . . . . . . . . . . . . 74
cognitive restructuring. . . . . . . . . . . . . . 80 prevention. . . . . . . . . . . . . . . . . . . . . . . . . 80 trichotillomania. . . . . . . . . . . . . . . . . . . . . 82
REVIEW QUESTIONS
LO 3.1
3.1 What are obsessions and how do they differ from other forms of worry?
3.2 What are compulsions and are they always linked to obsessions?
LO 3.2
3.3 Describe the cognitive model of OCD.
3.4 Australian researchers have argued that the dread of death may mediate compulsive behaviour and other
psychiatric problems experienced by individuals with OCD. What evidence is there for this proposal?
LO 3.3
3.5 What are the fundamental principles of ‘exposure and response prevention’ for the treatment of OCD?
3.6 Design an exposure and response prevention treatment for a client with OCD who avoids odd numbers due to
a fear of harm befalling him/herself and his/her family.
3.7 Describe the DIRT program for OCD.
LO 3.4
3.8 How do individuals with hoarding disorder explain their behaviour?
3.9 How do individuals with body dysmorphic disorder typically react to their negative beliefs and unhelpful thoughts
about their bodies? What do they do?

3.10 Excluding OCD itself, how well established are treatments for the OCD-related disorders?
REFERENCES
American Psychiatric Association (2000). Diagnostic and statistical Cororve, M. B., & Gleaves, D. H. (2001). Body dysmorphic disorder:
manual of mental disorders (4th ed., text revision). Washington, A review of conceptualizations, assessment, and treatment
DC: Author. strategies. Clinical Psychology Review, 21, 949–970.
American Psychiatric Association (2013). Diagnostic and statistical Crerand, C. E., Franklin, M. E., & Sarwer, D. B. (2006). Body
manual of mental disorders (5th ed.). Washington, DC: Author. dysmorphic disorder and cosmetic surgery. Plastic and
Antony, M. M., Downie, F., & Swinson, R. P. (1998). Diagnostic Reconstructive Surgery, 118, 167e–180e.
issues and epidemiology in obsessive-compulsive disorder. In R. Einstein, D., & Menzies, R. G. (2003). Atypical presentations.
P. Swinson, M. M. Antony, S. Rachman, & M. A. Richter (Eds.), In R. G. Menzies & P. de Silva (Eds.), Obsessive-compulsive
Obsessive compulsive disorder: Theory, research and treatment disorder: Theory, research and treatment (pp. 209–220). London:
(pp. 3–32). New York: Guilford Press. Wiley & Sons.
Baxter, L. R., Ackermann, R. F., Swerdlow, N. R., Brody, A., Saxena, Frampton, I. (2003). Neuropsychological models of OCD. In
S., Schwartz, J. M., . . . Phelps, M. E. (2000). Specific brain R. G. Menzies & P. de Silva (Eds.), Obsessive-compulsive disorder:
system mediation of obsessive-compulsive disorder responsive to Theory, research and treatment (pp. 39–58). London: Wiley & Sons.
either medication or behavior therapy. In W. K Goodman, M. V Frost, R. O., & Hartl, T. L. (2003). Compulsive hoarding. In
Rudorfer, & J. D. Maser (Eds.), Obsessive-compulsive disorder: R. G. Menzies & P. de Silva (Eds), Obsessive-compulsive disorder:
Contemporary issues in treatment (pp. 573–609). New Jersey: Theory, research and treatment (pp. 163–180). London: Wiley
Erlbaum. & Sons.
rie66620_ch03_073-086.indd 84 07/29/17 02:15 PM

Frost, R. O., Steketee, G., & Williams, L. F. (2000). Hoarding: Menzies, R. G., Menzies, R. E., & Iverach, L. (2015). The role of
A community health problem. Health and Social Care in the death fears in obsessive-compulsive disorder. Australian Clinical
Community, 8, 229–234. Psychologist, 1, 6–11.
Geller, D., Biederman, J., Jones, J., Park, K., Schwartz, S., Shapiro, Pigott, T. A. (1988). Obsessive-compulsive disorder: Symptom
S., & Coffey, B. (1998). Is juvenile obsessive-compulsive overview and epidemiology. Bulletin of the Menninger Clinic, 62,
disorder a developmental subtype of the disorder? A review of the A4–A32.
paediatric literature. Journal of the American Academy of Child Rachman, S. J. (2003). Compulsive checking. In R. G. Menzies
and Adolescent Psychiatry, 37, 420–427. & P. de Silva (Eds.), Obsessive-compulsive disorder: Theory,
Iverach, L., Menzies, R. G., & Menzies, R. E. (2014). Death research and treatment (pp. 139–162). London: Wiley & Sons.
anxiety and its role in psychopathology: Reviewing the status Rachman, S. J., & de Silva, P. (1978). Abnormal and normal
of a transdiagnostic construct. Clinical Psychology Review, 34, obsessions. Behaviour Research and Therapy, 16, 233–238.
580–593. Rapoport, J. L. (1989). The boy who couldn’t stop washing: The
Jones, M. K., & Krochmalik, A. (2003). Obsessive-compulsive experience and treatment of OCD. New York: Dutton.
washing. In R. G. Menzies & P. de Silva (Eds.), Obsessive- Salkovskis, P. M. (1996a). Frontiers of cognitive therapy. New York:
compulsive disorder: Theory, research and treatment (pp. 121–138). Guilford Press.
London: Wiley & Sons. Salkovskis, P. M. (1996b). Cognitive-behavioral approaches to the
Jones, M. K., & Menzies, R. G. (1997a). The cognitive mediation understanding of obsessional problems. In R. Rapee (Ed.), Current
of obsessive-compulsive handwashing. Behaviour Research and controversies in the anxiety disorders (pp. 103–133). New York:
Therapy, 35, 843–850. Guilford Press.
Jones, M. K., & Menzies, R. G. (1997b). Danger Ideation Reduction Salkovskis, P. M., & Harrison, J. (1984). Abnormal and normal
Therapy (DIRT): Preliminary findings with three obsessive- obsessions: A replication. Behaviour Research and Therapy, 22,
compulsive washers. Behaviour Research and Therapy, 35, 549–552.
955–960. Salkovskis, P. M., & McGuire, J. (2003). Cognitive-behavioural
Karno, M., Golding, J. M., Sorenson, S. B., & Burman, M. A. (1988). theory of OCD. In R. G. Menzies & P. de Silva (Eds.), Obsessive-
The epidemiology of obsessive-compulsive disorder in five US compulsive disorder: Theory, research and treatment (pp. 59–78).
communities. Archives of General Psychiatry, 45, 1094–1099. London: Wiley & Sons.
Kyrios, M. (2003). Exposure and response prevention. In R. G. Shafran, R. (2003). OCD in children and adolescents. In R. G. Menzies
Menzies & P. de Silva (Eds.), Obsessive-compulsive disorder: & P. de Silva (Eds.), Obsessive-compulsive disorder: Theory,
Theory, research and treatment (pp. 259–274). London: Wiley research and treatment (pp. 311–320). London: Wiley & Sons.
& Sons. St Clare, T., Menzies, R. G., & Jones, M. K. (2008). Danger
Macdonald, A. M. (2003). Personality and individual differences in Ideation Reduction Therapy for obsessive-compulsive washers:
OCD. In R. G. Menzies & P. de Silva (Eds.), Obsessive-compulsive A comprehensive guide to treatment. Bowen Hills: Australian
disorder: Theory, research and treatment (pp. 101–120). London: Academic Press.
Wiley & Sons. Summerfeldt, L. J., Antony, M., Downie, F., Richter, M., & Swinson,
McDonough, M. (2003). Pharmacological and neurosurgical R. (1997). Prevalence of particular obsessions and compulsions in
treatment of OCD. In R. G. Menzies & P. de Silva (Eds.), Obsessive- a clinical sample. In R. P. Swinson, M. M. Antony, S. Rachman,
compulsive disorder: Theory, research and treatment (pp. 291– & M. A. Richter (Eds.), Obsessive compulsive disorder: Theory,
310). London: Wiley & Sons. research and treatment (pp. 79–119). New York: Guilford Press.
Menzies, R. E., & Dar-Nimrod, I. (in press). Death anxiety and Viccaro, L. D., St Clare, T., Menzies, R. G., & Jones, M. K. (2010).
its relationship to obsessive-compulsive disorder. Journal of Danger ideation reduction therapy for obsessive-compulsive
Abnormal Psychology. checkers: A comprehensive guide to treatment. Bowen Hills:
Menzies, R. E., & Iverach, L. (2016). The dread of death and its Australian Academic Press.
relationship to mental health. In R. G. Menzies, M. Kyrios., & Weissman, M. M., Bland, R. C., Canino, G. J., & Greenwald, S.
N. Kazantzis (Eds.), Innovations and future directions in the (1994). The cross national epidemiology of obsessive compulsive
behavioural and cognitive therapies (pp. 219–223). Brisbane: disorder: The Cross National Collaborative Group. Journal of
Australian Academic Press. Clinical Psychiatry, 55, 5–10.
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CHAPTER 4
Trauma- and stressor-related

disorders
Richard Bryant
CHAPTER OUTLINE
● The diagnosis of posttraumatic stress disorder (PTSD)
● The epidemiology of posttraumatic stress disorder
● The aetiology of posttraumatic stress disorder
● The treatment and prevention of posttraumatic stress disorder
● Summary

4.1 Describe the current diagnostic criteria for posttraumatic stress disorder (PTSD).
4.2 Identify the prevalence of PTSD and the course of posttraumatic stress responses.
4.3 Compare the different models accounting for the development of PTSD.
4.4 Understand the components of effective treatments for PTSD and the current challenges in the treatment
of PTSD.
TRAUMA- AND STRESSOR-RELATED-DISORDERS: AN AUSTRALASIAN FOCUS

The history of writings on posttraumatic stress disorder can be traced back to the ancient Greek poem ‘The Odyssey’,
by Homer, which depicts the terrifying effects individuals may experience following war. In the contemporary era, much
has been documented about the potentially debilitating effects of trauma, especially during wartime. This attention
spiked during World War I, when soldiers faced horrendous atrocities during trench warfare in Europe, and there was
increasing awareness of the deep and persisting psychological scars caused by these experiences. Despite this long
history of trauma-related stress conditions, it was only in the aftermath of the Vietnam War, in 1980, that trauma-induced
psychological dysfunction was formally recognised as a mental disorder by the American Psychiatric Association and
was referred to as posttraumatic stress disorder.
This timeframe coincided with specific interest in Australia on the psychological effects of traumatic events.
During the 1970s, 1980s and 1990s, Australia was faced with a series of natural and man-made disasters that sparked
professional and community interest in the nature of posttraumatic stress. Events such as Cyclone Tracy in Darwin in
1974, the Granville train disaster in Sydney in 1977, the Ash Wednesday bushfires in Victoria and South Australia in 1983,
the Newcastle earthquake in 1989 and the Port Arthur mass shooting in Tasmania in 1996 posed challenging questions
for policymakers and health professionals about how to understand and manage PTSD. Given Australia’s susceptibility
to extreme weather conditions, such as seasonal cyclones, flooding and bushfires, this interest in PTSD has continued.
Moreover, with Australia’s military involvement in Vietnam, and more recently the Middle East, military agencies have
taken much interest in how PTSD affects people involved in wars. This national interest is reflected in major studies
undertaken by agencies such as the Australian Defence Force, which conducted a census of all of its personnel in
continued
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2014 to identify the rates of PTSD and other mental health

conditions. The finding that 8 per cent of the entire defence
force experiences PTSD has renewed efforts to address
this issue in military personnel. The mental health of war
veterans has also attracted much public and media attention,
and has led to much greater community awareness of PTSD
than in previous generations.
This knowledge of PTSD has been further fuelled
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over recent decades by many films depicting war and its
aftermath, with major protagonists clearly demonstrating
symptoms of PTSD; these include The Deer Hunter, Coming
Home, Born on the Fourth of July and Saving Private Ryan.
Of course, many of these depictions of PTSD have not
been entirely accurate; however, they reflect the ongoing Australia has been challenged by many natural
and increasing awareness of PTSD in the public arena. disasters. In 2009 the Black Saturday bushfires in
These films also reflect an increased sensitivity to the Victoria caused significant loss of life and property,
psychological costs that soldiers pay in serving their country, and led to high rates of posttraumatic stress disorder
and a degree of collective remorse in Australia specifically in the affected communities.
about the lack of attention given to the psychological needs
of Vietnam veterans when they returned from their service. It is interesting to compare the lack of community support
and psychological care afforded to Vietnam veterans with the effort made today to support soldiers post-war. This
shift is a stark reflection of how social and professional knowledge and attitudes have changed in the years since the
Vietnam War.
This chapter provides an up-to-date account of PTSD. It commences with a description of the current diagnostic
criteria for PTSD. It then outlines current knowledge of the epidemiology of the disorder and the risk factors for its
development. The causes of PTSD are then discussed in terms of prevailing models of PTSD, including cognitive,
learning and biological models. Finally, treatment and prevention approaches are discussed, including the major
challenge posed in this regard by the many millions of people currently affected by trauma across the world.
posttraumatic LO 4.1 The diagnosis of posttraumatic

stress disorder
(PTSD) stress disorder
Anxiety disorder
that may develop Posttraumatic stress disorder (PTSD) is classified among ‘Trauma- and Stressor-Related Disorders’
after a traumatic in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) of the
experience that American Psychiatric Association (APA, 2013). It is defined as a disorder that entails extreme stress
is characterised reactions after exposure to a traumatic event. The event must include threatened or actual harm to the
by: (a) repeated
self or others. Although PTSD can develop in response to a wide range of traumatic events, there is
re-experiencing
of the traumatic strong evidence of a relationship between the greater likelihood of PTSD development as the severity
event; of trauma increases. Common examples of traumatic events associated with PTSD include war, natural
(b) avoidance of disasters, rape, assault, car accidents and terrorism (March, 1993).
stimuli associated PTSD comprises four major clusters of symptoms: re-experiencing symptoms, avoidance
with the trauma symptoms, negative changes in cognitions and mood, and marked alterations in arousal. The first
or emotional symptom cluster involves re-experiencing symptoms that include intrusive memories, flashbacks and
numbing;
nightmares related to the traumatic event and distress when exposed to reminders of the trauma. The
(c) negative
changes in second cluster involves active avoidance symptoms, including avoidance of thoughts and reminders
cognitions and of the trauma. The third symptom grouping entails negative alterations in cognition and mood, which
mood; and (d) includes emotional numbing, being unable to recall an important aspect of the trauma, exaggerated
increased arousal. negative expectations about oneself or the world, excessive blaming of the self or others, and pervasive
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Chapter 4 Trauma- and stressor-related disorders 89
negative affective states (e.g., fear, anger, guilt and shame). The final cluster involves arousal
symptoms, including an exaggerated startle response (i.e., being very jumpy or reactive to stimuli),
hypervigilance (i.e., being on the lookout for possible sources of threat), sleeping and concentration
difficulties, reckless or self-destructive behaviour and anger outbursts. To qualify for a diagnosis of
PTSD, these symptoms must have been present for at least one month.
LO 4.2 The epidemiology of posttraumatic

stress disorder
The prevalence of posttraumatic stress disorder
Population studies have shown that many people in the community have been exposed to traumatic
stressors. For instance, the National Comorbidity Survey conducted in the United States indicated
that 61 per cent of randomly sampled adults reported exposure to a traumatic stressor (Kessler,
Sonnega, Bromet, Hughes, & Nelson, 1995). Even higher, a study of adults living in Detroit found that
90 per cent reported exposure to a traumatic stressor (Breslau, Davis, Andreski, & Peterson, 1991).
Yet despite the frequency of exposure to potentially traumatising events, relatively few people actually
develop PTSD. For example, the National Comorbidity Survey found that only 20.4 per cent of the
women and 8.2 per cent of the men who had experienced a traumatic event ever developed PTSD
(Kessler et al., 1995). Similarly, the Detroit study found that only 13 per cent of the women and
6.2 per cent of the men had developed PTSD (Breslau et al., 1991). These studies indicate that the
normative response following trauma exposure is to adapt to the experience and not to develop PTSD.
Although men are more likely to be exposed to trauma than women, women have at least a two-fold
risk of developing PTSD compared to men (Breslau, Davis, Andreski, Peterson, & Schultz, 1997).
More severe traumas tend to result in more severe PTSD. There is evidence that interpersonal violence
leads to more PTSD than impersonal trauma. For example, whereas 55 per cent of rape victims develop
PTSD, only 7.5 per cent of accident victims develop PTSD.
Interesting patterns have been observed in the prevalence of PTSD among Australian adults. In
the Australian National Survey of Mental Health and Wellbeing, conducted in 1997 by the Australian
Bureau of Statistics, it was found that although the rates of trauma exposure were similar to those found
in North American studies, the Australian study found lower rates of PTSD (Creamer, Burgess, &
McFarlane, 2001). Specifically, whereas the 12-month prevalence rate for PTSD was 3.9 per cent in the
United States (Kessler, Dupont, Berglund, & Wittchen, 1999), the Australian study reported 1.3 per cent
(Creamer et al., 2001). This study also highlighted the comorbidity that exists among people with PTSD.
Table 4.1 presents a summary of the comorbid psychiatric disorders that were reported in this study,
and highlights that developing PTSD is strongly associated with a range of other psychiatric disorders.
However, when the national survey was repeated in 2007, a higher prevalence rate of 4.4 per cent was
observed, which is more consistent with rates noted overseas (Australian Bureau of Statistics, 2007).
In considering the epidemiology of PTSD, it is worth noting that PTSD tends not to be static but
rather shifts over time. Longitudinal studies indicate that whereas the rate of PTSD remains fairly
stable in any given population, there is much fluidity in people shifting from having PTSD to having
subsyndromal PTSD, and even no PTSD (Bryant et al., 2013). To understand these shifting states of
PTSD more accurately, studies have used growth modelling statistics to map the different trajectories
that people follow after trauma, which can be achieved when people are repeatedly assessed. These
studies indicate that people tend to be either (a) resilient, (b) initially distressed but then gradually
recovering, (c) worsening over time or (d) chronically distressed. These patterns have been shown
repeatedly in survivors of traumatic injury (Bryant et al., 2015) and SARS infection (Bonanno et al.,
2008), women diagnosed with breast cancer (Lam et al., 2010), those who have experienced disasters
(Pietrzak, Van Ness, Fried, Galea, & Norris, 2013) or terrorist attacks (Norris, Tracy, & Galea, 2009)
and in military personnel (Bonanno et al., 2012).
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TABLE 4.1 The prevalence of psychological disorders in individuals with and without posttraumatic
stress disorder
WITH PTSD WITHOUT PTSD
Major depression 59% 6%
Dysthymia 5% 1%
Bipolar disorder 2% 0%
Generalised anxiety disorder 31% 2%
Panic disorder 16% 1%
Social phobia 18% 1%
Obsessive-compulsive disorder 11% 1%
Alcohol use disorder 25% 6%
Drug use disorder 18% 3%

Source: From Creamer, M., Burgess, P., & McFarlane, A. C. (2001). Posttraumatic stress disorder: Findings from the Australian National
Survey of Mental Health and Wellbeing. Psychological Medicine, 31, 1237–1247.
PREVALENCE IN CHILDREN
The prevalence of PTSD in children is generally similar to that reported in studies of trauma-exposed
adults (Fletcher, 1996). Despite the overall comparability between children’s and adults’ reactions,
there are suggestions that PTSD can be manifested differently across different stages of childhood
(Salmon & Bryant, 2002). That is, preschool children can display fewer cognitive symptoms
(e.g., fewer re-experiencing symptoms such as reliving, daydreaming or talking about the event) and
little avoidance (e.g., inability to recall an aspect of the trauma and avoidance of thoughts, feelings or
conversations about the event) compared to older children.
Risk factors for the development of posttraumatic

stress disorder
It is common for individuals to experience a broad array of PTSD-type symptoms in the initial weeks
after trauma exposure (Harvey & Bryant, 2002). Despite the prevalence of acute stress reactions, the
majority of these stress responses are transient. For example, whereas 94 per cent of rape victims
displayed sufficient symptoms two weeks after the trauma to meet the criteria for PTSD (excluding
the one-month time requirement), this rate dropped to 47 per cent 11 weeks later (Rothbaum, Foa,
Riggs, Murdock, & Walsh, 1992).
Research has attempted to identify those individuals who are at risk of developing chronic stress
reactions in the form of PTSD after exposure to a trauma. Across many studies, there is evidence that
PTSD development is associated with a history of psychological disturbance predating the trauma,
prior traumatic experience, lower intelligence levels, female gender, more severe traumatic exposure,
low social support after the traumatic experience, interpersonal trauma, and ongoing stressors in the
aftermath of the trauma (Breslau et al., 1991; Brewin, Andrews, & Valentine, 2000; Bryant, 2003;
McNally, Bryant, & Ehlers, 2003). Support for the latter point was obtained in a study that found
that the rates of PTSD actually increased over time in New Orleans after Hurricane Katrina in 2005,
perhaps due to the persisting stress involved in the aftermath of the hurricane (such as relocation, lack
of housing and the loss of basic infrastructure) (Kessler et al., 2008).
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LO 4.3 The aetiology of posttraumatic

stress disorder
In addition to factors predating the trauma that predispose individuals to developing PTSD (such as
a history of psychological disturbance), cognitive, learning and biological factors are believed to be
involved in the causation of PTSD.
Cognitive models
According to cognitive models of PTSD, maladaptive appraisals or interpretations of the traumatic
event (e.g., ‘I was weak because I did not stop the rape’), the individual’s responses to it (e.g., ‘I am
worthless because I am not coping better with the assault’) and the environment after the trauma (e.g.,
‘I can never feel safe again after the assault’) are pivotal in terms of perpetuating the individual’s
sense of threat (Ehlers & Clark, 2000). There is much evidence that maladaptive thoughts about
the trauma predict the development of the disorder (Ehlers, Mayou & Bryant, 1998; Warda &
Bryant, 1998).
Learning accounts
Learning accounts of PTSD involve the application of classical conditioning principles to trauma
(Pitman, Shalev, & Orr, 2000). Specifically, when a traumatic event (unconditioned stimulus) occurs,
people typically respond with fear (unconditioned response). It is argued that the strong fear elicited
fear-conditioning
by the trauma will lead to strong associative conditioning between the fear and the events surrounding
Process that
the trauma. As reminders of the trauma occur (conditioned stimuli), people then respond with fear involves
reactions (conditioned response). pairing a fear
response with
factors present
Biological accounts at the time of
Biological accounts highlight the role of arousal in strengthening the fear-conditioning process. experiencing
the fear, such
It is proposed that extreme sympathetic arousal at the time of a traumatic event may result in the
that subsequent
release of stress neurochemicals (including noradrenaline and adrenaline) into the cortex, resulting exposure to
in strong conditioning of fear responses with the associated memories (Pitman, 1989). In support of these factors
this proposal, there is evidence that people who eventually develop PTSD display elevated resting triggers a fear
heart rates in the initial week after the trauma (Shalev et al., 1998). Psychophysiological studies have reaction.
also explored the responses of individuals with PTSD using their own recollections of the trauma as
sympathetic
the eliciting stimulus. When individuals with PTSD are asked to recall past traumatic events, they
arousal
consistently produce larger psychophysiological responses, including heart rate and skin conductance, Activation of
compared to individuals with a similar trauma history without PTSD (Pitman et al., 2000). the sympathetic
nervous
system that is
Avoidance responsible
Across cognitive, learning and biological models, there is recognition that avoidance of trauma for increased
reminders maintains the PTSD. According to cognitive models, this is because avoidance prevents heart rate,
respiration rate
people from having the opportunity to access corrective information that the perceived threats are no
and blood flow
longer realistically dangerous. According to learning processes with their biological bases, avoidance to the organs,
serves to impede the extinction of classically conditioned fear. The combination of predisposing, allowing people
cognitive, learning and biological factors that are theorised to result in the development of PTSD are to respond to
shown in Figure 4.1. threats.
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Predisposing factors
Trauma
Maladaptive appraisals Fear conditioning
selective
serotonin
reuptake Avoidance strategies
inhibitor (SSRI)
Class of
antidepressant
drugs (such Impaired extinction
as fluoxetine) learning and no
that inhibit the opportunity to
challenge beliefs
reuptake of
regarding ongoing
serotonin. threat
cognitive
behaviour
therapy (CBT) PTSD
Type of
psychological FIGURE 4.1 The aetiology of posttraumatic stress disorder (PTSD)
treatment that
combines both
cognitive and
behavioural
LO 4.4 The treatment and prevention
concepts and of posttraumatic stress disorder
techniques.
cognitive Treatment
restructuring
Cognitive The study of pharmacological therapy for PTSD is relatively recent. The first medication approved
technique in by the United States Food and Drug Administration for treating PTSD was the selective serotonin
which the client reuptake inhibitor (SSRI) sertraline. Randomised controlled trials of sertraline versus a placebo pill
learns to identify, indicate significant symptom reduction in response to sertraline (Davidson et al., 2006). Overall, these
challenge and reports suggest that SSRIs are an effective class of medications for patients with PTSD.
replace his/her
The psychological treatment of choice for PTSD is cognitive behaviour therapy (CBT), and
dysfunctional
beliefs with more
typically comprises psychoeducation, anxiety management, cognitive restructuring, imaginal and
realistic or helpful in vivo exposure, as well as relapse prevention (Harvey, Bryant, & Tarrier, 2003):
beliefs. ∙ Psychoeducation comprises providing information about common symptoms following a
in vivo exposure traumatic event, legitimising the trauma reactions as an understandable response given the event,
Technique and establishing a rationale for treatment by describing the cognitive factors believed to be driving
of behaviour the symptoms.
therapy in ∙ Anxiety management techniques aim to provide individuals with coping skills to assist them to
which clients gain a sense of mastery over their fear, to reduce arousal levels and to assist the individual when
confront their
engaging in exposure to the traumatic memories. Anxiety management approaches often include
feared objects/
situations in real breathing re-training, relaxation skills and calming self-talk.
life (as opposed ∙ Cognitive restructuring, which is based on the premise that maladaptive appraisals underpin the
to imaginal maintenance of PTSD, involves teaching patients to identify and evaluate the evidence for their
exposure). beliefs about the trauma, the self and the environment.
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∙ Prolonged imaginal exposure requires the individual to vividly imagine the trauma for extended
periods. Prolonged exposure typically occurs for at least 30 minutes and is usually supplemented
by daily homework exercises in which the patient practises the exposure exercise at home. Most
exposure treatments supplement imaginal exposure with in vivo exposure that involves graded
exposure to trauma-related stimuli in real life.
The duration of CBT for PTSD is typically 9–12 sessions.
One of the earliest well-controlled studies of CBT for this disorder randomly assigned assault
survivors who had PTSD to prolonged exposure, stress management, supportive counselling or a
wait-list control group (Foa, Rothbaum, Riggs, & Murdock, 1991). Whereas stress management wait-list control
resulted in greater gains than supportive counselling or the wait-list control group at the end of group
treatment, the prolonged exposure condition led to a greater reduction in PTSD symptoms three In a treatment
months later. The researchers interpreted these findings as indicating that whereas stress management outcome
study, group of
led to short-term symptom reduction, prolonged exposure resulted in longer term benefits because
participants that
the cognitively based fear networks were activated and modified. The efficacy of CBT has been functions as a no-
reported in a range of other well-controlled studies (Harvey et al., 2003). This has led to most treatment control
international treatment guidelines, including the Australian National Health and Medical Research group while the
Council’s treatment guidelines, recommending trauma-focused CBT as the front-line treatment for experimental
PTSD (Forbes et al., 2007). group receives
the intervention.
Prevention
Attempts to prevent PTSD with early intervention after exposure to trauma have been challenged
by the pattern of most trauma survivors, who are initially distressed but go on to experience
natural remission of their symptoms in the following weeks or months (Bryant, 2003). This has
resulted in early-intervention programs being hampered as it has been difficult to demonstrate
that interventions are more effective than natural remission from these transient stress reactions.
There was an important shift in relation to this situation in the DSM-IV (APA, 1994), when a
new diagnosis of acute stress disorder was introduced to describe posttraumatic stress reactions
that occur in the initial month after trauma, and which were purportedly predictive of subsequent
PTSD (Bryant, 2016). Many longitudinal studies were subsequently conducted which indicated
that whereas at least half of trauma survivors with acute stress disorder did develop subsequent
PTSD, most people who eventually developed PTSD did not initially display acute stress disorder random
(Bryant, 2011). This pattern suggests that although acute stress disorder was not a foolproof means allocation
of predicting PTSD, it did mean that those who met the criteria for this disorder were at higher risk Assignment of
for developing PTSD later. participants in
The capacity of the acute stress disorder diagnosis to differentiate between temporary stress an experiment
responses and the beginning of persistent PTSD led to researchers attempting to prevent PTSD to groups based
through early-intervention programs using CBT strategies. It is important to note that CBT is on a random
process so that
different from psychological debriefing because whereas the latter requires the person to express
each participant
his/her responses to the trauma on a single occasion within days of the event, CBT requires repeated has an equal
systematic exposure for prolonged periods and this intervention does not commence until at least two chance of being
weeks after trauma exposure. One approach has focused on individuals who are already displaying allocated to the
PTSD-like symptoms in the initial weeks after the trauma. In a series of studies, these individuals various groups;
were randomly allocated to either CBT or supportive counselling (which entailed providing the this is done in an
individual with the support of a therapist without teaching any CBT strategies). It was found that attempt to ensure
that there are
fewer participants in the CBT group (20 per cent) later met the diagnostic criteria for PTSD compared
no systematic
to the supportive counselling participants (67 per cent) (Bryant, Harvey, Dang, Sackville, & Basten, differences
1998; Bryant, Sackville, Dang, Moulds, & Guthrie, 1999). These results strongly suggest that the between the
early implementation of CBT for individuals experiencing trauma symptoms is helpful in preventing participants in
the development of full-blown PTSD. each group.
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exposure therapy
Behavioural
Current challenges in treatment and prevention
technique in Across most trials of treating PTSD, nearly half of patients either drop out of treatment or do not
which the client respond. Accordingly, there is a need to develop procedures to augment the efficacy of PTSD
confronts the treatment. One approach has been to prepare patients with skills to better tolerate the distress
feared stimuli that
associated with exposure therapy, which has resulted in stronger benefits for PTSD patients following
s/he has avoided
until his/her child sexual abuse (Cloitre et al., 2010) and adults following civilian trauma (Bryant et al., 2013).
anxiety reduces; Another technique has been to augment CBT by enhancing extinction. The process of extinction
there are various involves neural plasticity in the basolateral nucleus of the amygdala, and it is strongly reliant on
types of exposure NMDA receptors, which are a type of glutamate receptor (Royer & Pare, 2002). This observation has
such as in vivo resulted in researchers testing whether NMDA agonists (i.e., drugs that stimulate NMDA receptors)
versus imaginal. such as d-cycloserine can enhance extinction when used in conjunction with CBT. Studies have found
extinction that d-cycloserine facilitates CBT for specific phobia (Guastella, Dadds, Lovibond, Mitchell, &
In learning theory, Richardson, 2007), social phobia (Hofman et al., 2006) and obsessive-compulsive disorder (Kushner
elimination of et al., 2007), as well as when administered to PTSD patients prior to CBT sessions (Davis, Myers,
a classically Ressler, & Rothbaum, 2005).
conditioned In the context of instances of massive trauma—including the September 11 terrorist attacks and
response by Hurricane Katrina in the United States, the 2004 Asian tsunami, the 2009 Black Saturday bushfires in
removal of the
unconditioned
Victoria, the 2011 Japanese earthquake and tsunami, and the 2017 floods in Queensland and northern
stimulus or the New South Wales—there is an important need to develop the means of disseminating evidence-
elimination of based treatments to large numbers of people. This issue has been drastically highlighted in the
an operantly wake of the current refugee crisis, in which there are 65 million refugees and internally displaced
conditioned people worldwide. However, no government has the resources to provide mental health treatment to
response by thousands of people who develop a disorder at the same time, such as after large-scale disasters of
removal of the these kinds.
reinforcement.
The internet is offering some promising avenues to provide CBT to people who cannot access
neural plasticity formal mental health services. Initial trials have shown promising results in terms of people benefiting
The brain’s from web-based delivery of CBT (Litz, Williams, Wang, Bryant, & Engel, 2004). Another approach
capacity to form has involved brief interventions in which non-specialists are trained to provide evidence-based
new connections strategies. For example, one trial showed that treating victims of terrorist attacks in Pakistan through
between neurons.
non-professional providers led to reduced PTSD symptoms (Rahman et al., 2016).
amygdala A related challenge facing the field of PTSD is to develop treatments that are more effective
Part of the brain’s when applied in community settings. Although there is abundant research support for CBT, there are
limbic system currently no studies indicating that this treatment can be successfully applied in community settings.
that is thought to Research studies typically involve tightly controlled trials in which there are strict inclusion criteria
regulate emotions. (e.g., patients with comorbid psychological conditions such as major depression are often excluded)
glutamate and the treatments are implemented by expertly trained clinicians. It is always questionable whether
The primary a treatment that has been proven to be efficacious in a research trial will also be effective when it is
excitatory conducted in community settings with non-specialist clinicians treating all types of PTSD patients.
neurotransmitter Thus there is a need to test whether CBT can be effective in community settings.
in the brain.
CASE STUDY: POSTTRAUMATIC STRESS DISORDER

Maggie is a 34-year-old woman who was involved in a serious motor accident while driving her young daughter to
school. Police reports indicated that Maggie was driving at 10 kilometres per hour faster than the speed limit when
her vehicle skidded on some oil on the road and slammed into a telegraph pole. Maggie suffered marked orthopaedic
injuries, required multiple operations and was left with significant lower back pain that restricted her activities.
Two years after the accident, Maggie reported to her doctor that she continued to have disturbed sleep and was
concerned about the frequent nightmares she was having about the accident. As a result of her sleeping difficulties, the
doctor referred Maggie to a clinical psychologist.
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Maggie reported to the clinical psychologist who assessed her that she definitely believed she and her daughter
were going to die at the time of the accident. Also a cause of much distress was the fact that throughout her lengthy
hospitalisation, Maggie was separated from her daughter, who also required two different surgeries, although she
eventually made a good recovery.
At her psychological assessment, Maggie described the nature of the frequent nightmares. In these dreams, Maggie
would wake screaming after reliving the accident at the point of impact against the telegraph pole. She also reported
daily intrusive memories of the accident that were characterised by visually seeing her car skidding towards the telegraph
pole. These memories were perceptually very rich, insofar as Maggie would actually feel the sense of the car moving
forward, sense the cutting sensations in her face as the shattering window glass cut her skin and taste the blood in her
mouth. Maggie was extremely distressed by these memories.
Following the accident she avoided driving, and was very distressed whenever she needed to be a passenger. Maggie
was also very protective of her daughter, rarely allowing her to leave the house and not permitting her to travel in cars
since the accident. Maggie displayed marked arousal, reflected in her poor sleep, marked anger outbursts, being very
jumpy and reactive to noises, and being very sensitive to potential threats in her environment. For example, she perceived
potential danger whenever she heard a loud noise, saw traffic or even heard the sound of cars or trucks. Maggie also
reported feeling much guilt about the accident. She was preoccupied on a daily basis with repetitive thoughts that she
had nearly killed her daughter because she was speeding, and commonly experienced bouts of thinking that she was an
unworthy mother more generally. These thoughts contributed to frequent episodes of depressive mood.
From the assessment it was clear that Maggie met the criteria for PTSD, and accordingly the clinical psychologist
commenced a course of trauma-focused CBT with her. Therapy commenced with psychoeducation about traumatic stress,
and instructing Maggie that therapy would aim to teach her (a) that reminders of the trauma need not be distressing, (b)
that avoiding these reminders is not necessary and that she can in fact master her fears by reducing her avoidance
behaviours and (c) that her thoughts of guilt and self-blame are excessive.
Treatment in the second session commenced with prolonged imaginal exposure in which Maggie was required to
‘relive’ the trauma memories by recounting the narrative of the trauma in a very realistic and detailed way. She did this
for 40 minutes and found that her anxiety began to subside by the end of the session. At the end of the exposure, the
therapist discussed with Maggie the fact that she and her daughter had survived the accident and that she needed to
remind herself of this every time she did an exposure session. She was then asked to repeat the exposure exercise every
second day for homework.This approach continued for five more sessions, with an additional focus on in vivo exposure,
in which Maggie was gradually required to approach actual reminders of the accident and remain in close proximity to
them until her distress subsided by at least half of its original intensity. She began by simply sitting in her car without the
car engine turned on, then progressing to turning the car on, then driving up and down her driveway, then around a quiet
suburban block, and eventually driving in traffic.
In the seventh session, the therapist commenced focusing on cognitive restructuring of Maggie’s self-blaming beliefs
and guilt about driving too fast, and her belief that she was responsible for her daughter’s injuries. This approach involved
testing her beliefs that she was a bad mother against all of the available evidence, and recognising that most people
occasionally drive marginally above the speed limit, and that an unfortunate accident does not equate with being a bad
mother. Therapy continued for another four sessions, after which Maggie reported much less distress and anxiety, better
sleep, fewer intrusive memories and less guilt about the accident.
SUMMARY
PTSD describes severe and persistent stress responses to traumatic events, characterised by distressing memories of the trauma,
avoidance of reminders of the trauma, disturbed thoughts and mood, and elevated arousal. The diagnosis was markedly altered
in the DSM-5 to extend traumatic stress beyond the domain of fear to also include other responses, such as guilt, anger and
shame. PTSD is highly comorbid with other disorders. Although many trauma survivors display PTSD reactions in the immediate
aftermath of trauma, most stress reactions abate with time. PTSD risk is greater in females, survivors of interpersonal trauma, and
the presence of stressors in the period after the trauma.
Our understanding of PTSD has been guided strongly by animal models of fear learning, which are based on conditioning
models. These models propose that the fear occurring at the time of trauma leads to strong associations, formed in the amygdala,
rie66620_ch04_087-098.indd 95 07/29/17 11:48 AM

between fear and factors present at the time of trauma. This results in strongly consolidated memories of the trauma, which are
experienced as flashbacks, intrusions or nightmares, and which contribute to ongoing avoidance of reminders of the trauma.
PTSD is one of the few disorders in which psychological treatments are much more effective than pharmacological interventions.
Trauma-focused CBT is the most strongly supported treatment modality, and typically comprises repeated exposure to trauma
memories as well as cognitive restructuring of maladaptive thoughts about the trauma and possible future threats. This approach
has been shown to effectively reduce chronic PTSD and to limit PTSD development when provided shortly after trauma exposure.
KEY TERMS
amygdala. . . . . . . . . . . . . . . . . . . . . . . . . . 94 fear-conditioning . . . . . . . . . . . . . . . . . . . 91 randomly allocated . . . . . . . . . . . . . . . . . 93
cognitive behaviour glutamate. . . . . . . . . . . . . . . . . . . . . . . . . . 94 selective serotonin
therapy (CBT) . . . . . . . . . . . . . . . . . . . . . . 92 in vivo exposure. . . . . . . . . . . . . . . . . . . . 92 reuptake inhibitor (SSRI). . . . . . . . . . . . . 92
cognitive restructuring. . . . . . . . . . . . . . 92 neural plasticity. . . . . . . . . . . . . . . . . . . . . 94 sympathetic arousal. . . . . . . . . . . . . . . . . 91
exposure therapy. . . . . . . . . . . . . . . . . . . 94 posttraumatic stress wait-list control group. . . . . . . . . . . . . . . 93
extinction. . . . . . . . . . . . . . . . . . . . . . . . . . 94 disorder (PTSD). . . . . . . . . . . . . . . . . . . . . 88
REVIEW QUESTIONS
LO 4.1
4.1 What sorts of events can trigger PTSD?
4.2 What are the major symptom clusters in PTSD, as defined by the DSM-5?
LO 4.2
4.3 What are the major risk factors for developing PTSD?
4.4 What are the primary trajectories of posttraumatic stress responses?
LO 4.3
4.5 What is some of the evidence for conditioning explanations for PTSD?
4.6 What are the fundamental propositions of cognitive models of PTSD?
LO 4.4
4.7 How accurately does the acute stress disorder diagnosis predict subsequent PTSD?
4.8 What strategies are being used to address PTSD in situations where there are massive numbers of trauma
survivors?
4.9 Is psychological debriefing a useful strategy to prevent subsequent PTSD?
4.10 Describe exposure therapy when it is used to treat PTSD.
REFERENCES
American Psychiatric Association (1994). Diagnostic and statistical dysfunction among hospitalized survivors of the SARS epidemic in
manual of mental disorders (4th ed.). Washington, DC: Author. Hong Kong: A latent class approach. Health Psychology, 27, 659–667.
American Psychiatric Association (2013). Diagnostic and statistical Bonanno, G. A., Mancini, A. D., Horton, J. L., Powell, T. M.,
manual of mental disorders (5th ed.). Washington, DC: Author. Leardmann, C. A., Boyko, E. J., . . . Millennium Cohort Study
Australian Bureau of Statistics (2007). National Survey of Mental Team (2012). Trajectories of trauma symptoms and resilience in
Health and Wellbeing: Summary of results (cat. No. 4326.0). deployed U.S. military service members: Prospective cohort study.
Canberra: Author. British Journal of Psychiatry, 200, 317–323.
Bonanno, G. A., Ho, S. M., Chan, J. C., Kwong, R. S., Cheung, C. K., Breslau, N., Davis, G. C., Andreski, P., & Peterson, E. (1991).
Wong, C. P., & Wong, V. C. (2008). Psychological resilience and Traumatic events and posttraumatic stress disorder in an urban
rie66620_ch04_087-098.indd 96 07/29/17 11:48 AM

population of young adults. Archives of General Psychiatry, 48, counselling. Journal of Consulting and Clinical Psychology, 59,
216–222. 715–723.
Breslau, N., Davis, G. C., Andreski, P., Peterson, E., & Schultz, L. R. Forbes, D., Creamer, M., Phelps, A., Bryant, R., McFarlane, A.,
(1997). Sex differences in posttraumatic stress disorder. Archives of Devilly, G. J., . . . Newton, S. (2007). Australian guidelines for the
General Psychiatry, 54, 1044–1048. treatment of adults with acute stress disorder and post-traumatic
Brewin, C. R., Andrews, B., & Valentine, J. D. (2000). Meta-analysis stress disorder. Australian and New Zealand Journal of Psychiatry,
of risk factors for posttraumatic stress disorder in trauma-exposed 41, 637–648.
adults. Journal of Consulting and Clinical Psychology, 68, 748–766. Guastella, A. J., Dadds, M. R., Lovibond, P. F., Mitchell, P., &
Bryant, R. A. (2003). Early predictors of posttraumatic stress Richardson, R. (2007). A randomized controlled trial of the effect
disorder. Biological Psychiatry, 53, 789–795. of D-cycloserine on exposure therapy for spider fear. Journal of
Bryant, R. A. (2011). Acute stress disorder as a predictor of Psychiatric Research, 41, 466–471.
posttraumatic stress disorder: A systematic review. Journal of Harvey, A. G., & Bryant, R. A. (2002). Acute stress disorder: A
Clinical Psychiatry, 72, 233–239. synthesis and critique. Psychological Bulletin, 128, 892–906.
Bryant, R. A. (2016). Acute stress disorder: What it is, and how to Harvey, A. G., Bryant, R. A., & Tarrier, N. (2003). Cognitive behaviour
treat it? New York: Guilford. therapy of posttraumatic stress disorder. Clinical Psychology
Bryant, R. A., Harvey, A. G., Dang, S. T., Sackville, T., & Basten, Review, 23, 501–522.
C. (1998). Treatment of acute stress disorder: A comparison of Hofmann, S. G., Meuret, A. E., Smits, J. A., Simon, N. M., Pollack,
cognitive behaviour therapy and supportive counseling. Journal of M. H., Eisenmenger, K., . . . Otto, M. W. (2006). Augmentation
Consulting and Clinical Psychology, 66, 862–866. of exposure therapy with D-cycloserine for social anxiety disorder.
Bryant, R. A., Mastrodomenico, J., Hopwood, S., Kenny, L., Cahill, C., Archives of General Psychiatry, 63, 298–304.
Kandris, K., & Taylor, K. (2013). Augmenting cognitive behavior Kessler, R. C., Dupont, R. L., Berglund, P., & Wittchen, H. (1999).
therapy for PTSD with emotion tolerance training: A randomized Impairments in pure and comorbid generalized anxiety disorder and
controlled trial. Psychological Medicine, 43, 2153–2160. major depression at 12 months in two national surveys. American
Bryant, R. A., Nickerson, A., Creamer, M., O’Donnell, M., Forbes, Journal of Psychiatry, 156, 1915–1923.
D., Galatzer-Levy, I., McFarlane, A. C., & Silove, D. (2015). The Kessler, R. C., Galea, S., Gruber, M. J., Sampson, N. A.,Ursano,
trajectory of posttraumatic stress following traumatic injury: A six- R. J., & Wessley, S. (2008). Trends in mental illness and suicidality
year follow-up. British Journal of Psychiatry, 206, 417–423. after Hurricane Katrina. Molecular Psychiatry, 13, 374–384.
Bryant, R. A., Sackville, T., Dang, S. T., Moulds, M., & Guthrie, R. Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B.
(1999). Treating acute stress disorder: An evaluation of cognitive (1995). Posttraumatic stress disorder in the National Comorbidity
behavior therapy and counselling techniques. American Journal of Survey. Archives of General Psychiatry, 52, 1048–1060.
Psychiatry, 156, 1780–1786. Kushner, M. G., Kim, S. W., Donahue, C., Thuras, P., Adson, D.,
Cloitre, M., Stovall-McClough, K. C., Nooner, K., Zorbas, P., Kotlyar, M., . . . Foa, E. B. (2007). D-cycloserine augmented
Cherry, S., Jackson, C. L., . . . Petkova, E. (2010). Treatment for exposure therapy for obsessive-compulsive disorder. Biological
PTSD related to childhood abuse: A randomized controlled trial. Psychiatry, 62, 835–838.
American Journal of Psychiatry, 167, 915–924. Lam, W. W., Bonanno, G. A., Mancini, A. D., Ho, S., Chan, M.,
Creamer, M., Burgess, P., & McFarlane, A. C. (2001). Post-traumatic Hung, W. K., . . . Fielding, R. (2010). Trajectories of psychological
stress disorder: Findings from the Australian National Survey of distress among Chinese women diagnosed with breast cancer.
Mental Health and Wellbeing. Psychological Medicine, 31, 1237– Psychooncology, 19, 1044–1051.
1247. Litz, B. T., Williams, L., Wang, J., Bryant, R. A., & Engel, C. C.
Davidson, J., Rothbaum, B. O., Tucker, P., Asnis, G., Benattia, I., & (2004). The development of an internet-based program to deliver
Musgnung, J. (2006). Venlafaxine extended release in posttraumatic therapist-assisted self-help behavioral treatment for traumatic
stress disorder: A sertraline- and placebo-controlled study. Journal stress. Professional Psychology: Science and Practice, 35,
of Clinical Psychopharmacology, 26, 259–267. 628–634.
Davis, M., Myers, K. M., Ressler, K. J., & Rothbaum, B. O. (2005). March, J. S. (1993). What constitutes a stressor? The ‘Criterion A’
Facilitation of extinction of conditioned fear by D-cycloserine: issue. In R. J. Davidson & E. B. Foa (Eds.), Posttraumatic stress
Implications for psychotherapy. Current Directions in disorder: DSM-IV and beyond (pp. 37–54). Washington, DC:
Psychological Science, 14, 214–219. American Psychiatric Press.
Ehlers, A., & Clark, D. (2000). A cognitive model of posttraumatic McNally, R. J., Bryant, R. A., & Ehlers, A. (2003). Psychological
stress disorder. Behaviour Research and Therapy, 38, 319–345. debriefing and its alternatives: A critique of early intervention for
Ehlers, A., Mayou, R. A., & Bryant, B. (1998). Psychological trauma survivors. Psychological Science in the Public Interest, 4,
predictors of chronic PTSD after motor vehicle accidents. Journal 45–79.
of Abnormal Psychology, 107, 508–519. Norris, F. H., Tracy, M., & Galea, S. (2009). Looking for resilience:
Fletcher, K. E. (1996). Childhood posttraumatic stress disorder. Understanding the longitudinal trajectories of responses to stress.
In E. J. Mash & R. Barkley (Eds.), Child psychopathology Social Science and Medicine, 68, 2190–2198.
(pp. 242–276).New York: Guilford Press. Pietrzak, R. H., Van Ness, P. H., Fried, T. R., Galea, S., & Norris,
Foa, E. B., Rothbaum, B. O., Riggs, D. S., & Murdock, T. B. F. H. (2013). Trajectories of posttraumatic stress symptomatology
(1991). Treatment of posttraumatic stress disorder in rape victims: in older persons affected by a large-magnitude disaster. Journal of
A comparison between cognitive-behavioural procedures and Psychiatric Research, 47, 520–526.
rie66620_ch04_087-098.indd 97 07/29/17 11:48 AM

Pitman, R. K. (1989). Post-traumatic stress disorder, hormones, and Royer, S., & Pare, D. (2002). Bidirectional synaptic plasticity in
memory. Biological Psychiatry, 26, 221–223. intercalated amygdala neurons and the extinction of condition
Pitman, R. K., Shalev, A. Y., & Orr, S. P. (2000). Posttraumatic stress feared responses. Neuroscience, 115, 455–462.
disorder: Emotion, conditioning and memory. In M. D. Corbetta & Salmon, K., & Bryant, R. A. (2002). Posttraumatic stress disorder
M. Gazzaniga (Eds.), The new cognitive neurosciences (2nd ed.) in children: The influence of developmental factors. Clinical
(pp. 687–700). New York: Plenum Press. Psychology Review, 22, 163–188.
Rahman, A., Hamdani, S. U., Riaz, N., Bryant, R. A., Dawson, K., Shalev, A. Y., Sahar, T., Freedman, S., Peri, T., Glick, N., Brandes,
Firaz, M., . . . van Ommeren, M. (2016). Effect of a multicomponent D., Orr, S. P., & Pitman, R. K. (1998). A prospective study of heart
behavioral intervention in adults with psychological distress in rate response following trauma and the subsequent development of
a conflict-affected area of Pakistan: A randomized clinical trial. posttraumatic stress disorder. Archives of General Psychiatry, 55,
JAMA, 316, 2609–2617. 553–559.
Rothbaum, B., Foa. E., Riggs, D., Murdock, T., & Walsh, W. (1992). Warda, G., & Bryant, R. A. (1998). Cognitive bias in acute stress
A prospective examination of post-traumatic stress disorder in rape disorder. Behaviour Research and Therapy, 36, 1177–1183.
victims. Journal of Traumatic Stress, 5, 455–475.
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CHAPTER 5
Depressive disorders
Richard O’Kearney
CHAPTER OUTLINE
● Historical and current approaches to the diagnosis of depression
● The epidemiology and associated features of depression
● The aetiology of depression
● The treatment of depression
● Summary

5.1 Describe the diagnostic criteria for depressive disorders.
5.2 Understand the prevalence of depression in various groups and its associated features.
5.3 Understand the current biological, psychological and social theories of the causes of major depressive disorders.
5.4 Understand the effective treatments for depressive disorders and approaches to reducing relapse and
preventing the onset of depression.
DEPRESSIVE DISORDERS: AN AUSTRALASIAN FOCUS

Depressive disorder is primarily characterised by persistent sad, empty or irritable mood accompanied by a range of
other features, such as feelings of worthlessness, a sense of failure and low energy. It is more intense or lasts longer than
the normal unhappiness that most individuals experience from time to time in response to a negative life event such as
the loss of a friendship or a disappointing exam result.
In addition to dealing with distressing and impairing symptoms, people with depression, like those with other mental
disorders, have to deal with the stigma that continues to be associated with mental health problems. This stigma has a
real effect on people’s recovery from depression, impacting on their ability to accept that they have a problem and how
quickly they seek help, as well as impairing family, work and social relationships, which in turn reduces the potential
support these relationships can provide.
Several organisations and initiatives in Australia, such as the Black Dog Institute, beyondblue and PANDA (Perinatal
Anxiety and Depression Australia), have put substantial effort into tackling the effects of stigma on people experiencing
conditions such as depression, along with the coordination and development of services and supports. As just one
example, in 2016 the Movember Foundation funded the television series Man Up (www.manup.org.au) that aims to
highlight, and hopefully reduce, the high risk of suicide in men, which is the leading cause of death for those aged 15 to
44. The series focuses on Australian stereotypes of masculinity that encourage men to be uncomplaining, to not express
their emotions, and to be overly self-reliant as a key part of the problem. These attitudes can stop men from recognising
and seeking help for psychological difficulties when they need it. The Man Up series provides information about the
nature of depression and its treatment in a way that seeks to engage men and challenge prominent but unhealthy
stereotypes of what it is to be a man and a mate in the face of depression.
continued
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The stigma reduction strategies used in public health

campaigns should be informed by research into the
psychological factors which create barriers for those who
suffer with depression from obtaining effective help and
the factors which might break down these barriers. How
to develop effective ways of combating the stigma of
depression and other mental disorders is an ongoing major
challenge for the community and one that psychological
science is playing a leading role in overcoming.
The current chapter focuses on the depressive
disorders, particularly major depressive disorder. The
chapter will begin by providing a brief overview regarding
DAL
historical approaches to depression and a description
of the current diagnostic criteria for key depressive Offering a new definition of what it means to ‘man up’,
disorders. Information will then be presented regarding the Man Up series encourages men to open up about
the epidemiology of depression, including its associated their concerns as a way of trying to reduce the male
problems. Finally, current biopsychosocial understandings suicide rate.
regarding the aetiology and treatment of depression will
be provided.
LO 5.1 Historical and current approaches to the

diagnosis of depression
Historical approaches to the diagnosis of depression
There have been many historical references to the existence of a pathologically depressed mood state
in both Western and Eastern literature (Jackson, 1986). For example, in ancient Greece, the term
‘melancholia’ was used to denote a mental condition characterised by fear and depression. Over the
centuries, the term ‘melancholia’ came to encompass broader concepts and was used to refer not only
to a state of illness but also to a depressed personality style.
During the late nineteenth century the German psychiatrist Emil Kraepelin (1896) identified
‘manic depressive insanity’ as one of the major categories of mental illness. Manic depressive insanity
encompassed the conditions that are currently categorised as bipolar disorders and depressive disorders.
However, there was controversy surrounding Kraepelin’s concept as it classified all disorders of mood
together rather than distinguishing between those individuals who experience depressive episodes
alone and those who experience both depressive and manic episodes (currently termed depressive
disorders and bipolar disorders, respectively). A distinction between depression and bipolar disorder
was eventually made by the German psychiatrist Karl Leonhard (1957) and has remained in the current
classification system.
major depressive
disorder
Depressive Current approaches to the diagnosis of depression
disorder involving
one or more The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (American
major depressive Psychiatric Association [APA], 2013) includes a chapter entitled ‘Depressive Disorders’. Among
episodes. these conditions is major depressive disorder, commonly referred to as ‘major depression’. It is known
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Chapter 5 Depressive disorders 101
as ‘recurrent depressive disorder’ in the International Classification of Diseases and Health Related
Problems (ICD-10) (World Health Organization [WHO], 1992).
Major depression is characterised by a continuous period of at least two weeks during which the
person feels depressed, sad, empty or hopeless, or has lost interest in nearly all of his/her activities
(referred to as anhedonia). In children the mood can be irritable rather than sad. This period of low anhedonia
mood must represent a change in the person’s functioning and be accompanied by at least four of the Inability to
following symptoms: experience
pleasure from
∙ significant weight loss when not dieting, or weight gain, or a decrease or increase in appetite nearly previously
every day pleasurable
∙ insomnia or hypersomnia nearly every day activities.
∙ loss of energy or fatigue nearly every day
∙ motor restlessness (‘psychomotor agitation’) or slowed movements (‘psychomotor retardation’)
nearly every day and observable to others
∙ diminished concentration or ability to think, or indecisiveness nearly every day
∙ feelings of worthlessness or excessive or inappropriate guilt nearly every day
∙ recurrent thoughts of death, recurrent suicidal ideation without a plan or a suicide attempt or a
specific plan for committing suicide.
To be considered an episode of major depression, these symptoms also need to cause significant
distress and impairment in the person’s life—impacting on his/her social, occupational and other important specifier
roles—and not be attributable to the physiological effect of a substance or other medical condition. An extension to
the diagnosis that
The DSM-5 also attempts to consider the great deal of variability in the clinical presentation of major
further clarifies
depressive disorder. It does this by including ‘specifiers’. A specifier is an extension to the diagnosis that the course,
further clarifies the course, severity or special features of the disorder. In the case of major depressive severity or
disorder, there are several specifiers that distinguish the disorder in terms of its severity (mild, moderate special features
or severe), the number of episodes (single or recurrent), the degree of recovery between depressive of the disorder.
episodes (in partial remission or in full remission) and whether there are accompanying psychotic
features. This last specifier is major depressive disorder ‘with psychotic features’, which refers to an anorexia
episode of depression in which the person experiences delusions and/or hallucinations. In addition, Loss of appetite.
the DSM-5 allows specification of particular features
of the sufferer’s depression. These include:

∙ major depressive disorder with melancholic
features, which is characterised by a profound,
nearly complete inability to experience pleasure.
Mood is usually worse in the mornings and the
sufferer may experience early-morning awakening,
marked psychomotor retardation or agitation,
significant anorexia (i.e., loss of appetite) or weight
loss and excessive guilt
∙ major depressive disorder with catatonic features,
which is characterised by movement disturbance
symptoms, such as immobility at one extreme or
excessive, purposeless activity at the other extreme
∙ major depressive disorder with peripartum
onset, which refers to episodes that occur during
pregnancy or within four weeks after childbirth.
DAL
While brief episodes of depressed mood (often

referred to as ‘the baby blues’) can occur in up Among the core symptoms of depressive disorders are feelings of
to 70 per cent of women within 1–10 days after sadness, depression, emptiness or hopelessness and/or a loss of
childbirth, depression with peripartum onset is a interest in activities.
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major depressive more serious disorder (Cooper & Murray, 1998). The risk of suffering from this form of depression
episode is thought to be greater among those women experiencing psychosocial stressors such as a
State perceived lack of support from their partner, family and friends, feeding and physical difficulties
characterised with the infant, stressful life events, a previous history of depression and complications during
by at least five
depressive
pregnancy
symptoms, one ∙ major depressive disorder with seasonal pattern, which is diagnosed when there is a regular
of which must relationship between the onset of the sufferer’s major depressive episodes and a particular time of
be either sad the year (most often with onset in the autumn or winter months)
mood or a loss of ∙ major depressive disorder of mixed features when some symptoms of elevated mood are present
pleasure/interest alongside depression
in usual activities. ∙ major depressive disorder with anxious distress, which identifies depression accompanied by
Additional
significant anxiety such as irrational worry, inability to relax or a sense of impending threat.
depressive
symptoms include This specifier recognises the strong comorbidity between depression and anxiety, with about
an increase 50 per cent of people with major depressive disorder reporting significant anxiety symptoms
or decrease (Kessler, Chiu, Demler, & Walters, 2005) as well as accumulating evidence that anxiety and
in appetite, depression are the expression of common biological and psychological dispositions including
insomnia or shared genetic factors (Hettema, Neale, Myers, Prescott, & Kendler, 2006). The presence of
hypersomnia, anxiety in depression also has important clinical implications as anxiety comorbid with depression
psychomotor
increases the risk of suicide (Boden, Fergusson, & Horwood, 2007) and predicts a longer length
agitation or
retardation,
of the depressive episode (Parker et al., 1999). These considerations suggest that major depressive
fatigue, feelings disorder often has its roots in difficulties in the expression and regulation of anxiety. The anxiety
of worthlessness specifier for depressive disorders will hopefully enable clinicians to identify and treat people
or severe before they develop an enduring major depressive disorder or a significant anxiety disorder such as
guilt, difficulty generalised anxiety disorder (GAD).
concentrating
and suicidal The DSM-5 diagnostic criteria for major depressive disorder no longer exclude those cases when
ideation. These the symptoms are better accounted for by bereavement as in the DSM-IV-TR (APA, 2000). In other
symptoms must words, bereaved individuals can now be diagnosed with major depression if they meet the necessary
be present for at criteria. This change has caused considerable controversy, with some clinicians concerned that it
least two weeks. will lead to the inappropriate diagnosis and treatment of bereaved individuals who are distressed yet
undergoing an adaptive adjustment process. The DSM-5 has attempted to minimise the chances of
generalised
anxiety disorder inappropriately diagnosing bereaved individuals with a mental disorder by listing some distinctions
(GAD) between non-pathological grief and major depression (e.g., a preoccupation with thoughts about the
Anxiety disorder deceased in the former versus self-critical thoughts in the latter).
characterised In addition to major depression, the DSM-5 chapter on ‘Depressive Disorders’ includes persistent
by chronic worry depressive disorder, previously referred to as dysthymic disorder or dysthymia. This change in
in daily life
terminology more clearly describes a depressive disorder where the mood disturbance and at least two
accompanied
by physical
other symptoms (e.g., insomnia, poor self-esteem and low energy) last for at least two years without a
symptoms of notable remission of symptoms.
tension. A new diagnostic category introduced in the DSM-5 is disruptive mood dysregulation disorder, that
is, a disorder of mood disturbance characterised by severe temper outbursts and persistent irritability
dysthymia
and anger. This is predominantly a disorder observed in children with severe recurrent problems
(dysthymic
disorder)
with anger, irritability and temper outbursts, which are severely out of proportion to the situation
Depressive and developmentally inappropriate. This symptom profile is highly prevalent in the United States
disorder that is but has been generally viewed sceptically in Europe and Australasia. Another potential problem is
less severe than that, given that there are a number of other diagnoses in the DSM-5 where behavioural and emotional
major depression dysregulation are core features (e.g., oppositional defiant disorder, attention-deficit/hyperactivity
but more chronic. disorder, impulse control disorders and bipolar disorder), reliably distinguishing disruptive mood
dysregulation disorder from these conditions could prove challenging.
Although the DSM-5 tries to deal with the heterogeneity of depressive disorders, the classification
system can be critiqued for ignoring potential distinctions based on different causal factors potentially
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involved in different types of depression. An Australian research team has argued for an alternative disruptive mood
subtyping model for the depressive disorders using possible aetiologies as well as symptom features dysregulation
(Parker, 2000; Parker et al., 2010; Parker & Hadzi-Pavlovic, 1996). This model suggests three broad disorder
classes of depressive disorders: psychotic, melancholic and non-melancholic. In terms of aetiology, A depressive
disorder
both psychotic and melancholic depression are theorised to be primarily biologically based, while characterised
non-melancholic disorders are thought to be driven by life-event stressors and psychological factors. In by severe and
terms of symptoms, melancholic depression is characterised by the presence of significant psychomotor persistent
disturbance, while psychotic depression is characterised by both psychomotor disturbance and irritability as
psychotic features. In combining information about symptoms and causal factors in the subtyping of evident in temper
depression, the model aims to provide greater direction regarding the most effective form of treatment outbursts that are
for each subtype (Parker, Roy, & Eyers, 2003). For instance, biological treatments (such as medication) extremely out of
proportion to the
may be most appropriate for the depressive disorders that are believed to be biologically based (i.e.,
situation.
psychotic and melancholic depression), whereas psychological approaches may be more effective for
non-melancholic depression. While there is significant merit in attempting to match individuals to the cognitive
type of treatment that is most effective for their type of depression, there is no evidence to date that the behaviour
presence of melancholia is more effectively treated with medication compared to psychotherapy such therapy (CBT)
as cognitive behaviour therapy (CBT) (Cuijpers et al., 2016). Type of
psychological
treatment that
LO 5.2 The epidemiology and associated combines both
cognitive and
features of depression behavioural
concepts and
techniques.
The prevalence of depression
Depressive disorders are among the most prevalent psychological problems in Australia. Rates of
depression are generally higher for women compared to men. Among Australian adults, prevalence
rates for major depressive disorder have been estimated at 3.1 per cent for men and 5.1 per cent for
women over a 12-month period (Australian Bureau of Statistics [ABS], 2007; Slade, Johnson, Oakley
Browne, Andrews, & Whiteford, 2009). Rates of dysthymia are lower, at about 1 per cent for men and
1.5 per cent for women (ABS, 2007; Slade et al., 2009). The impact of depression on families and the
wider community is far more widespread, however, and it has been estimated that 1 in 10 Australians
are affected by someone close to them suffering from a mood disorder (Australian Institute of Health
and Welfare, 1999). Despite the availability and widespread use of effective treatments for highly
prevalent disorders such as depression and anxiety disorders, research indicates that the level of
psychological distress in the Australian population has not changed between 1995 and 2011 (Jorm &
Reavley, 2012). These findings underline the importance of better understanding the psychological,
social and biological determinants of these common and increasingly burdensome disorders.
Research has demonstrated that women are, on average, twice as likely to experience both mild
depressive symptoms and severe depressive disorders as men (Nolen-Hoeksema, 2002). This finding
has been replicated in many countries and among several ethnic communities. Various theories
have been put forward to account for this gender difference, including the possibility that women,
compared to men, are more willing to admit that they are suffering from symptoms of depression or
that women are more vulnerable to the psychosocial stressors associated with modern life, such as
having to cope with the simultaneous demands of being a caregiver for children and ageing parents
while also participating in the workforce. As a similar sex disparity exists for anxiety disorders, the
imbalance may also represent differences in gender-related socialisation, with a greater emphasis
traditionally on females being more reliant on others and less assertive than males. This emphasis may
increase a sense of uncontrollability over stressors and feelings of helplessness during stressful times.
In addition, there is some evidence that psychological factors interact with hormonal and biological
influences more prevalent in women. In this regard, Ge, Conger, and Elder (2001) demonstrated that
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the marked gender disparity in the incidence of depression symptoms that begins in adolescence is
best explained by the interaction of pubertal biological changes, the interpersonal stressors of puberty,
and pre-existing gender-dependent vulnerabilities such as the over-reliance on interpersonal sources
as a basis for self-esteem in females compared to males.
Australian data released in 2015 indicated that 5 per cent of Australian adolescents (aged 12–17
years) had depressive disorders, including major depressive disorder and dysthymia, over a 12-month
period (Lawrence et al., 2015). Depressive disorders in children and adolescents have been steadily
increasing over the past 5–10 years in most developed countries. Like adults, girls tend to have
higher rates than boys after the onset of puberty and are approximately twice as likely to suffer from
depression as their male counterparts. The cause of this increase is as yet unknown, but possibilities
include hormonal fluctuations, psychological factors (such as body dissatisfaction) that accompany
puberty and the stress associated with entry to high school (Kessler, 2006). The rates of depression
in males and females during a one-year period from a study involving more than 1000 children and
young adults are shown in Figure 5.1.
30
25
Percentage with depression
20
Males
15 Females
10
5
0
11 13 15 18 21
Age in years
FIGURE 5.1 The percentage of males and females from the ages of 11–21 years who were diagnosed with
major depressive disorder or dysthymia during a one-year period
Source: From Hankin, B. L., Anderson, L. Y., Moffit, T. E., Silva, P. A., McGee, R., & Angell, K. E. (1998). Development of depression from
pre-adolescence to young adulthood: Emerging gender differences in longitudinal studies. Journal of Abnormal Psychology, 107, 128–104,
© 1988 The American Psychological Association. Used with permission.
High levels of anxiety, problem behaviours or the abuse of drugs and alcohol have all been
associated with a heightened risk of developing depression in young people. Among the other risk
factors are having a previous history of depression, ongoing family conflict, a history of sexual or
physical abuse, residing in a rural area, being of Aboriginal or Torres Strait Islander descent, and
having a parent with a psychological disorder. Several explanations may account for the fact that
children who live with a parent with a psychological disorder are at greater risk of experiencing
a depressive episode. This may be due to genetic factors that are transmitted from parents to their
children, problems in early attachment and bonding between a child and a parent with psychological
problems, ongoing parenting difficulties that lead to conflict between the child and parent, the child
experiencing a feeling of abandonment or neglect as their parent may not be able to adequately meet
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their needs, and the child needing to assume the role and responsibilities of being a ‘parent’ to their
father, mother and siblings.
The age of onset of depression

Depressive disorders can affect people at any age. Onset of a first episode of depression can occur
from as young as three years of age (Emde, Harmon, & Good, 1986; Rutter, 1986). Epidemiological
data suggest that the median age of onset for mood disorders is about 30 years of age (Kessler
et al., 2005).
In a report profiling depression in Australia, studies have found that approximately 20 per cent
of those who experience depression meet criteria by the age of 25 (Australian Institute of Health
and Welfare, 1999). Early adult depression is often preceded by an anxiety disorder in childhood or
adolescence (Maughan & Kim-Cohen, 2005). One study of longitudinal design conducted psychiatric longitudinal
assessments at regular intervals on individuals from the ages of 11 to 26 years (Kim-Cohen et al., design
2003). Of the individuals with major depressive disorder or dysthymia at the age of 26, almost Type of research
90 per cent had a prior diagnosis of a mental disorder, primarily adolescent anxiety or depression or evaluating
changes in the
childhood conduct or oppositional defiant disorder. These data emphasise that initial adult episodes of
same group of
depression often have precursors in mental health problems much earlier in life. people over time.
conduct disorder
The course of depression Disorder marked
by chronic
Follow-up studies have demonstrated that up to 50 per cent of those with a depressive disorder will disregard for the
recover within the first six months following treatment. Unfortunately, major depressive disorder rights of others,
has a highly recurrent character. About 50 per cent of people who recover from a first episode of including specific
depression will have no further episodes, but many will have a further episode or not recover fully behaviours such
from the first episode (Eaton et al., 2008). The risk of relapse is higher among those who continue to as stealing, lying
and engaging in
experience some depressive symptoms after an episode rather than experiencing a full resolution of
acts of violence.
their symptoms. The risk of recurrence also increases as the number of previous depressive episodes
increases (Bockting, Hollon, Jarrett, Kuyken, & Dobson, 2015). In addition, a history of depression in oppositional
family members, an earlier age of onset for the first episode and ongoing life stressors increase the risk defiant disorder
of further episodes after a first episode. Disorder

of chronic
misbehaviour in
Problems associated with depression children marked
by belligerence,
The main problems associated with depression include an increased risk of suicide and suicide irritability and
attempts, difficulties performing occupational and social activities, anxiety disorders and physical defiance.
health problems.
SUICIDE
In Australia in 2015, data indicate that 3027 people (12.7 per 100 000) took their own life, with
2292 males (19.4 per 100 000) and 735 females (6.2 per 100 000) dying by suicide (ABS, 2016).
Depression is associated with an increased rate of suicide attempts and successful suicide, with
as many as 75 per cent of people who take their own life suffering from depression (Harwitz &
Ravizza, 2000). Follow-up studies of previously hospitalised patients with depression or bipolar
disorder have shown that approximately 15 per cent of depressed patients commit suicide (Blair-
West, Cantor, Mellsop, & Eyeson-Annan, 1999). The rate of suicide in the community from
depressive disorders is estimated to be approximately 3.5 per cent, with a higher preponderance
of male suicides (6.9%) over female suicides (1.1%) (Blair-West et al., 1999). In addition to
male gender and having been hospitalised for depression, major risk factors for suicide in those
with depression include the co-occurrence of a substance use disorder, stressful life events, a
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previous history of suicide attempts and, among adolescents, parent–child conflict (Gould &
Kramer, 2001).
Suicide rates in Australia appear to have been declining since the late 1990s (Large & Nielssen,
2010). Possible reasons for this include improved recognition and treatment of depression, and reduced
access to lethal means such as firearms. These types of broad, societal-level preventive measures are
clearly important. To augment these approaches, other prevention strategies focus on the individual
level. Thoughts of suicide can be considered a necessary precondition to an attempt, and this suicide
ideation is much more common in the community than suicide attempts, with approximately 8 per cent
of people reporting thoughts about suicide compared to 0.8 per cent attempting suicide (Fairweather,
Anstey, Rodgers, & Butterworth, 2006). While suicide attempters and suicide ideators may be equally
likely to suffer from depression, factors such as unemployment, physical ill-health, relationship
difficulties and poor social support have been found to play a key role in differentiating those who
attempt suicide from those who have thoughts about it. There is evidence that addressing these issues
in those at risk of suicide because of a mental disorder such as depression can reduce suicide rates
(While et al., 2012). Among these strategies are active follow-up by mental health professionals with
the patient after acute treatment and regular training of clinicians on managing suicide risk.
OCCUPATIONAL AND SOCIAL ACTIVITIES

People with depression typically find it difficult to perform their usual occupational and social activities.
For example, depression results in lowered work productivity (e.g., higher rates of sick leave). For
younger individuals, depression can affect learning and academic achievement, as well as the ability
to develop and maintain social and intimate relationships. For families, one member suffering from
a depressive illness can result in a level of burden experienced by other members in providing care.
Families often experience financial problems if the sufferer is also the main breadwinner. Conflict
with family members and withdrawal from family obligations are characteristics of depression. The
fact that people with depression are at greater risk of suicide and suicide attempts also impacts heavily
on family members, friends and workmates.
ANXIETY DISORDERS
As already noted, depressive disorders are frequently associated with anxiety disorders and both are
extremely common in community settings. For example, one study found that one in five Australian
patients seeing a general practitioner was suffering from depression and/or anxiety disorders (Harris
et al., 1996). Anxiety disorders—especially generalised anxiety disorder, panic disorder and social
phobia—are often found to precede depressive disorders, to increase the risk of a depressive disorder,
and to be associated with longer episodes of depression and a higher risk of suicide (Kessler et al.,
1996; Parker et al., 1999).
PHYSICAL HEALTH PROBLEMS

Depression is associated with a number of physical health problems (Hickie et al., 1996). For instance,
rates of depression in people with cardiovascular disease range from 10 to 23 per cent (Musselman,
Evans, & Nemeroff, 1998). Depression is also associated with increased rates of death in the
18 months following a cardiac event, with individuals who are depressed following a heart attack
having an almost four-fold risk of death compared to those who are not depressed (Frassure-Smith &
Lesperance, 1995). Research has also found an association between depression and both diabetes
(Eaton, 2002) and cancer (Massie, 2004).
There may be several reasons for the association between depression and medical illness. For
instance, depression may result in individuals engaging in health-risk behaviours (such as smoking,
drug use, alcohol abuse, poor eating habits and low levels of physical activity). Depression has also
been found to be associated with poorer immune functioning, which may increase the risk of illness.
Conversely, medical illness may result in depression due to the ongoing stressors of dealing with a
chronic and life-threatening illness or to physical changes (e.g., hormonal disturbances) stemming
from the medical illness and/or its treatment.
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CASE STUDY: ANXIETY AND DEPRESSION

Mack is a 22-year-old second-year university student who was referred to a clinical psychologist by his GP for worsening
depressive symptoms. Mack reported persistent low mood over the past year and increasing lack of interest in his
usual exercise routines, in playing music and in family activities. He described how he had lost confidence in the quality
of his university work and felt he was not good enough to become a lawyer or even to complete his degree. He was
considering dropping out and was attending only compulsory tutorials and doing other work online or not at all. While
he was still going to his part-time job, he noticed himself being more irritable there: ‘I’m just doing the work, then going
home and not socialising because they all annoy me.’ Mack also noticed he had difficulty concentrating, was sleeping
longer in the mornings and had less of an appetite. He felt like ‘just giving up’ but stated that he had not experienced any
ideas of suicide or self-harm and had no plans to take his own life.
The course of Mack’s depression illustrates the role of anxiety and stress in the development of depression. Mack
was a high-achieving student who was doing well in Year 11 of high school, but he became increasingly stressed and
preoccupied by the need to achieve highly in Year 12. He believed that the stress of Year 12 contributed to his decision
to break up with his girlfriend ‘to give me more time to study’ while also contributing to conflict with friends at school.
He noticed himself becoming increasingly anxious in social situations outside of the family, being more concerned with
what others thought of him and worrying about ‘wasting time socialising instead of studying’. He found it more and more
difficult to get to sleep at night, which further added to his anxiety that ‘if I don’t get enough sleep I won’t have the energy
and concentration to study’.
While he did well in his Year 12 final exams and got into his first preference university degree, he deferred for a year
because he felt so stressed by the previous year and wanted to have a break from study. He got a part-time job and was
able to resume activities he had dropped in Year 12 such as going on camping trips with his family. However, when he
resumed study, his anxiety returned. He found the start of university very stressful, particularly the social interactions with
other students. He justified his pattern of avoidance of social activities by the need to get high marks, but this resulted
in his self-esteem being completely dependent on his grades as well as meaning he missed out on the pleasure and
support of contact with friends. Whenever he struggled with his studies he would become very irritable with family and
co-workers and then go over and over these conflicts in his mind for days.
As the academic year progressed, Mack avoided both being at university and having contact with friends as much
as possible. As his grades began to slip, his belief in his worth as a person also dropped. Mack resisted reaching out for
support and getting treatment for his anxiety and depression, but, with his family’s persistence, eventually agreed to see
his GP.
LO 5.3 The aetiology of depression

Depression is a complex and heterogeneous disorder and it is likely that the best accounts of its
aetiology will combine the impact of biological, psychological, social and environmental factors. The
contribution of each of these factors to explaining depression varies in regard to different presentations
of depression. For example, there is some evidence in the case of individuals who experience recurrent
episodes of major depression that severe stress plays less of a role in triggering their later depressive
episodes (Monroe & Harkness, 2005). Nevertheless, aetiological models of all types of depression
are increasingly attempting to integrate biological, psychological and social factors and to identify
vulnerabilities to depression in the face of stressful events or environments.
Biological factors
There is little doubt that genetic factors play a role in depression, particularly for severe and recurrent
forms of the disorder (Weissman et al., 2005). For example, heritability estimates from several studies
demonstrate that a family history of depression can double or triple an individual’s risk of developing
rie66620_ch05_099-124.indd 107 07/29/17 02:14 PM

neuro- a mood disorder. However, the precise nature of the vulnerability that is inherited remains unknown.
transmitters To highlight just one possibility, the findings from a large multi-generational study of female twins
Biochemicals (Kendler, Pedersen, Farahmand, & Persson, 1996) suggest that inherited traits in children (e.g., anxious
released from a traits) may contribute to the development of particular parenting styles (e.g., overprotectiveness or
sending neuron to
a receiving neuron
authoritarianism). Such parenting styles may in turn undermine the child’s sense of mastery over
so as to transmit his/her environment, rendering the child vulnerable to developing further anxiety problems and
messages in the depression.
brain and nervous Overall, current understandings highlight the interplay between genetic vulnerability and
system. stressful life events (i.e., gene–environment interactions) leading to the development of depression
(Caspi, Hariri, Holmes, Uher, & Moffitt, 2010; Quinn, Dobson-Stone, Outhred, Harris, & Kemp,
monoamines 2012). For example, the shorter allele of the 5-HTTLPT gene sequence is associated with lower
Neurotransmitters serotonin reuptake at brain synapses and hence is thought to be implicated in the development of
including depression (Caspi et al., 2010). Individuals carrying one or two copies of the short allele of this
catecholamines
gene sequence have been shown to exhibit higher levels of neuroticism and depression after stressful
(adrenaline,
noradrenaline life events and/or childhood maltreatment (Caspi et al., 2003; Lesch et al., 1996). In other words,
and dopamine) it is the occurrence of both a specific type of genetic vulnerability and stressful life events that
and serotonin contribute to depression.
that have been The main neurotransmitters implicated in depression are serotonin, noradrenaline (norepinephrine)
implicated in and dopamine, which are also involved in the regulation of sleep cycles, motivation and appetite.
mood disorders. These belong to the family of neurotransmitters called monoamines and are concentrated in the limbic
system, a part of the brain associated with integrating goal-directed activities. Early theories suggested
limbic system that depression was caused by a reduction in the availability of monoamine neurotransmitters in the
Part of the brain synapses between neurons. More recent theories of depression, however, have implicated abnormalities
that relays
in the number and sensitivity of receptors available to take up monoamine neurotransmitters in
information from
the primitive synapses, which then affects the balance of the various available neurotransmitters.
brain stem about Neuroendocrine (hormonal) theories suggest a role for hyperactivity in the hypothalamic-pituitary-
changes in bodily adrenal (HPA) axis in the development of depression. The HPA axis is critical to the body’s response to
functions to the stress and produces stress hormones involved in the fight or flight response. People who are depressed
cortex where the tend to demonstrate chronic overactivity in the HPA axis, resulting in the production of excess stress
information is hormones (such as cortisol), which in turn affects the way in which monoamine neurotransmitters work
interpreted.
in the brain (Southwick, Vythilingam, & Charney, 2005). Chronic high levels of stress hormones may
also impact on important brain structures involved in the regulation of stress such as the hippocampus,
synapse
Space between
perhaps leading to longer-term vulnerability to emotional dysregulation in times of stress.
a sending and Neurophysiological theories focus on structural or functional abnormalities in certain structures
receiving neuron in the brain such as the pre-frontal cortex, hippocampus, anterior cingulate cortex and the amygdala
into which (Davidson, Pizzagalli, Nitschke, & Putnam, 2002). However, research has yet to determine whether
neurotransmitters these abnormalities are a cause or a consequence of depression.
are released.
neuron Environmental factors

Nerve cell;
activates or There is strong evidence that stressful life events can act as causal triggers for depressive episodes.
inhibits other These events typically precede the episode by 6–9 months (Brown, Harris, & Hepworth, 1994) and
neurons by may be acute (e.g., a severe financial disaster) or chronic (e.g., living with an abusive partner or
releasing neuro- caring for a person with an ongoing physical or mental disorder). In particular, life events that entail
transmitters.
experiences of loss and failure (e.g., the break-up of a close relationship, the loss of a loved one or
unemployment) are frequently associated with the onset of a depressive episode. Growing up in a
receptors
Molecules on the hostile, disruptive and violent family environment is also thought to contribute to the development of
membranes of depression in adult life (Nolen-Hoeksema, Girgus, & Seligman, 1992). But these types of experiences
neurons to which and environments are more likely to trigger depression when they interact with biological and learnt
neurotransmitters psychological vulnerabilities. In addition, the negative impact of stressful life experiences can be
bind. reduced by the degree of social support available to the individual.
rie66620_ch05_099-124.indd 108 07/29/17 02:14 PM

Psychological factors hypothalamic-

pituitary-adrenal
A number of psychological vulnerabilities and processes have been proposed to explain the onset and (HPA) axis
maintenance of depressive disorder. Three
components of the
COGNITIVE THEORIES neuroendocrine
system that work
Cognitive theories have dominated psychological accounts of depression. An important early theory
together in a
was that depression is a learnt response to adverse events that are perceived as uncontrollable. The feedback system
learned helplessness model of depression was based on the observation that when laboratory animals interconnected
were subjected to unavoidable adverse outcomes (i.e., electric shocks) that were independent of their with the brain’s
behaviour (i.e., uncontrollable), they gave up trying to do something about their situation (Seligman, limbic system and
1975). This model was reformulated (Peterson & Seligman, 1984) to be a better fit for depression in cerebral cortex.
humans by including the role of the type of attributions (i.e., causal explanations) people make for hormone
adverse events. The depressive attributional style is one that interprets negative life events as being Chemical
due to internal (the individual’s own fault), global (applicable to all situations) and stable (unchanging produced by
or invariable) factors. For example, according to this theory, a person who interprets the ending of a the endocrine
romantic relationship as being due to an aspect of him/herself that pervades all of his/her relationships glands that
and that cannot be changed will be more likely to experience a sense of hopelessness regarding carries messages
the possibility of establishing a meaningful relationship in the future and hence will be at risk of throughout
the body and
developing depression.
potentially affects
In another major cognitive theory of depression, Aaron Beck (1976; 1991) proposed that negative a wide array of
experiences in childhood may result in the development of dysfunctional core beliefs about the self, functioning such
others and the world (such as a highly critical parenting style resulting in the child’s belief that s/he as an individual’s
is unlovable). Individuals generally deal with these negative core beliefs by adopting compensatory mood, level
strategies or rules that protect them from developing depression (e.g., ‘as long as I’m in a relationship of energy and
then I’m lovable’). However, Beck proposes that these negative core beliefs can be triggered by reaction to stress.
relevant negative life events (e.g., the ending of a relationship activating the belief ‘I am unlovable’) cortisol
and thus result in a depressive episode. He argues that the thought patterns of depressed people are Hormone
characterised by self-criticism, a negative view of others and life events and pessimistic expectations produced by the
regarding the future. According to Beck, this negative view of the self, the world and the future (known adrenal cortex
as the negative cognitive triad) is maintained by a number of cognitive distortions in which depressed that helps the
body respond
people are likely to engage. Among these errors in thinking are the following:
to stressors,
inducing the fight
∙ Arbitrary inference takes place when a person draws a conclusion in the absence of supporting or flight response.
evidence or despite the presence of contradictory evidence (e.g., ‘I did not get invited to Jenny’s
party. That must mean that I have offended her in some way’). pre-frontal cortex
∙ Magnification and minimisation occur when a person magnifies or exaggerates his/her perceived Region at the
failures (e.g., ‘I couldn’t answer that question in class. Everyone thinks I am such an idiot’) and front of the
brain important
minimises or discounts his/her achievements (e.g., ‘I managed to get a part-time job in the company in language,
but they were probably desperate to hire someone’). emotional
∙ Personalisation entails relating events to oneself in the absence of any clear evidence (e.g., ‘Terry expression, the
was frowning when he saw me in the shop. I must have done something to make him angry’). planning and
∙ Overgeneralisation occurs when a person draws a conclusion based on a single event (e.g., ‘My production of
boyfriend broke up with me last week. I’m hopeless with relationships’). new ideas, and
the mediation of
Beck (1991) maintains that the dysfunctional, negative cognitions characterising individuals with social interactions.
depression result in symptoms of depression (such as low mood) and that these symptoms in turn amygdala
result in further negative cognitions. For instance, an individual who believes that s/he is unpopular Part of the brain’s
may feel depressed and withdraw from friends, which appears to provide further support for the limbic system
individual’s belief that s/he is undesirable to others. In other words, there is a cyclical relationship that is thought
between dysfunctional thinking and the symptoms of depression. Beck’s cognitive model of depression to regulate
is illustrated in Figure 5.2. emotions.
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Negative early experiences

(e.g., critical parenting)
Dysfunctional beliefs
(e.g., ‘I am unlovable’)
Critical incident
(e.g., the end of a relationship)
Dysfunctional beliefs activated

(e.g., ‘I am unlovable’)
Negative cognitive triad

(e.g., ‘It’s my fault he left me’,
‘I don’t have any support’,
‘I’ll be alone forever’)
Symptoms of depression
(e.g., depressed mood, loss of
interest in activities such as
socialising)
FIGURE 5.2 Beck’s (1976) cognitive model regarding the development of depressive episodes
negative Beck’s theory of depression has been extensively investigated and has received considerable
cognitive triad support. For instance, in one study involving 176 depressed patients who were being treated with
Perspective seen 12 weeks of cognitive therapy, it was found that reduced dysfunctional cognitions over the course
in depressed of therapy predicted reduced depressive symptoms, and that a reduction in depressive symptoms
individuals in
which they have
predicted a reduction in dysfunctional thinking (Oei, Bullbeck, & Campbell, 2006). These results are
negative views consistent with a circular model in which both negative cognitions and depressive symptoms influence
of themselves, one another. Another study examined the ability of a reduction in dysfunctional thinking to predict
the world and the ‘sudden gains’ (i.e., large decreases in depressive symptoms from one therapy session to the next)
future. (Tang, DeRubeis, Beberman, & Pham, 2005). The participants included 83 patients with depression
who were receiving one of two types of cognitive behaviour therapy. The amount of improvement in
dysfunctional thinking that patients experienced during therapy sessions was rated by trained observers,
while symptoms of depression were measured using a self-report questionnaire at the beginning of
each session. In support of the cognitive model, it was found that there was a significantly greater
amount of cognitive change in the session preceding the ‘sudden gain’ in symptom improvement
compared to other sessions. In other words, a decrease in dysfunctional thinking in one session was
followed by a large reduction in depressive symptoms in the following session. The results of patients
receiving the two types of cognitive behaviour therapy are shown in Figure 5.3.
BEHAVIOURAL THEORIES
Behavioural theories of depression focus on the contingencies associated with depressed and non-
depressed behaviours. A dominant behavioural theory regarding the aetiology and maintenance of
depression proposes that some life events or stresses can reduce the opportunity to experience positive
reinforcers, which in turn increases the risk of depression (Jacobson, Martell, & Dimidjian, 2001;
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Amount of cognitive change 6

Control session
Pre-gain session
4
0
CBT 1 CBT 2
FIGURE 5.3 In both forms of cognitive behaviour therapy (CBT 1 and CBT 2), there was a significantly
greater amount of improvement in negative thinking in the pre-gain session (the session before there was
a large improvement in depressive symptoms) compared with the control session (held just before the pre-
gain session)
Source: From Tang, T. Z., DeRubeis, R., Beberman, R., & Pham, T. (2005). Cognitive changes, critical sessions, and sudden gains in
cognitive-behavioural therapy for depression. Journal of Consulting and Clinical Psychology, 73, 168–172, © 2005 The American
Psychological Association. Used with permission.
Lewinson & Gotlib, 1995). For example, if someone loses his/her job the person may experience
financial difficulties and miss the opportunity for regular social interaction with work colleagues.
Chronic financial constraints and lack of social support over time could lead to the development and
maintenance of a depressive illness in this person.
Other behavioural theories of depression highlight the role of poor coping skills. For some people,
a lack of effective coping skills to deal with life stressors can contribute to the onset of a depressive
episode (Arean et al., 1993). For example, individuals who lack effective problem-solving skills may
experience increasing helplessness in the face of mounting stressors.
PSYCHOANALYTIC THEORIES
Psychoanalytic theories hold that depression is a form of pathological grief. These grief-like responses expressed
may occur within the context of the break-up of a close relationship, loss of a job with income and emotion (EE)
status, deterioration in health and even the shattering of one’s ideals and beliefs. Disruptions in early Family interaction
style in which
childhood bonding experiences with caregivers are thought to sensitise people to losses in adulthood,
family members
which, in turn, leads to vulnerability to depression. Such individuals are thought to be ambivalent are overly
in their relationships and excessively dependent on others for support, encouragement, guidance, protective and
admiration and confirmation of their self-worth. Ambivalent feelings in relationships are heightened self-sacrificing
with experiences of loss, which results in anger directed towards the self. Such self-directed anger is towards the
thought to manifest as guilt and self-blame. person with a
psychological
disorder while
Social factors also expressing
high levels of
A range of interpersonal difficulties may be involved in the development and maintenance of criticism and
depressive episodes. One type of interpersonal difficulty is the family communication style of hostility; this may
expressed emotion (EE), which entails high levels of criticism, hostility and/or over-involvement. contribute to the
Researchers have found an association between high levels of expressed emotion in the families of person’s relapse.
rie66620_ch05_099-124.indd 111 07/29/17 02:14 PM

depressed patients and the patient’s risk of relapsing after a depressive episode (Hooley & Teasdale,
1989). Lack of an intimate relationship has also been found to be a risk factor for depression,
especially for women (Brown & Harris, 1978). Interpersonal theories of depression highlight the
cyclical nature of these episodes, where disturbances in social functioning (e.g., relationships
characterised by high levels of criticism) trigger depressive symptoms (such as depressed mood, low
energy and social withdrawal) that in turn lead to a further deterioration in social functioning, and
hence a worsening of the depression in a vicious cycle. In addition, because depressive behaviours
in a social context can be aversive to others, they can lead to others spending less time with the
depressed person and in this way amplify both the self-criticism and withdrawal of the depressed
individual, which further maintains his/her depression.
Protective factors
While the focus thus far has been on factors that are believed to contribute to the development of
depression, other factors are thought to be protective of developing a depressive episode (Australian
Institute of Health and Welfare, 1999). Some of the factors that may reduce an individual’s chances of
developing depression are as follows:
∙ good interpersonal skills and positive relationships with others
∙ high levels of family cohesion (i.e., strong supportive ties with at least one parent or significant
other)
∙ a sense of being connected with one’s community
∙ a sense of achievement in a valued area of pursuit (e.g., academically or athletically)
∙ a temperament characterised by optimism and low anxiety
∙ an openness to the possibility of exploring new experiences
∙ effective coping skills such as constructive problem-solving and negotiation skills.
protective As with risk factors for depression, many of these protective factors tend to cluster together,
factors making it difficult to tease out the relative importance of any one of them. For example, an individual
Conditions who comes from a close, supportive family environment and who has developed a good relationship
or variables with one or both parents may also have developed good interpersonal skills and thus may be better
associated with
equipped to participate in local sporting activities. Active participation in sporting activities may help
a reduced risk
or chance of to develop a sense of achievement and boost self-esteem, thus lessening the likelihood of developing
developing a a depressive episode.
disorder.
antidepressants LO 5.4 The treatment of depression

Drugs used
to treat the Some depressive disorders, especially those associated with acute stressors, may improve with time in
symptoms of the absence of treatment. However, effective treatment can speed up recovery and reduce the risk of
depression such relapse. Depressive episodes that are prolonged and untreated can often result in chronic psychosocial
as sad mood,
negative thinking,
difficulties, including poor academic and work histories, damaged social relationships, and a lowered
and disturbances sense of self-worth and self-confidence. Unfortunately, most people with depression never seek care
of sleep and or they wait, sometimes for years, before seeking help (Kohn, Saxena, Levav, & Saraceno, 2004).
appetite; three For the purpose of treatment planning and evaluation, it is important to assess the severity and
common types profile of the sufferer’s symptoms using reliable and valid measures of depression. Besides the
are monoamine instruments used to screen for depression at a population or community level such as the K10 (Kessler
oxidase inhibitors, et al., 2002) or the Centre for Epidemiologic Studies Depression Scale (Radloff, 1991), a number
tricyclics and
of psychometrically sound patient-focused instruments are commonly used in treatment settings to
selective
serotonin assess depression severity and treatment response. There are a range of general measures as well as
reuptake those that are designed for specific populations of patients such as elderly people, those presenting
inhibitors. with depression in the context of medical illness or youth and children. Frequently used measures
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include the Beck Depression Inventory (Beck, Steer, & Garblin, 1988), Hopkins Symptom Checklist tricyclic
(Hesbacher, Rickels, Morris, Newman, & Rosenfeld, 1980), Symptom Checklist 90 (Derogatis & antidepressants
Savitz, 2000), Geriatric Depression Inventory (Sheikh & Yesavage, 1986), Reynolds Adolescent (TCAs)
Depression Scale (Osman, Gutierrez, Bagge, Fang, & Emmerich, 2010) and the Children’s Depression Class of
antidepressant
Inventory (Kovacs, 1985).
drugs such as
Treatments for depressive disorders comprise both medical and psychological interventions, which imipramine and
may also be combined. Research suggests that a combined approach is especially beneficial for more amitriptyline.
severe, chronic or recurrent depression (Pampallona, Bollini, Tibalbi, Kupelnick, & Munizza, 2004;
selective
Petersen, 2006; Thase et al., 1997).
serotonin
reuptake
Pharmacological and physical approaches inhibitors (SSRIs)
Class of
Antidepressants are the most frequently used medications for depression. This class of medications antidepressant
includes the tricyclic antidepressants (TCAs), the selective serotonin reuptake inhibitors (SSRIs), drugs (such
serotonin-noradrenaline reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs) as fluoxetine)
that inhibit the
and several other newer medications that do not easily fit into the previous four categories.
reuptake of
Antidepressants are thought to work by increasing the availability of neurotransmitters or serotonin.
increasing the sensitivity of neuron receptors in the brain. Antipsychotic medications may also
be used to control psychotic symptoms (e.g., delusions or hallucinations) in some types of severe monoamine
oxidase
depressive disorders.
inhibitors
There is ongoing debate regarding which class of antidepressants is the most beneficial.
(MAOIs)
The findings from a review of studies indicated that, among depressed patients being treated in Class of
general practice settings, the newer forms of antidepressants (such as the SSRIs) were similar antidepressant
in efficacy to tricyclic antidepressants for the treatment of depression, both of which were more drugs.
effective than placebo (Mulrow et al., 2000). However, newer antidepressants were associated
antipsychotic
with a decreased risk of treatment dropout due to the reduced negative side effects of these medications
medications. Drugs used to
In addition to medication, a number of non-pharmacological medical interventions are treat psychotic
being investigated for the treatment of depressive disorders. Repetitive transcranial magnetic symptoms such
stimulation (rTMS) comprises the application of repeated, high-intensity magnetic pulses to as delusions and
the brain, which is thought to change the way in which neurotransmitters function. Preliminary hallucinations.
evidence has supported its efficacy in the treatment of depression when compared to placebo psychotic
treatment (Loo & Mitchell, 2005) and it has been approved for clinical use in the United States. symptoms
However, further research is required to refine and develop rTMS as a general treatment for According to the
depressive disorders. narrow definition,
Another approach, vagus nerve stimulation via a small implanted electrical device in the chest wall, delusions and
hallucinations;
is thought to increase activity in the hypothalamus and amygdala, which in turn alleviates depressive
according to
symptoms. Bright light therapy may be especially relevant to the treatment of seasonal affective the broader
disorder. This treatment involves regular exposure to light of a particular frequency and intensity that definition,
is thought to affect levels of melatonin, serotonin and noradrenaline (Wehr et al., 2001). In one study, also includes
bright light therapy was compared to antidepressant medication in 102 depressed participants. Those disorganised
who received bright light therapy demonstrated greater reductions in their depression symptoms at the speech and
end of the five-week trial period (Martiny, Lunde, Undén, Dam, & Bech, 2005). Non-pharmacological disorganised
or catatonic
medical therapies of this kind tend to have minimal side effects and thus hold particular promise for
behaviour.
managing depressive disorders in children, adolescents and adults who may be sensitive to the side
effects of antidepressant medications.
Severe depressive disorders are often treated successfully with electroconvulsive therapy (ECT),
which involves the application of an electrical current to the brain. The use of ECT has been controversial
because it was allegedly used as a form of punishment in some facilities in the past. Furthermore,
it can lead to permanent memory loss and difficulties in learning new information. However, the
modern use of ECT typically involves the delivery of an electrical current to only one side of the brain
rie66620_ch05_099-124.indd 113 07/29/17 02:14 PM

repetitive (usually the right side), which minimises the

transcranial likelihood of long-term memory and learning
magnetic problems. Several studies have found that
stimulation ECT is an effective and suitable treatment
(rTMS) especially for severe depression (Carney et al.,
Biological 2003; Pagnin, de Queiroz, Pini, & Cassano,
treatment that
exposes patients
2004). Variations in the placement of the
BLACK DOG INSTITUTE

to repeated, ECT electrodes and the width of the electrical
high-intensity pulse have been shown to enhance the
magnetic pulses efficacy of this treatment while minimising
that are focused adverse cognitive effects (Sackeim et al.,
on particular 2008). Although the treatment is considered
brain structures in to be safe, it is generally contraindicated UNSW Professor Colleen Loo from Black Dog Institute
order to stimulate
among those with a history of myocardial or demonstrates how transcranial magnetic stimulation
them.
cerebrovascular accidents. (TMS) is applied on a fellow staff member.
vagus nerve A potential alternative to ECT is direct
stimulation current stimulation, which is a mild form
Biological of brain stimulation being trialled for depression (Loo et al., 2012). This approach is thought to
treatment in
increase brain activity in areas of the brain that are underactive and to decrease brain activity in those
which the vagus
nerve (the part areas that are overactive. This novel treatment holds promise especially for young people or those
of the autonomic where ECT is contraindicated (e.g., those who have experienced a recent myocardial infarction or
nervous system vascular aneurysm).
that carries
information
from the head, Psychological approaches
neck, thorax
and abdomen Each of the major psychological therapies for depression seeks to address specific vulnerabilities that
to several areas are thought to contribute to the onset and/or maintenance of a depressive episode. Many psychological
of the brain) is interventions are relatively short term (approximately 12–20 sessions) and may be administered in
stimulated by a an individual or group format. They usually incorporate relapse-prevention strategies for long-term
small electronic
improvement. Most psychological therapies also share important components such as developing
device similar
to a cardiac a strong therapeutic relationship between the client and therapist and increasing the client’s coping
pacemaker, which skills, which are thought to play a crucial role in therapy outcome.
is surgically Cognitive behaviour therapy (CBT) is one of the most widely used and well-supported psychological
implanted under interventions for depression (Beck, Rush, Shaw, & Emery, 1979; Ellis & Harper, 1961). CBT utilises
a patient’s skin in a combination of cognitive and behavioural strategies. Treatment often begins with the behavioural
the left chest wall. strategy of pleasant activity scheduling, whereby the therapist and client work together to gradually
bright light increase the number of rewarding activities the client engages in each day as a way of improving his/her
therapy mood. Another behavioural technique involves teaching clients the skills of effective problem solving
Treatment so that they can overcome feelings of hopelessness and helplessness in the face of negative life events.
that involves A key cognitive technique is cognitive restructuring. Here, the client is introduced to the ABC model
exposure to in which activating events trigger dysfunctional beliefs that in turn result in negative consequences
bright light; used (i.e., negative mood and behaviours). The client is encouraged to keep a daily record of the thoughts
particularly during
associated with depressed mood, known as a ‘thought monitoring form’. Once dysfunctional thinking
the winter months
for individuals patterns have been identified, the therapist assists the client to challenge these thoughts and replace
with seasonal them with more realistic ones. The client is asked to examine the evidence supporting or contrary
affective disorder. to the dysfunctional thought and to consider alternative ways of viewing the situation that are more
accurate. These more realistic thoughts in turn give rise to more positive feelings and behaviours. An
example of a cognitive restructuring exercise is shown in Table 5.1.
The efficacy of CBT has been extensively evaluated since the first controlled study was carried
out in the 1970s. Gloaguen, Cottraux, Cucherat, and Blackburn (1998) conducted a meta-analysis
of 48 controlled trials that investigated the efficacy of CBT in the treatment of mild to moderately
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TABLE 5.1 A common exercise in CBT is to ask clients to record the thoughts that trigger negative mood and behaviours
and then to replace these thoughts with more realistic ones that are supported by evidence
CONSEQUENCES:
ACTIVATING FEELINGS, RATIONAL OUTCOME: FEELINGS,
EVENT BELIEFS BEHAVIOURS RESPONSE BEHAVIOURS
Trying to find a I’m so stupid—I Depressed and There’s no way I could Still a bit frustrated by
vacant car space should have angry at myself. have known the car park the situation but no
in a busy car park known I wouldn’t Tempted to turn would be like this—the longer down on myself.
find a spot. around and go supermarket isn’t usually Kept looking until I
home. busy this early in the eventually found a spot.
morning.
severe unipolar depression. Across studies, CBT was found to be significantly more effective than no- seasonal
treatment control groups, antidepressant medication and some other forms of psychological treatment affective disorder
for depression. For non-hospitalised individuals with severe depression, CBT and medication appear Depressive
to have comparable effects (DeRubeis, Gelfand, Tang, & Simons, 1999), although medication disorder
characterised
is recommended as a first-line treatment for severe melancholic depression or for depression with by a two-year
psychotic features (Royal Australian and New Zealand College of Psychiatrists Clinical Practice period in which
Guidelines Team for Depression, 2004). CBT is also well supported as a treatment for depression the individual
in adolescents (Clarke, Rohde, Lewinsohn, Hops, & Seeley, 1999) and may be more effective than experiences
medication in this age group (Melvin et al., 2006). In addition to its beneficial effects in the treatment major depression
of depression, CBT has also been found to be extremely cost-effective (Vos, Corry, Haby, Carter, & during winter
Andrews, 2005). months and then
recovers during
Interpersonal psychotherapy (IPT) focuses on interpersonal problems that may be related to the
the summer.
onset and/or maintenance of a depressive episode (Klerman, Weissman, Rounsaville, & Chevron,
1984). In the most recent form of IPT, the interpersonal problem areas that are believed to have electro-
triggered the depressive episode and are therefore targeted during treatment are: (a) grief over convulsive
an interpersonal loss; (b) interpersonal disputes (e.g., a wife may not feel adequately supported
therapy (ECT)
by her husband); and/or (c) life transitions (e.g., becoming a parent) (Stuart & Robertson, 2012). Treatment for
IPT aims to help clients resolve dysfunctional interpersonal relationships and/or encourages them mood disorders
that involves
to develop new relationships as a means of improving their mood. IPT also considers the role of
the induction of
problems in the depressed person’s social and interpersonal skills and behaviour as maintaining or a brain seizure
exacerbating factors for depression. These problems include excessive reassurance seeking, overtly by passing an
clingy or dependent behaviours, focus on self and negative issues in conversations with others, poor electrical current
conflict-resolution skills and non-verbal behaviour that shows low interpersonal engagement and through the
responsiveness. patient’s brain
IPT has received considerable support in the treatment of depressive disorders and is now regarded while s/he is
anaesthetised.
as one of the standard treatments for these conditions (Feijo de Mello, de Jesus Mari, Bacaltchuk,
Verdeli, & Neugebauer, 2005). Current treatment guidelines state that IPT is as effective as CBT pleasant activity
in the treatment of moderately severe depression (Royal Australian and New Zealand College of scheduling
Psychiatrists Clinical Practice Guidelines Team for Depression, 2004). Behavioural
Based on a purely behavioural model of depression, Jacobson’s behavioural activation approach technique
for the treatment of depression focuses on helping clients re-engage in their lives through strategies entailing planning
(such as getting in touch with an old friend or participating in a team sport) that act to offset patterns a gradual
increase in the
of withdrawal and inactivity that contribute to depressive episodes (Dimidjian et al., 2006). Strategies
level of pleasant
are designed to help individuals approach and access sources of positive reinforcement in their lives activities the client
that can serve as a natural antidepressant. engages in as a
In psychodynamic therapy, the therapist attempts to reconstruct past experiences and interpret way of improving
patterns of emotions and behaviours, in order to enhance the patient’s insight about the repetitive his/her mood.
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meta-analysis conflicts maintaining his/her current problems (Leichsenring & Leibing, 2007). While there are fewer
Statistical high-quality studies testing its efficacy than there are studies of CBT and IPT, there is growing support
technique for for the conclusion that the different psychotherapies for depression, including psychodynamic therapy,
summarising
have comparable benefits (Barth et al., 2013).
results across
several studies.
interpersonal
Relapse prevention
psychotherapy Since major depressive disorder is often a recurring condition, and the occurrence of an episode can
(IPT) increase the risk of future episodes, one of the major challenges for the treatment of depression is how
Short-term to reduce the likelihood of further episodes once the person is well.
psychological As most people in Australia who seek help for major depression receive antidepressant medication,
treatment
originally
it is not surprising that the most common method to prevent relapse is to continue with antidepressant
developed by medication. While the continued use of antidepressants to reduce the risk of a subsequent episode
Gerald Klerman, has been shown to be beneficial, this reduction in risk is only modest and may be less than that
Myrna Weissman obtained through specific psychological relapse-prevention strategies (Bockting et al., 2015). In
and their addition, continuing antidepressant use after remission of a depressive episode may carry harms for
colleagues for some groups of patients such as the elderly (Coupland et al., 2011).
the treatment Other approaches to preventing future depressive episodes involve continuing the active-phase
of depression;
psychological treatment (e.g., CBT and IPT). Relapse-prevention training within CBT focuses on
addresses
the client’s planning how to cope with potential future triggers to depressed mood by continued use of cognitive
interpersonal strategies and problem-solving skills, as well as identifying early signs of a deterioration in functioning
problems (e.g., sleeping problems re-emerging) and developing a plan for how to respond if depressive
as a way of symptoms do re-emerge. A number of studies have shown that simply continuing CBT after remission
improving his/ from major depression is at least comparable to continuing antidepressant use in reducing the risk of
her psychological relapse, and that both are more effective than a pill placebo (Jarrett & Thase, 2010).
symptoms.
Several psychological treatments have been specifically developed for the prevention of depression
psychodynamic in those at risk of relapse following treatment. Wellbeing cognitive therapy (Fava et al., 2004) and
therapies preventive cognitive therapy (Bockting et al., 2005) have shown good outcomes as ways to prevent
Therapies relapse in preliminary studies and may be preferable to continuing antidepressants because of a lower
focused on risk-to-benefit ratio, although larger-scale studies are needed. The components of these adaptations
uncovering
of cognitive therapy include using CBT strategies to target residual symptoms such as anxiety and
and resolving
unconscious irritability, lifestyle modification to promote appropriate lifestyle choices (e.g., identifying new positive
conflicts activities or previously valued ones and assisting individuals in making progressive steps to engage
that drive in these and to monitor and review their attempts) and techniques to stimulate awareness of personal
psychological growth and recovery (e.g., noticing one’s gains and treating setbacks as temporary challenges to be
symptoms. met). Another type of psychological intervention combining elements of meditation and CBT, namely
mindfulness-based cognitive therapy (Segal, Williams, & Teasdale 2002), has shown promising results
in preventing relapse in depressed people successfully treated with CBT or medication (Eisendrath
et al., 2008; Kenny & Williams, 2007; Ma & Teasdale, 2004; Teasdale et al., 2000). While the aim
in cognitive therapy approaches is to help the patient develop a capacity to challenge the content of
their thoughts, mindfulness-based cognitive therapy focuses on cognitive processes with the key aim
of teaching individuals to develop a different relationship with their negative thinking. For example,
instead of repeatedly engaging with and focusing on negative thoughts (which produces a downward
spiral in mood), individuals are taught to simply notice their thoughts (as mental phenomena that come
and go, just as clouds move across the sky). Further research is needed to evaluate the effectiveness of
mindfulness-based cognitive therapy compared to other psychological interventions for depression.
The prevention of depression

As stated, depression is highly prevalent, often beginning in adolescence or early adulthood and becoming
a major and lifelong burden for sufferers, their families and the community. In addition, the occurrence
of a first depressive episode may itself cause enduring psychological and neurological changes that in
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turn increase the risk of further depressive episodes. For these reasons, over the past decade there has
been a growing focus on preventing depression. Most interventions to prevent depression have had a
CBT and/or an interpersonal focus and teach cognitive, interpersonal and coping skills for dealing with
life stress. Outcomes in controlled trials have been mixed, with the largest positive effects for preventing
depression observed when the targeted group has some risk of developing depression, either because
they already have some symptoms of depression, have a family history of depression, or because of
adverse environmental factors (Horowitz & Garber, 2006). In contrast, programs that are directed at
all members of a population (e.g., high-school students), regardless of their level of risk for developing
depression, have shown inconsistent effects (Merry, McDowell, Hetrick, Bir, & Muller, 2004). These
universal programs have also been criticised because they typically require substantial resources to
reach large numbers of the population, which makes it difficult for them to be sustained over time
(O’Kearney, Kanwal, Christensen, & Griffiths, 2009). The use of internet delivery of both treatment
and prevention programs for depression may help overcome some of these issues (Calear, Christensen,
Griffiths, McKinnon, & O’Kearney, 2009; Clarke et al., 2005).
CASE STUDY: THE SYMPTOMS AND TREATMENT OF MAJOR DEPRESSIVE DISORDER

Judy is a 32-year-old lawyer who reported a gradual change in her satisfaction with work and her relationship over the
previous 12–18 months. She initially attributed this to working longer hours and the fact that her husband was increasingly
required to spend more time away from home for work. But she became concerned when she noticed that she was
being uncharacteristically irritable with her work colleagues and that she was frequently avoiding meetings and social
activities because she found them ‘too much of a hassle’. Judy felt particularly low on the weekends when her husband
was working. She started staying at home more and had to push herself to get out. Even when she did manage to go
out, she no longer enjoyed her usual activities and was anxious that she would see someone she knew. She described
feeling anxious when her phone rang and would often ignore it. She also had begun to feel very anxious at night and
was preoccupied with the thought that she was a burden on her husband and that he was going to leave her and that
her work supervisor was unhappy with her performance. She frequently awoke during the night and most nights she was
awake at 4 am, when she would be unable to get back to sleep. She had lost considerable weight because ‘she wasn’t
cooking with her husband away’ and really she didn’t feeling like eating anyway.
Judy had seen her mother go through a period of depression after her parents’ marriage broke up when she was
a teenager. The break-up had affected her too and she had dieted to excess and then started binge eating. But these
eating problems lasted for only a few months and it was just recently that she began to experience problems with eating
again, this time in the form of not feeling like eating rather than deliberately restricting her food intake in order to lose
weight.
Judy was reluctant to seek help for her current problems and was very critical of herself—she believed that the
fact that she was not able to ‘pull herself together’ showed that she was a failure. She started to feel that there was no
solution to how she was feeling. Her husband became concerned enough after a weekend of frequent, distressed phone
calls from Judy when he was at a conference to insist that they both go to the family GP.
After seeing the GP, Judy accepted the need for treatment for her depression and she began to see a clinical
psychologist for psychotherapy and to take antidepressant medication. As her sleep and eating improved and she began
to engage more again with her friends, family and work colleagues, her mood returned to its usual ups and downs. The
psychotherapy she undertook helped her to better understand her feelings of anger and loss during her husband’s
absences and also her avoidance of these feelings because of a strong need not to be dependent. She also took the risk
of talking about these feelings with her husband. Over a period of time, Judy developed more confidence in recognising
and accepting these feelings but also in trying to find solutions to solve what was triggering them.
SUMMARY
Depressive disorders are characterised by periods of depressed mood and/or a loss of interest in activities, together with a range
of other symptoms. These symptoms often include a sense of hopelessness that may result in attempted or completed suicide. The
main depressive disorders included in the DSM-5 are major depressive disorder and persistent depressive disorder (dysthymia). An
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alternative subtyping model for the depressive disorders has been proposed by an Australian research group that identifies three
broad classes of depressive disorders: psychotic, melancholic and non-melancholic depression. This model combines information
about symptoms with aetiological factors and, through its attention to causal factors, aims to guide the selection of the most
effective types of treatment.
Depressive disorders are among the most prevalent psychological problems in Australia and it is estimated that 1 in 10 Australians
is affected by someone close to them suffering from a mood disorder. International data indicate that women are twice as likely
to experience depressive episodes compared to men. These prevalence figures are of concern given the range of serious
psychological and medical problems associated with depression, including suicide, anxiety disorders and a number of health-risk
behaviours such as drug and alcohol abuse.
The aetiology of depressive disorders is thought to be related to biological, social, environmental and psychological factors,
and this multiplicity of factors is reflected in the diverse treatments for depression, which include a range of pharmacological,
physical and psychosocial approaches. One focus of current research is to identify strategies that may be useful in preventing the
development of depression and the recurrence of depressive episodes.
KEY TERMS
amygdala. . . . . . . . . . . . . . . . . . . . . . . . 108 generalised anxiety disorder (GAD). . . 102 oppositional defiant disorder. . . . . . . 105
anhedonia. . . . . . . . . . . . . . . . . . . . . . . 101 hormones. . . . . . . . . . . . . . . . . . . . . . . . 108 pleasant activity scheduling. . . . . . . . 114
anorexia. . . . . . . . . . . . . . . . . . . . . . . . . 101 hypothalamic-pituitary-adrenal pre-frontal cortex. . . . . . . . . . . . . . . . . 108
antidepressants . . . . . . . . . . . . . . . . . . 113 (HPA) axis. . . . . . . . . . . . . . . . . . . . . . . . 108 protective factors. . . . . . . . . . . . . . . . . 112
antipsychotic medications . . . . . . . . . 113 Interpersonal psychotherapy (IPT). . . 115 psychodynamic therapy . . . . . . . . . . . 115
bright light therapy. . . . . . . . . . . . . . . . 113 limbic system . . . . . . . . . . . . . . . . . . . . 108 psychotic symptoms . . . . . . . . . . . . . . 113
cognitive behaviour therapy longitudinal design. . . . . . . . . . . . . . . . 105 receptors. . . . . . . . . . . . . . . . . . . . . . . . 108
(CBT). . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 major depressive disorder. . . . . . . . . 100 repetitive transcranial magnetic
conduct . . . . . . . . . . . . . . . . . . . . . . . . . 105 major depressive episodes . . . . . . . . 102 stimulation (rTMS). . . . . . . . . . . . . . . . . 113
cortisol. . . . . . . . . . . . . . . . . . . . . . . . . . 108 meta-analysis . . . . . . . . . . . . . . . . . . . . 114 seasonal affective disorder . . . . . . . . 113
disruptive mood dysregulation monoamine oxidase inhibitors selective serotonin reuptake
disorder. . . . . . . . . . . . . . . . . . . . . . . . . 102 (MAOIs). . . . . . . . . . . . . . . . . . . . . . . . . . 113 inhibitors (SSRIs). . . . . . . . . . . . . . . . . . 113
dysthymic disorder. . . . . . . . . . . . . . . . 102 monoamines. . . . . . . . . . . . . . . . . . . . . 108 specifier. . . . . . . . . . . . . . . . . . . . . . . . . 101

electroconvulsive therapy negative cognitive triad. . . . . . . . . . . . 109 synapses. . . . . . . . . . . . . . . . . . . . . . . . 108
(ECT). . . . . . . . . . . . . . . . . . . . . . . . . . . . 113 neurons. . . . . . . . . . . . . . . . . . . . . . . . . 108 tricyclic antidepressants (TCAs). . . . . 113
expressed emotion (EE) . . . . . . . . . . . 111 neurotransmitters. . . . . . . . . . . . . . . . . 108 vagus nerve stimulation . . . . . . . . . . . 113
REVIEW QUESTIONS
LO 5.1
5.1 What are the defining features of the main depressive disorders included in the DSM-5 and what aspects of the
DSM-5 categories of depressive disorders have proven to be controversial?
5.2 The DSM-5 criteria provide a number of ways in which clinicians can differentiate between individuals in regard
to the particular features of their depressive disorder. Describe how some of these differences are specified in
the DSM-5.
LO 5.2
5.3 While depressive disorders are among the most common psychological disorders for both females and males,
females are especially vulnerable to these disorders. What factors might account for this gender difference?
5.4 People with depressive disorders are at a much higher risk of suicide and of attempting suicide. Outline some
ways in which the risk of suicide and suicide attempts can be lowered in Australasian communities.
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LO 5.3
5.5 List the factors that feature within a biopsychosocial model of the aetiology of depression.
5.6 Some cognitive and behavioural models of depression suggest it reflects a process of learned helplessness.
What are the proposed factors that give rise to learned helplessness in Seligman’s revised model?
LO 5.4
5.7 Describe the key components of cognitive behaviour therapy for depression. What are some of the advantages
of this approach?
5.8 Depressive disorder is often triggered by interpersonal stresses, losses or conflict. How does interpersonal
psychotherapy address these interpersonal concerns in treating depression?
5.9 Why is it important to focus on reducing the risk of relapse when treating major depressive disorder? What are
the best psychological options for reducing the risk of relapse following treatment for depression?
5.10 Why have preventive approaches been developed for depression and what prevention strategies are best
supported by the research?
REFERENCES
American Psychiatric Association (2000). Diagnostic and statistical contributions of psychological interventions in preventing relapse
manual of mental disorders (4th ed., text revision). Washington, and recurrence. Clinical Psychology Review, 41, 16–26.
DC: Author. Bockting, C., Schene, A., Spinhoven, P., Koeter, M., Wouters, L.,
American Psychiatric Association (2013). Diagnostic and statistical Huyser, J., & Kamphuis, J. (2005). Preventing relapse/recurrence
manual of mental disorders (5th ed.). Arlington: Author. in recurrent depression with cognitive therapy: A randomized
Arean, P. A., Perri, M. G., Nezu, A. N., Schein, R. L., Christopher, F., & controlled trial. Journal of Consulting and Clinical Psychology,
Joseph, T. X. (1993). Comparative effectiveness of social problem- 73, 647–657.
solving therapy and reminiscence therapy as treatments for Brown, G. W., & Harris, T. O. (1978). Social origins of depression: A
depression in older adults. Journal of Consulting and Clinical study of psychiatric disorder in women. London: Tavistock.
Psychology, 61, 1003–1010. Brown, G. W., Harris, T. O., & Hepworth, C. (1994). Life events and
Australian Bureau of Statistics (2007). National survey of mental endogenous depression: A puzzle reexamined. Archives of General
health and wellbeing. Canberra: Author. Psychiatry, 51, 525–534.
Australian Bureau of Statistics (2016). Causes of death, Australia, Calear, A., Christensen, H., Griffiths, K., McKinnon, A., &
2015 (cat. no. 3303.0). Canberra: Author. O’Kearney, R. (2009). The Youth Mood Project: A clustered
Australian Institute of Health and Welfare (1999). National health randomised controlled trial of an online cognitive-behavioural
priority areas report on mental health 1998: A report focusing program with adolescents. Journal of Consulting and Clinical
on depression (cat. no. PHE 11). Canberra: Commonwealth Psychology, 77, 1021–1032.
Department of Health and Aged Care. Retrieved from www.aihw Carney, S., Cowen, P., Geddes, J., Goodwin, G., Rogers, R., Dearness,
.gov.au/publications/index.cfm/title/4482. K., . . . Scott, A. (2003). Efficacy and safety of electroconvulsive
Barth, J., Munder, T., Gerger, H., Nüesch, E., Trelle S., Znoj, therapy in depressive disorders: A systematic review and meta-
H., Jüni, P., Cuijpers, P. (2013). Comparative efficacy of seven analysis. Lancet, 361, 799–808.
psychotherapeutic interventions for patients with depression: A Caspi, A., Hariri, A., Holmes, A., Uher, R., & Moffitt, T. (2010).
network meta-analysis. PLoS Med, 10, e1001454. Genetic sensitivity to the environment: The case of the serotonin
Beck, A. (1976). Cognitive therapy and the emotional disorders. New transporter gene and its implications for studying complex diseases
York: International Universities Press. and traits. American Journal of Psychiatry, 167, 509–527.
Beck, A. (1991). Cognitive therapy: A 30-year retrospective. Caspi, A., Sugden, K., Moffitt, T. E., Taylor, A., Craig, I. W.,
American Psychologist, 46, 368–375. Harrington, H., . . . Poulton, R. (2003). Influence of life stress on
Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive depression: Moderation by a polymorphism in the 5-HTT gene.
therapy of depression. New York: Guilford Press. Science, 301, 386–389.
Beck, A. T, Steer, R. A, Garbin, M. G. J. (1988). Psychometric Clarke, G., Eubanks, D., Reid, E., Kelleher, C., O’Connor, E.,
properties of the Beck Depression Inventory: Twenty-five years of DeBar, L. L., . . . Gullion C. (2005). Overcoming depression on the
evaluation. Clinical Psychology Review, 8, 77–100. internet (ODIN) (2): A randomised trial of a self-help depression skills
Blair-West, G. W., Cantor, C. H., Mellsop, G. W., & Eyeson-Annan, program with reminders. Journal of Medical Internet Research, 7, e16.
M. L. (1999). Lifetime suicide risk in major depression: Sex and Clarke, G. N., Rohde, P., Lewinsohn, P. M., Hops, H., & Seeley, J. R.
age determinants. Journal of Affective Disorders, 55, 171–178. (1999). Cognitive-behavioral treatment of adolescent depression:
Bockting, C. L., Hollon, S. D., Jarrett, R. B., Kuyken, W., & Dobson, Efficacy of acute group treatment and booster sessions. Journal of the
K. (2015). A lifetime approach to major depressive disorders: The American Academy of Child and Adolescent Psychiatry, 38, 272–279.
rie66620_ch05_099-124.indd 119 07/29/17 02:14 PM

Cooper, P. J., & Murray, L. (1998). Postnatal depression. British Frassure-Smith, N., & Lesperance, F. (1995). Depression and
Medical Journal, 316, 1884–1886. 18-month prognosis after myocardial infarction. Circulation, 91,
Coupland, C., Dhiman, P., Morriss, R., Arthur, A., Barton, G., 999–1005.
Hippisley-Cox, J. (2011). Antidepressant use and risk of adverse Ge, X., Conger, R. D., & Elder, G. H. (2001). Pubertal,
outcomes in older people: Population based cohort study. British stressful life events and the emergence of gender differences in
Medical Journal, 343, 4551. adolescent depressive symptoms. Developmental Psychology, 37,
Cuijpers, P., Weitz, E., Lamers, F., Pennix, B., Twisk, J., . . . Hollon, 404–417.
S. D. (2016). Melancholic and atypical depression as predictor Gloaguen, V., Cottraux, J., Cucherat, M., & Blackburn, I. (1998).
and moderator of outcome in cognitive behavior therapy and A meta-analysis of the effects of cognitive therapy in depressed
pharmacotherapy for adult depression. Depression and Anxiety, 34, patients. Journal of Affective Disorders, 49, 59–72.
246–256. doi:10.1002/da.22580 Gould, M. S., & Kramer, R. A. (2001). Youth suicide prevention.
Davidson, R. J., Pizzagalli, D., Nitschke, J. B., & Putnam, K. (2002). Suicide and Life-Threatening Behaviour, 31 (Supp. 1), 6–31.
Depression: Perspectives from affective neuroscience. Annual Hankin, B. L., Anderson, L. Y., Moffit, T. E., Silva, P. A., McGee,
Review of Psychology, 53, 545–574. R., & Angell, K. E. (1998). Development of depression from
Derogatis, L. R., & Savitz, K. L. (2000). The SCL-90-R and the Brief pre-adolescence to young adulthood: Emerging gender differences
Symptom Inventory (BSI) in primary care. In M. E. Maruish (Ed.), in longitudinal studies. Journal of Abnormal Psychology, 107,
Handbook of psychological assessment in primary care settings, 128–104.
Volume 236 (pp 297–334). Mahwah: Lawrence Erlbaum Associates. Harris, M., Silove, D., Kehag, E., Barratt, A., Manicavasagar, V.,
DeRubeis, R. J., Gelfand, L. A., Tang, T. Z., & Simons, A. D. (1999). Pan, J., . . . Pond, D. (1996). Anxiety and depression in general
Medications versus cognitive behavior therapy for severely depressed practice patients: Prevalence and management. Medical Journal of
outpatients: Meta-analysis of four randomised comparisons. Australia, 164, 526–529.
American Journal of Psychiatry, 156, 1007–1013. Harwitz, D., & Ravizza, L. (2000). Suicide and depression.
Dimidjian, S., Hollon, S. D., Dobson, K. S., Schmaling, K. B., Emergency Medicine Clinics of North America, 18, 263–271.
Kohlenberg, R., Addis, M., . . . Jacobson, N. S. (2006). Randomized Hesbacher, T., Rickels, K., Morris, R. J., Newman, H., Rosenfeld, H.
trial of behavioral activation, cognitive therapy, and antidepressant (1980). Psychiatric illness in family practice. Journal of Clinical
medication in the acute treatment of adults with major depression. Psychiatry, 41, 6–10.
Journal of Consulting and Clinical Psychology, 74, 658–670. Hettema, J. M., Neale, M. C., Myers, J. M., Prescott, C. A., &
Eaton, W. (2002). Epidemiologic evidence on the comorbidity of Kendler, K. S. (2006). A population-based twin study of the
depression and diabetes. Journal of Psychosomatic Research, 53, relationship between neuroticism and internalizing disorders.
903–906. American Journal of Psychiatry, 163, 857–864.
Eaton, W., Huibo, S., Nestadt, G., Lee, B., Beienvenu, J., & Zandi, Hickie, I., Hooker, A., Hadzi-Pavlovic, D., Bennett, B. K., Wilson, A. J., &
P. (2008). Population-based study of first onset and chronicity of Lloyd, A. R. (1996). Fatigue in selected primary care settings:
major depressive disorder. Archives of General Psychiatry, 2008, Sociodemographic and psychiatric correlates. Medical Journal of
513–520. Australia, 164, 585–588.
Eisendrath, S. J., Delucchi, K., Bitner, R., Fenimore, P., Smit, M., Hooley, J., & Teasdale, J. D. (1989). Predictors of relapse in unipolar
& McLane, M. (2008). Mindfulness-based cognitive therapy for depressives: Expressed emotion, marital distress and perceived
treatment-resistant depression: A pilot study. Psychotherapy and criticism. Journal of Abnormal Psychology, 98, 229–235.
Psychosomatics, 77, 319–320. Horowitz, J. L., & Garber, J. (2006). The prevention of depressive
Ellis, A., & Harper, R. A. (1961). A guide to rational living. symptoms in children and adolescents: A meta-analytic review.
Englewood Cliffs: Prentice Hall. Journal of Consulting and Clinical Psychology, 74, 401–415.
Emde, R. N., Harmon, R. J., & Good, W. (1986). Depressive feelings Jackson, S. W. (1986). Melancholia and depression: From Hippocratic
in children: A transactional model for research. In M. Rutter, times to modern times. New Haven: Yale University Press.
C. E. Izard, & P. B. Read (Eds.), Depression in young people: Jacobson, N. S., Martell, C. R., & Dimidjian, S. (2001). Behavioural
Developmental and clinical perspectives (pp. 135–162). New activation treatment for depression: Returning to contextual roots.
York: Guilford Press. Clinical Psychology: Science and Practice, 8, 255–270.
Fairweather, A. K., Anstey, K. J., Rodgers, B., & Butterworth, P. Jarrett, R. B., & Thase, M. E. (2010). Comparative efficacy and
(2006). Factors distinguishing suicide attempters from suicide durability of continuation phase cognitive therapy for preventing
ideators in a community sample: Social issues and physical health recurrent depression: Design of a double-blinded, fluoxetine- and
problems. Psychological Medicine, 36, 1235–1246. pill placebo-controlled, randomized trial with 2-year follow-up.
Fava, G. A., Ruini, C., Rafanelli, C., Finos, L., Conti., S., & Grandi, Contemporary Clinical Trials, 31, 355–377.
S. (2004). Six-year outcome of cognitive behavioral therapy Jorm, A. F., & Reavley, N. J. (2012). Changes in psychological
for prevention of recurrent depression. American Journal of distress in Australian adults between 1995 and 2011. Australian
Psychiatry, 161, 1872–1876. and New Zealand Journal of Psychiatry, 46, 352–356.
Feijo de Mello, M., de Jesus Mari, J., Bacaltchuk, J., Verdeli, H., & Kendler, K. S., Pedersen, N. L., Farahmand, B. Y., & Persson, P. G.
Neugebauer, R. (2005). A systematic review of research findings (1996). The treated incidence of psychotic and affective illness
on the efficacy of interpersonal therapy for depressive disorders. in twins compared with population expectation: A study in the
European Archives of Psychiatry and Clinical Neuropsychiatry, Swedish Twin and Psychiatric Registries. Psychological Medicine,
255, 75–82. 26, 1135–1144.
rie66620_ch05_099-124.indd 120 07/29/17 02:14 PM

Kenny, M. A., & Williams, J. M. (2007). Treatment-resistant Handbook of depression (2nd ed.) (pp. 352–375). New York:
depressed patients show a good response to mindfulness-based Guilford Press.
cognitive therapy. Behaviour Research and Therapy, 45, 617–625. Loo, C. K., Alonzo, A., Martin, D., Mitchell, P. B., Galvez, V., &
Kessler, R. C. (2006). The epidemiology of depression among Sachdev, P. (2012). A three-week, randomized, sham-controlled
women. In C. Keys & S. Goodman (Eds.), A handbook for trial of transcranial direct current stimulation in depression. British
the social, behavioural and biomedical sciences: Women and Journal of Psychiatry, 200, 1–8.
depression (pp. 22–37). New York: Cambridge University Press. Loo, C., & Mitchell, P. B. (2005). A review of the efficacy of
Kessler, R. C., Andrews, G., Colpe, L. J., Hiripi, E., Mroczek, D. transcranial magnetic stimulation (TMS) treatment for depression,
K., Normand, S. L., . . . Zaslavsky, A. M. (2002). Short screening and current and future strategies to optimise efficacy. Journal of
scales to monitor population prevalences and trends in non-specific Affective Disorders, 88, 255–267.
psychological distress. Psychological Medicine, 32, 959–956. Ma, S. H., & Teasdale, J. D. (2004). Mindfulness-based cognitive
Kessler, R. C., Bergland, P., Demler, O., Jin, R., Merikangas, K. R., therapy for depression: Replication and exploration of differential
& Walters, E. E. (2005). Lifetime prevalence and age-of-onset relapse prevention effects. Journal of Consulting and Clinical
distributions of DSM-IV disorders in the National Comorbidity Psychology, 72, 31–40.
Survey Replication. Archives of General Psychiatry, 62, 593–602. Martiny, K., Lunde, M., Undén, M., Dam, H., & Bech, P. (2005).
Kessler, R. C., Chiu, W. T., Demler, O., & Walters, E. E. (2005). Adjunctive bright light in non-seasonal major depression:
Prevalence, severity, and comorbidity of 12-month DSM-IV Results from clinician-rated depression scales. Acta Psychiatrica
disorders in the National Comorbidity Survey Replication. Archives Scandinavica, 112, 117–125.
of General Psychiatry, 62, 617–627. Massie, M. J. (2004). Prevalence of depression in patients with
Kessler, R. C., Nelson, C. B., McGonagle, K. A., Liu, J., Swartz, cancer. Journal of National Cancer Institute Monographs, 32,
M., & Blazer, D. G. (1996). Comorbidity of DSM-III-R major 56–71.
depressive disorder in the general population: Results from the US Maughan, B., & Kim-Cohen, J. (2005). Continuities between childhood
National Comorbidity Survey. British Journal of Psychiatry, 168, and adult life. British Journal of Psychiatry, 187, 301–303.
17–30. Melvin, G. A., Tonge, B. J., King, N. J., Heyne, D., Gordon, M. S.,
Kim-Cohen, J., Caspi, A., Moffitt, T., Harrington, H., Milne, B., & & Klimkeit, E. (2006). A comparison of CBT, sertraline, and their
Poulton, R. (2003). Prior juvenile diagnoses in adults with mental combination for adolescent depression. Journal of the American
disorder: Developmental follow-back of a prospective-longitudinal Academy of Child and Adolescent Psychiatry, 45, 1151–1161.
cohort. Archives of General Psychiatry, 60, 709–717. Merry, S., McDowell, H., Hetrick, S., Bir, J., & Muller, N. (2004).
Klerman, G. L., Weissman, M. M., Rounsaville, B., & Chevron, E. Psychological and/or educational interventions for the prevention
(1984). Interpersonal psychotherapy of depression. New York: of depression in children and adolescents. Cochrane Database
Basic Books. Systematic Reviews (1): CD003380.
Kohn, R., Saxena, S., Levav, I., & Saraceno, B. (2004). The treatment Monroe, S. M., & Harkness, K. L. (2005). Life stress, the ‘kindling’
gap in mental health care. Bulletin of World Health Organization, hypothesis, and the recurrence of depression: Considerations from
82, 858–866. a life stress perspective. Psychological Review, 112, 417–445.
Kovacs, M. (1985). The Children’s Depression Inventory (CDI). Mulrow, C. D., Williams, J. W., Chiquette, E., Aguilar, C., Hitchcock-
Psychopharmacology Bulletin, 21, 995–998. Noel, P., Lee, S., . . . Stamm, K. (2000). Efficacy of newer
Kraepelin, E. (1896). Psychiatrie Auflage. Leipzig: Barth. medications for treating depression in primary care patients.
Large, M., & Nielssen, O. (2010). Suicide in Australia: Meta-analysis American Journal of Medicine, 108, 54–64.
of rates and methods of suicide between 1988 and 2007. Medical Musselman, D. L., Evans, D. L., & Nemeroff, C. B. (1998). The
Journal of Australia, 192, 432–437. relationship of depression to cardiovascular disease. Archives of
Lawrence, D., Johnson, S., Hafekost, J., Boterhoven de Haan, K., General Psychiatry, 55, 580–592.
Sawyer, M., Ainley, J., Zubrick, S. R. (2015). The Mental Health Nolen-Hoeksema, S. (2002). Gender differences in depression. In I.
of Children and Adolescents. Report on the second Australian H. Gotlib & C. L. Hammen (Eds.), Handbook of depression (pp.
Child and Adolescent Survey of Mental Health and Wellbeing. 492–509). New York: Guilford Press.
Department of Health, Canberra. Nolen-Hoeksema, S., Girgus, J. S., & Seligman, M. E. (1992).
Leichsenring, F., & Leibing, E. (2007). Psychodynamic Predictors and consequences of childhood depressive symptoms:
psychotherapy: A systematic review of techniques, indications A 5-year longitudinal study. Journal of Abnormal Psychology, 101,
and empirical evidence. Psychology and Psychotherapy: Theory, 405–422.
Research and Practice, 80, 217–228. Oei, T. P., Bullbeck, K., & Campbell, J. M. (2006). Cognitive change
Leonhard, K. (1957). The classification of endogenous psychoses. process during group cognitive behavior therapy for depression.
In E. Robins (Ed.), Aufteilung der endogenen Psychosen (1st ed.). Journal of Affective Disorders, 92, 231–241.
Berlin: Akademic-Verlag. O’Kearney, R., Kanwal, K., Christensen, H., & Griffiths, K. (2009).
Lesch, K., Bengel, D., Helis, A., Sabol., S. Z., Greenberg, B. D., Petri, A controlled trial of a school-based internet program for reducing
S., . . . Murphy, D. L. (1996). Association of anxiety related traits depression in adolescent girls. Depression and Anxiety, 26, 65–72.
with a polymorphism in the serotonin transporter gene regulatory Osman, A., Gutierrez, P. M., Bagge, C. L., Fang, Q., & Emmerich,
region. Science, 274, 1527–1531. A. (2010). Reynolds adolescent depression scale-second edition: A
Lewinson, P. M., & Gotlib, I. H. (1995). Behavioural therapy and reliable and useful instrument. Journal of Clinical Psychology, 66,
treatment of depression. In E. E. Beckham & W. R. Leber (Eds.), 1324–1345.
rie66620_ch05_099-124.indd 121 07/29/17 02:14 PM

Pagnin, D., de Queiroz, V., Pini, S., & Cassano, G. B. (2004). Seligman, M. E. P. (1975). Helplessness: On depression, development
Efficacy of ECT in depression: A meta-analytic review. Journal of and death. San Francisco: Freeman, Cooper.
ECT, 20, 13–20. Sheikh, J. I., & Yesavage, J. A. (1986). Geriatric Depression
Pampallona, S., Bollini, P., Tibalbi, G., Kupelnick, B., & Munizza, Scale (GDS). Recent evidence and development of a shorter
C. (2004). Combined pharmacotherapy and psychological version. In T.L. Brink (Ed.), Clinical gerontology: A guide to
treatment for depression: A systematic review. Archives of General assessment and intervention (pp. 165–173). New York: The
Psychiatry, 61, 714–719. Haworth Press, Inc.
Parker, G. (2000). Classifying depression: Should paradigms lost be Slade, T., Johnson, A., Oakley Browne, M., Andrews, G., &
regained? American Journal of Psychiatry, 157, 1195–1203. Whiteford, H. (2009). 2007 National Survey of Mental Health and
Parker, G., Fink, M., Shorter, E., Taylor, M., Akiskal, H., Berrios, G., Wellbeing: Methods and key findings. Australian and New Zealand
. . . Swartz, C. (2010). Issues for DSM-5: Whither melancholia? Journal of Psychiatry, 43, 594–605.
The case for its classification as a distinct mood disorder. American Southwick, S. M., Vythilingam, M., & Charney, D. S. (2005). The
Journal of Psychiatry, 167, 745–747. psychobiology of depression and resilience to stress: Implications
Parker, G., & Hadzi-Pavlovic, D. (1996). Melancholia: A disorder for prevention and treatment. Annual Review of Clinical
of movement and mood. A phenomenological and neurobiological Psychology, 1, 255–292.
review. Cambridge: Cambridge University Press. Stuart, S., & Robertson, M. (2012). Interpersonal psychotherapy: A
Parker, G., Roy, K., & Eyers, K. (2003). Cognitive behavior therapy clinician’s guide (2nd ed.). London: Hodder Arnold.
for depression? Choose horses for courses. American Journal of Tang, T. Z., DeRubeis, R., Beberman, R., & Pham, T. (2005).
Psychiatry, 160, 825–834. Cognitive changes, critical sessions, and sudden gains in cognitive-
Parker, G., Wilhelm, K., Mitchell, P., Austin, M. P., Roussos, J., & behavioural therapy for depression. Journal of Consulting and
Gladstone, G. (1999). The influence of anxiety as a risk to early Clinical Psychology, 73, 168–172.
onset major depression. Journal of Affective Disorders, 52, 11–17. Teasdale, J. D., Segal, Z. V., Williams, J. M. G., Ridgeway, V.
Petersen, T. (2006). Enhancing the efficacy of antidepressants with A., Soulsby, J. M., & Lau, M. A. (2000). Prevention of relapse/
psychotherapy. Journal of Psychopharmacology, 20, 19–28. recurrence in major depression by mindfulness-based cognitive
Peterson, C., & Seligman, M. E. (1984). Causal explanations as a risk therapy. Journal of Consulting and Clinical Psychology, 68,
factor for depression: Theory and evidence. Psychological Review, 615–623.
91, 347–374. Thase, M. E., Greenhouse, J. B., Frank, E., Reynolds, C. F., Pilkonis,
Quinn, C. R., Dobson-Stone, C., Outhred, T., Harris, A., & Kemp, A. P. A., Hurley, K., . . . Kupfer, D. J. (1997). Treatment of major
H. (2012). The contribution of BDNF and 5-HTT polymorphisms depression with psychotherapy or psychotherapy-pharmacotherapy
and early life stress to the heterogeneity of major depressive combinations. Archives of General Psychiatry, 54, 1009–1015.
disorder: A preliminary study. Australian and New Zealand Journal Vos, T., Corry, J., Haby, M., Carter, R., & Andrews, G. (2005).
of Psychiatry, 46, 55–63. Cost-effectiveness of cognitive-behavioural therapy and drug
Radloff, L. S. (1991). The CES-D Scale: A self-report depression interventions for major depression. Australian and New Zealand
scale for research in the general population. Applied Psychological Journal of Psychiatry, 39, 683–692.
Measurement, 1, 385–401. Wehr, T. A., Duncan, W. C., Sher, L., Aeschbach, D., Schwartz, P.
Royal Australian and New Zealand College of Psychiatrists Clinical J., Turner, E. H., . . . Rosenthal, N. E. (2001). A circadian signal
Practice Guidelines Team for Depression (2004). Australian and of change of season in patients with seasonal affective disorder.
New Zealand clinical practice guidelines for the treatment of Archives of General Psychiatry, 58, 1108–1114.
depression. Australian and New Zealand Journal of Psychiatry, 38, Weissman, M. M., Wickramaratne, P., Nomura, Y., Warner, V.,
389–407. Verdeli, H., Pilowsky, D. J., . . . Bruder G. (2005). Families at
Rutter, M. (1986). The developmental psychopathology of depression: high and low risk for depression: A 3-generation study. Archives of
Issues and perspectives. In M. Rutter, C. E. Izard, & P. B. Read General Psychiatry, 62, 29–36.
(Eds.), Depression in young people: Developmental and clinical While, D., Bickley, H., Roscoe, A., Windfuhr, K., Rahman, S.,
perspectives (pp. 3–30). New York: Guilford Press. Shaw, J., . . . Kapur, N. (2012). Implementation of mental health
Sackeim, H., Prudic, J., Nobler, M., Fitzsimons, L., Lisanby, S., service recommendations in England and Wales and suicide rates,
Payne, N., . . . Devanand, D. (2008). Effects of pulse width and 1997–2006: A cross-sectional and before and after observational
electrode placement on the efficacy and cognitive effects of study. The Lancet, 379, 1005–1012.
electroconvulsive therapy. Brain Stimulation, 1, 71–83. World Health Organization (1992). The ICD-10 classification of
Segal, Z. V., Williams, M., & Teasdale, J. D. (2002). Mindfulness- mental and behavioural disorders: Clinical descriptions and
based cognitive therapy for depression: A new approach to diagnostic categories. Geneva: Author.
preventing relapse. New York: Guilford Press.
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124
GRADUATE SPOTLIGHT
NAME: ELON GERSH
Degree studied: Bachelor of Arts (Honours in Psychology),

Combined Masters/PhD in Clinical Psychology
University: Undergraduate, Monash University;

postgraduate, University of Melbourne
Current position: Clinical Case Manager/Therapist and

Clinical Psychologist
Employer: Orygen, The National Centre of Excellence in

Youth Mental Health and private practice

It was important to have a career that would be interesting and also one where I felt like I was making a
positive difference in people’s lives.

I’ve been working at Orygen, The National Centre of Excellence in Youth Mental Health, which is a public
youth mental health service. I initially worked with young people with psychosis and now work with youth
experiencing depression and suicide risk. I also worked for Berry Street as a family therapist and now work
part-time in private practice. I’ve recently secured a postdoctoral research position in Seattle, so I’m very
excited to be moving to the United States for work.

In the private setting I provide individual psychological therapy to a range of people. In my public role I do
the same and also undertake case management, which entails more practical support. I am also involved in
conducting research.

Having the opportunity to be someone who people turn to during their most difficult periods in life is a real
honour. Watching people develop and grow through our sessions can be a very rewarding experience.

Unfortunately, the path to getting qualified as a psychologist is a long and sometimes challenging one. If
you do think it’s the right path for you, then work hard and don’t be afraid to bring your unique personality
and passions to the field.
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CHAPTER 6
Bipolar disorder
Philip B. Mitchell
Greg Murray
CHAPTER OUTLINE
● Historical and current approaches to the diagnosis of bipolar disorder
● The epidemiology of bipolar disorder
● The aetiology of bipolar disorder
● The treatment of bipolar disorder
● Summary

6.1 Differentiate bipolar I disorder, bipolar II disorder and cyclothymic disorder.
6.2 Understand the epidemiological aspects of bipolar disorder.
6.3 Describe the possible causes of bipolar disorder.
6.4 Describe the medical and psychological interventions used to treat and prevent bipolar disorder.
BIPOLAR DISORDER: AN AUSTRALASIAN FOCUS

Bipolar disorder refers to a group of conditions where people typically experience the two poles of mood disturbance—
that is, episodes of depression and episodes with manic or hypomanic symptoms (such as an excessively agitated or
euphoric mood). ABC News journalist Jane Ryan, who had been living with bipolar disorder for a decade before she
made her condition publicly known, provided a vivid description of her most recent episode of this condition:
First I became severely depressed. The strength went out of my arms and legs and it was hard to
walk . . . Everything became grey and hazy and hard to focus on. My brain slowed down to a snail’s pace . . .
I fixated on death—not because I wanted to kill myself, but because it seemed like the only way I could get
some rest. I knew it couldn’t last forever and that I’d survived it before, but somehow in the depths of that
despair I convinced myself that I would never be better, I would never recover, I would stay like this forever.
Then a switch was flicked . . . I became agitated . . . I stopped listening when people were talking because
my thoughts were racing and I couldn’t concentrate. I talked loud and fast without realising it, I felt so funny
and clever. Then I became irritable. Deeply irritable . . . Soon after, I became psychotic. I lost my grip on reality
and started to imagine the natural environment harboured terrible dangers [such as] a group of cyclists
approaching from behind was a swarm of buzzards swooping to peck me to death. It’s hard to describe the
terror you feel when you know your mind has become totally unhinged and you can’t tell what’s real and
what’s not. During that time I experienced incredible fear and anxiety that people at work might discover
the truth.
It was Jane’s fear of negative attitudes and discrimination from others regarding her bipolar disorder that led her to keep
her condition a secret. Fortunately, the stigma around the condition is decreasing as more people such as Jane are opening
continued
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up about their experience of bipolar disorder. She describes her

decision to speak out about her condition as follows:
Lying on that hospital bed waiting for the anti-psychotics
to kick in, I began to think. Why am I so afraid of people
finding out? One in 100 Australians lives with this illness, so
why the secrecy? I work hard—really hard—to manage it so
that it doesn’t impact on my work or relationships, so what’s
the problem here? I decided it was time to come clean. It
was liberating, but I also felt pretty sick about it. I had held
this secret so close to my chest for so many years that the
prospect of coming out was really frightening. But I wanted
DAL
to do it for all the other people out there who feel the need
In recent years, the stigma around bipolar disorder
to keep their diagnosis a secret, and to let the rest of the
has been decreasing as more people open up
world know you can live a normal life with bipolar.
about their experience of living with the disorder.
Source: Reproduced by permission of Australian Broadcasting Corporation—
Library Sales © ABC
This chapter focuses on bipolar disorder, providing a brief overview regarding historical approaches, a description of
the diagnostic criteria, information regarding epidemiology and a discussion of current biopsychosocial understandings
regarding aetiology and treatment. The chapter also aims to continue the work of Jane Ryan and many others around
the world—taking the stigma out of this diagnosis, and underlining that good quality of life is possible for people with
bipolar disorder.
LO 6.1 Historical and current approaches

to the diagnosis of bipolar disorder
The history of bipolar disorder
Bipolar disorder has a long history (Mitchell, 2017). The earliest descriptions of mania and melancholia
can be traced back to classical Greek times. Throughout most of history, mania and depression were
viewed as separate illnesses. However, a turning point for the contemporary view of bipolar disorder
took place in the nineteenth century in France when Jean-Pierre Falret (1851) referred to the condition
as ‘la folie circulaire’ (the cycle of madness), thus describing a single entity involving the sequential
change between mania and melancholia.
It was also during the late nineteenth century that Emil Kraepelin formally made the landmark
distinction between ‘manic depressive insanity’ and other forms of severe mental illness, particularly
‘dementia praecox’ (an early term for schizophrenia). Kraepelin (1896) observed that patients with
dementia praecox generally experienced ongoing symptoms of cognitive impairment and social
bipolar disorder withdrawal whereas manic-depressive patients tended to experience better functioning between
Mood disorder episodes of mood disturbance. The next landmark occurrence in the classification of mood disorders
marked by manic/ was made by Karl Leonhard (1957), who argued that the term ‘manic depressive insanity’ was too
hypomanic inclusive. He coined the term bipolar disorder to refer to a condition where individuals experience
episodes and both depressive and manic episodes, and distinguished this condition from one involving depressive
depressive
episodes
episodes alone.
(previously The treatments for bipolar disorder have changed dramatically, as illustrated by historical
called manic- records of the lives of some great artists. For example, the composer Robert Schumann was struck
depression). down by manic-depressive psychosis and admitted to an asylum in the mid-1800s. He succumbed
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Chapter 6 Bipolar disorder 127
to madness, experiencing auditory hallucinations that

consisted alternately of glorious music and being
tormented with terrible threats. Later descriptions
suggest that when he was not arguing with the demons
inside his head or shouting at the doctors, he would sit
for days feverishly composing fugues. However, none
of these compositions satisfied him and he burnt them
COURTESY OF THE FAMILY OF PROFESSOR JOHN CADE

all. Schumann had lost everything: his inspiration, his
job, his home, his children and his wife.
These tragic effects on the lives of so many people
made the discovery of lithium carbonate in the treatment lithium
of mania so significant. It was a quiet and unassuming carbonate
Australian psychiatrist, John Cade, who made the Drug classified as
serendipitous yet remarkable discovery of the benefits a mood stabiliser
that is used in
of lithium in an old wooden building on the grounds of
the treatment of
the Repatriation Mental Hospital, Bundoora, Victoria bipolar disorder.
(Mitchell & Hadzi-Pavlovic, 1999). He believed
that urea (a protein breakdown product in urine)
was a causal factor in what he referred to as ‘manic
depressive insanity’. While trying to overcome a John Cade, the Australian psychiatrist who
technical difficulty in experiments on guinea pigs, he discovered the beneficial effects of lithium,
began using lithium urate (being the most soluble of which was to transform the treatment of
the urates) to alter the toxicity of urea. Cade witnessed, individuals with bipolar disorder.
unexpectedly, that the lithium itself was acting as
a protective agent against the toxicity of urea. He
deduced that lithium alone may have a therapeutic effect in mania, and further experiments found this
to be true. Therein lies one of the most profound discoveries in modern medicine. After conducting
the trials on guinea pigs and then on himself and finding no adverse effects, Cade administered the
lithium (in an uncontrolled trial) to 10 patients with mania, six with schizophrenia and three with
depression. In contrast to the minimal benefits experienced by the patients with the other conditions,
the effect on the patients with mania was dramatic. A number of other Australian researchers
extended Cade’s research, leading to some pivotal clinical studies on bipolar disorder in the 1950s
(Cade, 1979). In honouring the significant contribution made by Cade in the treatment of mania,
some researchers have proposed that bipolar I disorder (defined below) be known as ‘Cade’s disease’
(Ghaemi, Ko, & Goodwin, 2002).
The following four decades were marked by a growth in genetic studies that revealed the high
heritability of bipolar disorder. In addition, new classes of mood stabiliser and antidepressant
medications began to emerge. More recently, there has been exponential interest in studies
exploring diagnostic models and the neurobiological and psychological factors underpinning the
condition.
The diagnosis of bipolar disorders

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (American
Psychiatric Association [APA], 2013) includes a chapter entitled ‘Bipolar and Related Disorders’ in
recognition of the fact that the term ‘bipolar disorder’ actually embraces a spectrum of disorders,
primarily consisting of bipolar I disorder, bipolar II disorder and cyclothymic disorder. Depressive
symptoms and major depressive episodes are important features of the bipolar disorders, but what
distinguishes these conditions from depressive disorders is the fact that affected individuals also
experience symptoms of pathologically elevated mood.
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MANIC AND HYPOMANIC EPISODES

manic episode A manic episode as defined by the DSM-5 requires that a person show an elevated, expansive or
State of irritable mood and abnormally and persistently increased goal-directed activity or energy (APA,
persistently 2013). The individual must experience these abnormalities in mood and goal-directed activity for at
elevated or least one week, plus at least three of the following symptoms:
irritable mood
and abnormally ∙ inflated self-esteem or grandiosity—that is, a pathologically exaggerated belief in one’s own
increased goal- abilities, which may be non-delusional (e.g., a businessman believing that he has greater but
directed activity unrealistic insights into investment opportunities) or delusional (e.g., a person believing that s/he is
accompanied
Christ or Mary, or a belief that one can fly)
by symptoms
such as inflated ∙ sleep disturbance—that is, a decreased subjective need for sleep
self-esteem, ∙ pressure of speech, in which the individual is more talkative than usual or experiences a sense of
decreased pressure to keep talking
need for sleep, ∙ flight of ideas, in which the individual’s thoughts race from one idea to another
racing thoughts, ∙ distractibility—that is, difficulty focusing on one thing and ignoring irrelevant stimuli
pressured speech ∙ heightened activity, in which the individual is restless and overly zealous in pursuing goals
and impulsive,
∙ risk taking, whereby the individual becomes excessively involved in potentially dangerous
self-destructive
behaviours.
activities (such as spending large amounts of money, driving dangerously or engaging in risky
sexual practices).
grandiosity
Inflated belief These behaviours, thoughts and emotions are regarded as symptoms of mania only if they are
about one’s out of character for the individual. To meet the diagnosis of a manic episode, the mood disturbance
worth, power, must be severe enough to impair the individual’s functioning, and hospitalisation is often required.
knowledge, Psychotic symptoms (such as delusions and hallucinations) are often seen in severe episodes of mania.
ability or identity; A noteworthy change in the DSM-5 was the fact that increased activity or energy was now required
when extreme,
(along with mood changes) to meet the criteria for a manic or hypomanic episode. This change to
may constitute
a grandiose the DSM diagnosis is consistent with the longstanding idea that bipolar disorder is fundamentally a
delusion. disorder of motivation (Scott et al., 2016).
Hypomania has the same symptom profile as mania, with the key distinction being that in
bipolar I disorder
hypomania the symptoms are not severe enough to markedly interfere with daily functioning, do not
Form of bipolar
disorder necessitate hospitalisation, and do not involve hallucinations or delusions. Also, the disturbance is of
characterised by shorter duration, with the DSM-5 criteria for hypomania specifying a period of persistently elevated,
manic episodes; expansive or irritable mood that is clearly different from the individual’s usual non-depressed mood,
major depressive lasting for at least four days.
episodes often
occur but are not THE BIPOLAR DISORDERS
necessary for the As shown in Table 6.1, the recognised bipolar disorders are characterised in terms of the occurrence
diagnosis. of various combinations of manic, hypomanic and major depressive episodes across time. According
bipolar II to the DSM-5, bipolar I disorder is defined by the presence of one or more manic episodes across the
disorder person’s life. The individual has also usually experienced major depressive episodes but these are
Form of bipolar not necessary for the diagnosis. In contrast, to be diagnosed with bipolar II disorder the individual
disorder
characterised by
hypomanic and
major depressive TABLE 6.1 The DSM-5 (APA, 2013) diagnoses of bipolar I and bipolar II disorders according to the
episodes. constellation of major depressive, manic and hypomanic episodes that have occurred throughout
the person’s life
MOOD EPISODE BIPOLAR I BIPOLAR II
Major depressive episode Common, but not necessary for a diagnosis Yes
Manic episode Yes No
Hypomanic episode Common, but not necessary for a diagnosis Yes
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must at some time have experienced at least one episode of major depression as well as at least one
period of hypomania. Also in contrast to bipolar I disorder, manic episodes are not seen in bipolar
II disorder. Dunner and Fieve (1974) were the first to distinguish between bipolar I and II disorders,
although there is ongoing debate as to whether these represent distinct forms of the condition or
simply differences in severity.
About 90 per cent of individuals with bipolar disorder experience multiple episodes of mood
disturbance during their lifetime (Mitchell, Hadzi-Pavlovic, & Loo, 2011). The period of mood
disturbance is variable for the individual but generally occurs over weeks or months rather than a
matter of days. Over time, the episodes may for some people become more frequent and closer together,
though for others the frequency does not change. The subtype of rapid cycling bipolar disorder is rapid cycling
diagnosed in those individuals who experience four or more bipolar episodes (mania, hypomania or bipolar disorder
depression) within a year. This definition includes those who recover between episodes and those who Diagnosis
switch continually from one polarity to the other. given when
an individual
A less severe but more chronic disorder is referred to as cyclothymic disorder, in which the
has four or
symptoms lack the severity to meet the criteria for bipolar I or II disorders. In the case of cyclothymic more bipolar
disorder, the individual experiences numerous periods of elevated and depressive symptoms, none episodes (mania
of which is severe enough to meet the criteria for a hypomanic, manic or major depressive episode. or depression)
There are increased rates of cyclothymic disorder in the family members of individuals with bipolar I within a
or II disorders. These findings suggest a connection between cyclothymic disorder and bipolar I and II single year.
disorders, although the nature of the relationship is still not fully understood. cyclothymic
The DSM-5 also includes a condition referred to as ‘other specified bipolar disorder’. This is disorder
designed to take into account people who may, for example, have a history of depression and meet all Milder but more
of the criteria for hypomania except the duration. This diagnosis may also be appropriate for someone chronic form of
who has too few symptoms to meet the criteria for bipolar II disorder but who has been symptomatic bipolar disorder.
for more than four days.
In addition to the diagnosis of a bipolar disorder, further information can be denoted with a specifier.
In the DSM-5, one such specifier is ‘with mixed features’. This means, for example, that a person might
have a manic episode with mixed features (if some depressive features are present), or on the other
hand, a major depressive episode with some hypo/manic features. Another specifier is ‘with anxious
distress’, which is added if the person with a bipolar disorder is also experiencing elevated anxiety.
PROBLEMS WITH THE UNDERDIAGNOSIS AND OVERDIAGNOSIS

OF BIPOLAR DISORDER
Bipolar disorder can be prone to both underdiagnosis and overdiagnosis. The most common forms
of underdiagnosis are for patients with bipolar disorder to be misdiagnosed as having schizophrenia
(particularly in men) or unipolar depression (particularly in women). The misdiagnosis of
schizophrenia probably reflects similarities between the psychotic features (especially the delusions
and hallucinations) of acute mania and schizophrenia. A major population study from Scandinavia
convincingly demonstrated that there are shared genetic factors between schizophrenia and bipolar
disorder, as well as distinct genetic contributions (Lichtenstein et al., 2009). The existence of
shared and distinct features between these two major psychotic disorders can make their differential
diagnosis challenging.
In addition to schizophrenia, individuals with bipolar disorder can be misdiagnosed with unipolar
depression. This is more likely to occur when past episodes of hypomania or mania are not actively
explored by the clinician when assessing individuals presenting with depression.
The diagnosis of bipolar disorder may also be missed in patients with anxiety disorders and
substance use disorders, perhaps reflecting a lack of appreciation that these disorders frequently coexist
with bipolar disorder. Sometimes patients with bipolar disorder are misdiagnosed with personality
disorders, particularly borderline and antisocial types.
The overdiagnosis of bipolar disorder can also be a problem (Mitchell, 2012). Specifically, there
is concern that bipolar disorder (especially bipolar II disorder) may be overdiagnosed, particularly
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in those individuals with unipolar depression or borderline personality disorder. Some authorities
recommend diagnosing hypomania even for brief periods of elevated mood (i.e., of only a few hours
in duration), rather than the DSM-5 criterion of hypomania lasting for at least four days. Such a
diagnostic shift risks either labelling normal exuberance and enthusiasm as a pathological mood
disturbance, or misconstruing the mood instability common in those with borderline personality
traits as hypomania. This is not a mere esoteric academic debate. Overdiagnosis could mean
inappropriate and excessive use of mood-stabilising medications, as well as insufficient attention
paid to the psychological aspects of unipolar depression or the personality disorder.
LO 6.2 The epidemiology of bipolar disorder

Prevalence, age of onset and course of the disorder
PREVALENCE
Australian data from the 2007 National Survey of Mental Health and Wellbeing indicate that
0.9 per cent of Australians have major symptoms of bipolar disorder in any 12-month period and
1.3 per cent over the lifetime (Mitchell et al., 2013). The United States National Comorbidity Survey
Replication study estimated a lifetime prevalence of 3.9 per cent for bipolar disorders I and II (Kessler
et al., 2005), although the interview instrument used in this study has been criticised for its tendency
to overdiagnose bipolar disorder.
In addition to the fact that unipolar depression is more common than bipolar disorder, the two
conditions differ in their gender ratio. While unipolar depression is more common in females, women
and men are equally likely to develop bipolar I disorder. Women are more likely to meet the criteria
for bipolar II disorder.
AGE OF ONSET
The median age of onset for bipolar disorder has been found to be 25 years, with approximately
25 per cent of individuals experiencing onset of the disorder by age 17. Relatively few individuals
experience their first episode of hypo/mania after the age of 30 years. There appears to be a
poorer outcome if the onset occurs in childhood or adolescence (National Institute of Mental
Health, 2012).
COURSE OF THE DISORDER

In terms of the course of the illness, it is becoming increasingly apparent that the depressive phase of
bipolar disorder (bipolar depression) is the predominant mood disturbance (Mitchell, Johnston, Corry,
Ball, & Malhi, 2009). A longitudinal study following patients over an average of 13 years reported that
those with bipolar I or II disorder spent much more of their lives depressed than manic or hypomanic
(Judd, Akiskal, & Schettler, 2002; 2003). Those with bipolar I disorder experienced 32 per cent of
their time in depression compared with 9 per cent in mania or hypomania. For those with bipolar II
disorder, the disparity was even greater, with 50 per cent of the time spent depressed compared with
1 per cent spent in hypomania. The median duration is 15 weeks for bipolar depressive episodes, seven
hypomanic weeks for manic episodes and three weeks for hypomanic episodes (Solomon et al., 2010).
episode The recurrent nature of bipolar disorder is a major challenge for sufferers. Despite considerable
Less severe advances in medications, about 40 per cent of bipolar disorder patients relapse within one year,
form of a manic 60 per cent in two years and 73 per cent over five years. Lithium fully protects only 25–50 per cent of
episode that
patients against further episodes and there are often problems with gaining compliance from patients
is an essential
feature of bipolar
in taking their medication. A high correlation has been found between poor medication adherence
II disorder. and low levels of acceptance of the diagnosis of bipolar disorder, highlighting the importance of
psychological treatments that, in part, help people to accept their diagnosis and understand the critical
role of medication.
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Problems associated with bipolar disorder

Not only are there immense psychological, financial and social costs for sufferers and their families,
but the economic costs of bipolar disorder to society are also substantial. Comorbidity of bipolar
disorder with other psychiatric illnesses is common, particularly with anxiety disorders and
substance abuse. Other associated problems include social and economic costs and the increased
risk of suicide.
ANXIETY DISORDERS
The link between anxiety disorders and depressive disorders has long been recognised. However,
epidemiological and clinical studies have also highlighted a significant comorbidity between
anxiety disorders and bipolar disorder (Mitchell et al., 2013; Mitchell et al., 2015; Perugi, Akiskal,
Toni, Simonini, & Gemignani, 2001; Pavlova et al., 2016). In fact, it has become evident that the
comorbidity between anxiety disorders and bipolar disorder may be even higher than the association
between anxiety disorders and depressive disorders (Chen & Dilsaver, 1995).
A meta-analysis by Pavlova et al. (2016) reported that nearly one in two individuals with bipolar
disorder have a lifetime diagnosis of at least one anxiety disorder. Furthermore, a third of people with
bipolar disorder meet diagnostic criteria for an anxiety disorder during periods of euthymia (normal
mood). In an Australian national survey (Mitchell et al., 2013), about 50 per cent of people with bipolar
disorder had a concurrent anxiety disorder (most commonly panic disorder, generalised anxiety
disorder or social phobia). Another study revealed that the lifetime prevalence of panic disorder was
20.8 per cent in patients with bipolar disorder, compared with 10 per cent in those with a depressive
disorder and 0.8 per cent in the general population (Chen & Dilsaver, 1995). The same study found
that the lifetime prevalence rate of obsessive-compulsive disorder among bipolar patients was
21 per cent as compared to 12.2 per cent in those with a depressive disorder and 2.5 per cent
in the general population. In the National Comorbidity Survey, 47.2 per cent of patients with
bipolar I disorder were found to have comorbid social phobia compared to 13.3 per cent of the
general population (Kessler, Rubinow, Holmes, Abelson, & Zhao, 1997). The same survey revealed
a lifetime diagnosis of posttraumatic stress disorder in 38.8 per cent of patients with bipolar
I disorder.
This high level of comorbidity between bipolar and anxiety disorders raises the question of their
temporal sequence. Perugi and colleagues (2001) studied the temporal relationship between bipolar
disorder and a range of comorbid disorders, specifically anxiety disorders (i.e., panic disorder and
social anxiety disorder) and obsessive-compulsive disorder. The study included 63 patients with
panic disorder, social phobia (social anxiety disorder) or obsessive-compulsive disorder who also had
comorbid bipolar I or II disorder. As seen in Figure 6.1, the results revealed that the comorbid disorder
preceded (hypo)mania in 33.3 per cent of individuals with panic disorder, 94.7 per cent of individuals
with social phobia and 52.2 per cent of individuals with obsessive-compulsive disorder. The comorbid
disorder had its onset during the (hypo)manic episode in 28.6 per cent of those with panic disorder,
yet in none of those with social phobia and only one of the participants with obsessive-compulsive
disorder. Finally, the comorbid disorder followed the onset of (hypo)mania in 38.1 per cent of those
with panic disorder, 5.3 per cent of those with social phobia and 43.5 per cent of those with obsessive-
compulsive disorder. In other words, anxiety symptoms preceded, occurred during and followed
(hypo)manic symptoms at different rates depending on the type of comorbid disorder. For instance, in
the case of social phobia, the anxiety symptoms almost always preceded (hypo)mania. These findings
have several implications. First, they suggest that anxiety may at times be an initial sign of an evolving
bipolar disorder. Second, anxiety disorders are often treated with antidepressants, which, given these
findings, suggests that antidepressants may at times be triggering manic or hypomanic symptoms.
Finally, there is a clear pattern of social phobia preceding (hypo)mania, which warrants further
study since it may suggest a causal role of social fears (e.g., thoughts about the self as inadequate) in
triggering mania or hypomania.
rie66620_ch06_125-146.indd 131 07/29/17 01:03 PM

100
80
Percentage of patients
60 Panic disorder
OCD
40
Social phobia
20
0
Before During After
FIGURE 6.1 The percentage of patients who developed panic disorder, obsessive-compulsive disorder
(OCD) or social phobia before, during or after their first manic or hypomanic episode
Source: From Perugi, G., Akiskal, H. S., Toni, C., Simonini, E., & Gemignani, A. (2001). The temporal relationship between anxiety disorders
and (hypo)mania: A retrospective examination of 63 panic, social phobic and obsessive-compulsive patients with comorbid bipolar disorder.
Journal of Affective Disorders, 67, 199–206, Elsevier.
SUBSTANCE MISUSE
Substance misuse has been reported in 39 per cent of people with bipolar disorder. In fact, bipolar
disorder has frequently been found to be the psychological disorder most strongly associated with
substance misuse (Todd & Sellman, 2004). There are various possible interactions between substance
amphetamines misuse and bipolar disorder. Drug use (particularly marijuana, amphetamines and alcohol) is thought
Stimulant drugs to be commonly used to self-medicate against emotional disturbances. Unfortunately, many of
that can produce these drugs, particularly marijuana, inadvertently lead to mood destabilisation. Furthermore, manic
symptoms of
symptoms such as elevated mood, increased activity and decreased need for sleep may be part of
euphoria, self-
confidence,
substance intoxication and withdrawal. It is therefore considered important to delay diagnosis until
alertness, drugs or alcohol are no longer affecting the patient’s presentation. Since these coexisting disorders
agitation, may interact and influence the course of each other, appropriate assessment and effective treatment of
paranoia, substance misuse is an essential part of the treatment of bipolar disorder (Goodwin & Sachs, 2004).
perceptual
illusions and SOCIAL AND ECONOMIC COSTS
depression. Given the severely disabling symptoms of manic and depressive episodes, together with the high rates
of comorbidity with other psychological disorders, it is not surprising that the social and economic
costs to individuals with bipolar disorder and society are substantial. Following manic episodes,
almost one-third of patients cannot work for six months and only one-fifth return to work at their
former skill level. In an Australian survey, people with bipolar disorder were found to be almost five
times more likely than the general population to have disrupted relationships, and more than twice as
likely as those with depression to have such difficulties (Mitchell et al., 2013).
SUICIDE
The suicide rate in people with bipolar disorder is about 15 times that of the general population,
with 80 per cent of these suicides occurring during the depressive phase of the disorder (Harris &
Barraclough, 1997). At least 25 per cent of patients will attempt suicide and 10–20 per cent will
complete suicide. It would appear that rates of suicide are higher among individuals with bipolar II
disorder compared to those with bipolar I disorder, most probably due to the more frequent episodes
of depression in the former compared to the latter.
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LIVING WITH BIPOLAR DISORDER

Meg Smith, an Australian Associate Professor in Psychology and a highly respected writer and
community researcher, gives a poignant personal account of life with bipolar disorder, with its broad
range of associated problems and perhaps even some gains:
There is a current debate going on in my support group about whether one has bipolar disorder
or is bipolar. My first inclination was to say that I have bipolar disorder—in the sense that I
experience episodes of manic illness and depression and that this constitutes the syndrome of
bipolar disorder. But somehow this does not really encompass the effect that bipolar disorder
has had on my life. There was the long period of undiagnosed and untreated episodes of mood
disorder. My mother described me as a miserable child—and so I was with a number of early
episodes of depression that turned me from a happy and interesting child to a whiny, miserable
one prone to constipation, headaches, social withdrawal and attacks of anxiety where I would
cry hopelessly. By the time I reached adolescence, I conceptualised myself as a shy, withdrawn
and uninteresting person. Then the hypomanic episodes started. I discovered an extroverted,
somewhat grandiose, confident, outgoing and attractive person. I remember thinking that life
would be all right if it weren’t for the ups and downs—with no idea about why I should think such
a thing.
I am still searching for a conceptualisation of what I have and who I am. Bipolar disorder
has affected my life profoundly. It has ended relationships, changed my career and carried me to
places I would probably never have gone without the mood swings and the changes in perception
that the moods bring to the world. I can’t say that I regret having experienced a mood disorder
but I do regret not knowing more about it a long time ago. Maybe I would have ended up as an
English teacher in some country high school without it. It has been said that people with bipolar
disorder have interesting lives and I have certainly had that. I don’t know if I would have been
happier not having bipolar. I do know that I value my stability now.
Personal communication, 7 November 2006
Bipolar disorder and creativity

While the focus thus far has been on the problems associated with bipolar disorder, researchers
have proposed that there may be at least one positive aspect of bipolar disorder, namely its
potential association with creativity. Since the late twentieth century, researchers have been
intrigued by an apparent relationship between creativity and psychopathology, particularly
bipolar disorder, with theorists noting the similarities in the cognitive and affective processes of
those with the disorder and creativity. For example, according to Winnicott (1971), creativity is
an expression of vitality, while Murray and Johnson (2010) have described the main features of
the creative process as fluency of associations, positive affect, divergent thinking and cognitive
over-inclusion—features evident in those with bipolar disorder. There is certainly much anecdotal
evidence of a connection between bipolar disorder and creativity as evident in the lives of eminent
people such as Stephen Fry, who, in the BBC2 documentary, The Secret Life of Manic Depression
(Gallagher, 2013), stated that, ‘I rely on it to give my life a sense of adventure and I think that motivational
most of the good about me has developed as a result of my mood swings. It has tormented me all interviewing
my life with the deepest of depressions, but also given me the energy and creativity which has A counselling
perhaps made my career.’ strategy, originally
While research findings are inconsistent in terms of a connection between bipolar disorder used in the
and creativity, there is no doubt that many people with bipolar disorder identify as creative. The addictions area,
subjective valuing of creativity has implications for the psychological treatment of bipolar disorder. that encourages
clients to think
For example, in some cases it is important to address patient concerns that bipolar medications may
about both the
blunt creativity (Murray & Johnson, 2010). This motivational interviewing discussion can include positives and
emerging evidence about the pros and cons of elevated mood states for the quality and quantity of the negatives
creative outputs (above). The creative lifestyle (characterised by unstable sleep/wake cycles) and the of a particular
Rieger, Elizabeth. Abnormal Psychology : Leading Researcher Perspectives, McGraw-Hill Education (Australia) Pty Limited, 2017. ProQuest Ebook Central, behaviour.
rie66620_ch06_125-146.indd 133 07/29/17 01:03 PM

known links between creativity and high achievement

striving may also be important therapeutic topics
for some people with bipolar disorder: both of these
factors are believed to play important causal roles in
bipolar disorder.
Bipolar disorder and creativity may be linked by
features that are strongly related to both. The shared
vulnerability model (Carson, 2011), for example,
proposes that vulnerability to pathology and creativity
share factors such as cognitive disinhibition (so that
more stimuli enter into awareness), an attentional bias
towards novel stimuli and neural hyperconnectivity
(which is proposed to increase associations between
SHUTTERSTOCK.COM/FEATUREFLASH
different stimuli). Carson suggests that these factors

result in an increased range of stimuli available in
conscious awareness that can then be combined in
novel ways.
Yet there are also important qualifications on the
postulated association between bipolar disorder and
creativity. For instance, Weisberg (1994) analysed the
musical compositions of Robert Schumann (known to
Actor and comedian Stephen Fry has spoken have had bipolar disorder) and found that periods of
publicly about his life with bipolar disorder, positive mood were associated with an increase in the
including his belief that the disorder has quantity but not the quality of his compositions. This
contributed to his creative achievements. distinction between no objective change in the quality of
creative output versus the subjective perception of being
more creative when ‘high’ has important clinical implications. It is useful for people with bipolar
disorder to understand that elevated mood states are not necessary for high-quality creativity, and that
moderation of extreme moods (e.g., via medication) can actually benefit their creative expression.
LO 6.3 The aetiology of bipolar disorder

Traditionally, theories of bipolar disorder have focused almost exclusively on biological factors, with
the recognition of psychosocial factors a more recent phenomenon. Thus current understandings of
bipolar disorder are consistent with the biopsychosocial approach.
BIOLOGICAL FACTORS
Genetic factors are among the biological vulnerabilities to bipolar disorder. The lifetime risk of
bipolar disorder in the family members of bipolar disorder patients is about 10 per cent compared
with a rate of about 1.0 to 1.5 per cent in the general population. The strong genetic component of
bipolar disorder has been supported by both a large study of twins, which estimated a heritability
rate of about 85 per cent, and a Danish population study sample of several million participants,
which reported a 13-fold increased risk of bipolar disorder in the first-degree relatives of affected
individuals (Mortensen, Pedersen, & Melbye, 2003). Bipolar disorder therefore runs in families. The
specific genes that increase the risk of developing bipolar disorder are gradually being identified, with
genome-wide association studies (GWAS) of large international samples now confirming involvement
of a number of genes (Psychiatric GWAS Consortium Bipolar Disorder Working Group, 2011).
STRESSFUL LIFE EVENTS

As described in the chapter on depressive disorders, the role of stressful life events in precipitating
depression has been well researched. A meta-analysis concluded that, while more research is required,
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life events are also implicated in the onset and course of bipolar disorder (Lex, Bazner, & Meyer,
2016). For example, individuals with bipolar disorder who experience high levels of stress are four
and a half times more likely to have a mood relapse than individuals with low levels of life stress
(Ellicott, Hammen, Gitlin, Brown, & Jamison, 1983).
The diathesis-stress model holds that psychological disorders result from interactions between diathesis-stress
underlying vulnerabilities and stressful life events. This model is well established in relation to model
schizophrenia, and has subsequently been applied to bipolar disorder (Jones, 2004). As shown in Originally
Figure 6.2, the model emphasises the role of stressful life events that result in disrupted routines and developed in
the context of
sleep deprivation in triggering episodes of mania (Frank, Swartz, & Kupfer, 2000). Examples of such
schizophrenia,
events include time zone travel, childrearing, jobs involving shift work and highly stimulating social the view that
events (especially those involving alcohol or other drugs). These life events interact with an underlying abnormality is
biological vulnerability that, in the case of bipolar disorder, is thought to involve a circadian system caused by the
that is unusually sensitive to disruption. This disruption of circadian function results in the early signs combination of
of mood disturbance (such as restlessness, sleeplessness and feeling wired). The individual may use a vulnerability or
poor coping strategies (such as substance abuse) to deal with these symptoms, which in turn can result predisposition
in a full-blown manic or depressive episode. These episodes in turn constitute a considerable source of (the diathesis)
and life events
stress (e.g., straining the individual’s relationships), thereby exacerbating the cycle. (the stressor).
Stressful life circadian system

Biological
events causing A part of the
vulnerability
disrupted
(e.g., circadian nervous system
routines or sleep
rhythm instability) adapted to
deprivation
coordinate the
organism’s
interaction
with the light-
Manic, Early symptoms dark cycle, and
hypomanic or of mood
depressive
ensure optimal
disturbance
episode timing of internal
physiological
processes.
Poor coping
strategies
FIGURE 6.2 The diathesis-stress model of bipolar disorder

Source: Adapted from Jones, S. (2004). Psychotherapy of bipolar disorder:
A review. Journal of Affective Disorders, 80, 101–114.
One type of life event that may have particular relevance in terms of disrupting routines and hence
triggering manic or hypomanic episodes is the excessive pursuit of goals. The goal dysregulation goal
model suggests that mania is the result of excessive goal engagement (Johnson et al., 2000). Even when dysregulation
not in an episode, individuals with a history of bipolar I disorder have been found to place a higher model
emphasis on rewards and to be excessively engaged in the pursuit of achieving goals compared to Theory that manic
those without the disorder. The model proposes that abnormalities in the reward system, particularly episodes may
be triggered by
excessive sensitivity to reward, may heighten the experience of positive states following success and
dysregulated goal
therefore increase the probability of mania. Supporting the goal dysregulation model, it has been pursuit, which
found that increases in goal-setting and time spent pursuing goals accelerate the development of entails the person
hypomanic or manic symptoms such as inflated self-esteem, decreased need for sleep, flight of ideas being excessively
and increased talkativeness. Johnson et al. (2000) examined whether goal-directed behaviour would involved in the
predict increases in mania among individuals with bipolar disorder. They found that specifically pursuit of goals.
goal-directed life events, and not positive life events in general, were associated with elevations
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in subsequent manic symptoms. In contrast, goal attainment was not associated with changes in
depression.
PSYCHOLOGICAL FACTORS
Similar to the research on depressive disorders, particular patterns of cognition (relating to the content
of thoughts, beliefs and attitudes) are believed to be a causal factor for bipolar disorder. Individuals
with bipolar disorder endorse a greater number of dysfunctional attitudes compared to healthy
controls, even when euthymic (i.e., normal in mood) (Alloy, Reilly-Harrington, Fresco, Whitehouse, &
Zechmeister, 1999). For instance, in contrast to controls, it has been reported that those with bipolar
disorder have greater negative beliefs regarding their worth, leading to lower self-esteem.
It is proposed that individuals prone to mania may be characterised by particular styles of thinking.
Specifically, when negative events activate low self-esteem, the person may respond defensively with
grandiose ideas, which inhibit negative thoughts about the self (Winters & Neale, 1985). Thomas and
Bentall (2002) have similarly proposed that hypomania and mania represent a deliberate, defensive
attempt to avoid the negative cognitions and emotions associated with depression and low self-esteem.
Consistent with their prediction, they found that a combination of rumination (i.e., thinking the same
thought over and over again), distraction and risk-taking coping styles predicted higher scores on a
measure of hypomania in a sample of university students.
As a final comment on cognitive approaches to mania, it seems that some aspects of the thinking
styles evident in individuals with bipolar disorder are a consequence of the disorder rather than a
causal factor. For example, many individuals with bipolar disorder experience a change in their self-
concept after episodes of hypomania, mania or depression (Lam, Jones, Haywood, & Bright, 1999).
In particular, negative self-evaluation accompanied by feelings of guilt, shame and anger are common
responses as a result of experiencing an episode of illness. This is particularly relevant in mania as
individuals often behave in an uncharacteristically disinhibited manner (such as inappropriate social
and sexual interactions and overspending), which has potentially adverse, humiliating and debilitating
consequences.
temperament In addition to cognitive factors, temperament may be another psychological factor relevant to the
Personality traits development of bipolar disorder. Temperament refers to enduring personality traits and characteristics
believed to (such as introversion and interpersonal sensitivity). It has been found to be a significant factor in
be genetically
the tendency to develop manic and/or depressive episodes and may affect the course and outcome
based.
of bipolar disorder once it has developed. Several studies have found significant temperamental
differences between those with bipolar I disorder, bipolar II disorder, depressive disorders and controls
(Akiskal et al., 2006). For example, traits such as perfectionism and sociotropy (a high need for social
acceptance) have been found to be more prevalent in individuals with bipolar disorder than those
with a depressive disorder. In addition, studies have found that symptom severity in bipolar disorder
is significantly associated with sociotropy, negative interpersonal events (e.g., ongoing conflicts with
others) and the interaction of the two (Hammen, Ellicott, & Gitlin, 1992; Reilly-Harrington, Alloy,
Fresco, & Whitehouse, 1999). In other words, bipolar symptoms may be triggered if an individual
with an extreme need for social approval perceives that s/he has been rejected.
Temperamental tendencies can adversely affect a person’s ability to accept and adapt to the illness,
which can lead to poor compliance with treatment and a high risk of relapse. It is therefore extremely
important to examine and address temperament factors when working with patients who have a
diagnosis of bipolar disorder (Ball, Mitchell, Malhi, Skillecorn, & Smith, 2003).
MEASURES OF STATES AND TRAITS RELATED TO BIPOLAR DISORDER

Self-report measures commonly used in Australia to assess the features of bipolar disorder include:
1. Depression Anxiety Stress Scale (DASS-21) (Lovibond & Lovibond, 1995). The DASS-21 is a
42-item measure with three subscales: depression (e.g., ‘I couldn’t seem to experience any positive
feeling at all’), anxiety (e.g., ‘I had a feeling of shakiness’) and stress (e.g., ‘I found myself getting
upset by quite trivial things’).
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2. Dysfunctional Attitudes Scale 24 (DAS-24) (Weissman, 1979; Power et al., 1994). The DAS-24
assesses attitudes towards achievement (e.g., ‘If I don’t set the highest standards for myself, I am
likely to end up a second-rate person’), dependency (e.g., ‘I am nothing if a person I love doesn’t
love me’) and self-control (e.g., ‘A person should do well at everything s/he undertakes’).
3. BIS/BAS Scales (Carver & White, 1994). These combined scales assess behavioural inhibition
and behavioural activation and comprise four subscales: behavioural inhibition (e.g. ‘I worry
about making mistakes’), drive (e.g., ‘When I want something, I usually go all out to get it’), fun
seeking (e.g., ‘I crave excitement and new sensations’) and reward responsiveness (e.g., ‘When I
get something I want, I feel excited and energised’).
4. Response Style Questionnaire (RSQ) (Thomas & Bentall, 2002). This is a 48-item measure that
inquires about people’s responses to feelings of depression: rumination (e.g., ‘isolate yourself and
think about the reasons you feel sad’), adaptive coping (e.g., ‘do something that has made you feel
better in the past’) and risk taking (e.g., ‘take recreational drugs or drink alcohol’).
5. Internal State Scale (ISS) (Bauer et al., 1991). The ISS is a 16-item measure assessing current mood
state in bipolar disorder. It has four subscales: activation (e.g., ‘Today I feel impulsive’), wellbeing
(e.g., ‘Today I actually feel great inside’), depression (e.g., ‘Today I feel depressed’) and perceived
conflict (e.g., ‘Today I feel like people are out to get me’).
LO 6.4 The treatment of bipolar disorder

Pharmacological approaches
Drug treatments for bipolar disorder vary according to the acute or maintenance phases of the condition.
Acute drug treatments target the existing episode of mood disturbance while maintenance treatments
focus on minimising the chances of relapse. The task of mood stabilisers is to effectively treat or mood stabilisers
prevent bipolar episodes (manic, depressive or mixed episodes) without triggering a mood shift to the Group of drugs
opposite pole. Today, there are six mood stabilisers commonly administered: lithium, carbamazepine, including
lithium and
valproate, olanzapine, quetiapine and lamotrigine. A number of other ‘atypical antipsychotics’ are
anticonvulsants
also effective in treating (and, in some cases, preventing relapse of) mania: these include aripiprazole,
that are
risperidone and ziprasidone. There have been some excellent reviews and meta-analyses of the current used to treat
evidence for the role of medications in the treatment of bipolar disorder (Cipriani et al., 2011; Geddes psychological
& Miklowitz, 2013; Malhi et al., 2015). disorders
characterised by
unstable mood
Psychological approaches (such as bipolar
disorder).
There is now convincing evidence that psychological therapies, used in conjunction with drug
treatments, contribute to a significant improvement in the symptoms and quality of life for people with
bipolar disorder as well as being cost effective (e.g., reducing the costs of further use of health services
due to relapse). Psychological interventions aim to reduce symptoms, prevent relapse and recurrence,
restore healthy psychological functioning and provide support to the patient and family. The specific psychoeducation
evidence-based psychological therapies for bipolar disorder are described in this section. There is no Treatment
evidence for the superiority of one therapy over another, and each of the therapies shares the diathesis- technique that
stress framework mentioned previously. Additional shared features across the various psychological entails providing
the client with
therapies include: establishing medication adherence, promoting regular cycles of activity and sleep,
information
improving coping strategies and emotional regulation techniques, addressing the psychosocial effects regarding the
of the illness and identifying early signs of relapse. nature, causes,
effects and
PSYCHOEDUCATION treatment of his/
Psychoeducation is a component of all psychological interventions for bipolar disorder (and also a her psychological
tested stand-alone therapy) and entails providing the patient and family with information regarding the problem.
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illness and its treatment. The main strategies include providing education regarding the importance
of identifying early signs of relapse so that preventative action can be taken, medication adherence,
minimising risk factors (e.g., substance abuse) and maximising protective factors (e.g., maintaining
a regular sleep/wake cycle). One study found that the addition of 7–12 sessions of psychoeducation
to medication resulted in a 30 per cent reduction in the rate of manic relapse compared to medication
alone (Perry, Tarrier, Morriss, McCarthy, & Limb, 1999).
Mood monitoring is an important intervention in the early stages of therapy. Encouraging clients
to keep structured mood diaries helps in identifying the triggers to mood shifts and the associated
changes in thoughts and feelings. Patterns may become apparent in the role of particular stressors (or
‘triggers’) such as a series of late nights, pressure at work or interpersonal difficulties. Early-warning
signs may also be identified through monitoring (e.g., irritability or anxiety preceding hypomania).
The Black Dog Institute has a number of Mood Diaries that individuals can access, and a variety of
mood-monitoring apps are freely available.
COGNITIVE BEHAVIOUR THERAPY

Cognitive behaviour therapy (CBT) is a well-established psychological treatment for many disorders,
including anxiety disorders and depressive disorders, and has been adapted for the needs of patients
with bipolar disorder. The aims of CBT are to alleviate acute symptoms and prevent relapse and
recurrence through identifying and challenging unhelpful thoughts and assumptions; improving
adherence to medication; and implementing adaptive coping and problem-solving strategies. A key
technique of CBT for bipolar disorder is cognitive restructuring, which involves identifying and
challenging hyper-positive cognitions (e.g., ‘No one else can see it, but I will be highly successful if
I race ahead with this business plan’) as well as negative underlying beliefs (e.g., ‘I need to be highly
successful to prove that I am worthwhile’). Cognitive adaptation to the experience of mental illness
refers to the meaning a patient assigns to the illness, including his/her beliefs regarding its causes and
how best to manage it. These are key beliefs that are addressed in CBT as they play an important role
in determining a patient’s acceptance of appropriate treatment and hence the ultimate level of social
and psychological functioning that s/he is able to attain.
self-efficacy The advantages of CBT are its brevity, its coherent theoretical framework, and the fostering of self-
Person’s belief efficacy as patients learn the skills of managing their symptoms. The first randomised controlled trial
that s/he has the of CBT for bipolar disorder was conducted by Cochrane in 1984. Since then, a number of studies have
ability to succeed
supported the efficacy of CBT for bipolar disorder (Ball, Mitchell, Corry, Skillecorn, & Malhi, 2006;
in a specific
situation.
Lam et al., 2003; Lam, Hayward, Watkins, Wright, & Sham, 2005; Patelis-Siotis et al., 2001; Scott,
Garland, & Moorhead, 2001; Zaretsky, Segal, & Gemar, 1999).
Lam et al. (2003; 2005) conducted one of the largest randomised controlled trials of patients with
bipolar disorder using a relapse-prevention approach. Patients with bipolar I disorder were randomly
assigned to the control group (minimal psychiatric care that primarily consisted of medication) or the CBT
group (an average of 14 CBT sessions combined with minimal psychiatric care) for a six-month period.
The CBT sessions focused on the monitoring of symptoms, modification of behaviours (e.g., ensuring
regular sleeping times), and addressing extreme goal-pursuit attitudes and behaviours. Both groups were
followed up for a total of two years after treatment ended. As shown in Figure 6.3, patients who received
CBT experienced significantly fewer manic/hypomanic and depressive episodes compared to those in
the control group. Thus the addition of CBT to pharmacological treatment was found to be beneficial in
reducing relapse rates compared to medication alone. However, the beneficial effect of CBT was greatest
during the six months of treatment and in the six months following treatment, with the effect diminishing
over the next 18 months. Given that the results were strongest in the first six months following treatment,
it was concluded that extended CBT may be useful in maintaining treatment gains over time.
INTERPERSONAL AND SOCIAL RHYTHM THERAPY

Interpersonal and social rhythm therapy (IPSRT) was developed by Frank, Swartz, and Kupfer
(2000) based on their earlier work on interpersonal psychotherapy for depression. IPSRT is targeted
towards reducing disruptions in daily routines and sleep/wake cycles that trigger bipolar episodes
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0.7
0.6
Proportion of subjects
experiencing relapse
0.5
Patients assigned to
0.4 control condition (N = 52)
0.3 Patients assigned to
cognitive therapy (N = 51)
0.2
0.1
0.0
Any bipolar Manic Depressive
episode episode episode
FIGURE 6.3 Relapse rates for bipolar disorder patients assigned to treatment with cognitive therapy or a
control condition (over an 18–month period)
Source: From 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 Journal of Psychiatry, 162, 324–329, American Psychiatric Association. Reprinted with
permission from the American Journal of Psychiatry (Copyright © 2005). American Psychiatric Association. All Rights Reserved.
(via the circadian mechanism mentioned previously). Patients are taught to regulate their social
rhythms (e.g., establish good routines for eating, socialising and particularly sleeping), especially
during times of stress, and to address interpersonal difficulties that may be triggering or maintaining
emotional instability. In the Pittsburgh Maintenance Therapies study (Frank et al., 2005), patients with
bipolar disorder were randomly assigned to receive one of two psychosocial treatments in addition
to medication: IPSRT or standard management. IPSRT delivered in the acute phase was found to be
more effective than standard management in preventing relapses.
FAMILY INTERVENTIONS
Family interventions have been used effectively
for patients with bipolar disorder since the 1970s.
Miklowitz and Goldstein (1990) designed a family-
focused therapy program for patients with bipolar

disorder who had recently experienced an episode
of mood disturbance. This approach aims to reduce
relapse through improving the family’s knowledge
about bipolar disorder, communication and problem-
solving skills. In one study, patients randomised to
family-focused therapy were less likely to relapse
(during and after treatment) than those receiving a
brief psychoeducation control group (Miklowitz,
George, Richards, Simoneau, & Suddath, 2003).
RELAPSE PREVENTION
Relapse prevention is an essential component Family-focused therapy can be an effective treatment option for people
of interventions for bipolar disorder since it is a with bipolar disorder.
highly recurrent condition with 70–75 per cent of
patients having at least one relapse within four to five years after recovering from an episode of mania
(Gitlin, Swendsen, Heller, & Hammen, 1995). Consequently, increasing emphasis is being placed on
implementing relapse-prevention strategies after recovery from an acute episode.
Until recently, relapse-prevention treatment for bipolar disorder focused on medication alone.
However, the medical approach in isolation has been shown to have limitations, including poor
adherence due to factors such as unpleasant side effects of medication (Sorenson, Done, & Rhodes,
2007). Furthermore, medication has been found to have limited long-term effectiveness, with one
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longitudinal study reporting relapse rates of 37 per cent after one year and 73 per cent after five years
or more among patients on mood stabilisers alone (Gitlin et al., 1995). This has led to a move towards
a biopsychosocial approach to managing bipolar disorder, and recognition that the best relapse-
prevention treatment combines pharmacological and psychological interventions.
Psychological approaches to relapse prevention have highlighted the role of risk factors predisposing
individuals to manic and depressive episodes. CBT strategies for relapse prevention include
psychoeducation for patients and their families regarding the risk factors for relapse (e.g., drug and
alcohol misuse) and the importance of both medication compliance and establishing a daily routine.
Patients are taught to self-monitor early symptoms of relapse and to have a plan of action available
should early-warning signs arise. Family, friends and other sources of support are also educated about
the early-warning signs of relapse. This is especially important in bipolar disorder, as a lack of insight
into symptoms or a reluctance to receive help (e.g., if symptoms are valued by the patient) is often
present in mania. Given the role of the patient’s belief system in his/her acceptance of and adjustment
to the illness, emphasis is placed on identifying and challenging any unhelpful cognitions that may
predispose him/her to a relapse (e.g., ‘I don’t feel unwell so I must not need treatment’). Comorbid
problems, particularly anxiety disorders and substance abuse, need to be addressed as they interact
with bipolar disorder and can negatively affect outcome.
Sorenson and colleagues (2007) developed a brief psychological intervention based on what they
termed ‘the instability model of bipolar disorder relapse’. This model assumes that there are four key
mechanisms that trigger relapse in bipolar disorder. The four mechanisms, as illustrated in Figure 6.4,
are a biological vulnerability (e.g., neurotransmitter disturbance) in combination with medication
non-adherence, disrupted routines (e.g., working longer hours) and dysfunctional interpretations of
life events (including past episodes of mood disturbance that the individual might misinterpret as a
sign of personal failure). The model proposes that any of these mechanisms can lead to relapse via a
common pathway of sleep disruption.
Medication
non-adherence
Biological
vulnerability Disrupted MANIA OR
Sleep disruption
to bipolar routines DEPRESSION
disorder
Dysfunctional
interpretations of
life events
FIGURE 6.4 The instability model of relapse in bipolar disorder

Source: Adapted from Sorenson, J., Done, D. J., & Rhodes, J. (2007). A case series evaluation of a brief, psychoeducation approach
intended for the prevention of relapse in bipolar disorder. Behavioural and Cognitive Psychotherapy, 35, 93–107.
According to the authors, it follows that each of these four mechanisms should be addressed with
specific interventions that all have the aim of reducing the risk of relapse. Key components include
identifying the early-warning signs of relapse, ensuring medication adherence, interpersonal social
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rhythms therapy and cognitive therapy. In one study, patients with bipolar disorder received four
treatment sessions and were followed up for five weeks after they completed treatment (Sorenson
et al., 2007). The results revealed that patients achieved significant reductions in hopelessness (and
thus suicide risk) and greater perceived control over internal states, both of which are known to be
key aspects in recovery from bipolar disorder. This provided initial evidence for the efficacy of a brief
psychological intervention in preventing relapse in bipolar disorder, although clearly a longer follow-
up period is necessary to determine the longer-term benefits.
In summary, the existing evidence demonstrates the efficacy of using psychological relapse-
prevention strategies in addition to medication in the management of bipolar disorder. However, more
studies are needed to identify the most effective type, format and duration of treatment.
HOSPITALISATION
Bipolar disorder can be a serious condition, with the person sometimes posing a risk to him/herself or
others if his/her behaviour becomes suicidal or psychotic. During a manic episode, the acutely unwell
person may well lose insight and become non-compliant to treatment. Manic episodes are often
associated with increased risk-taking behaviour and sometimes aggression in reaction to attempts
to contain the person. In such instances, hospitalisation in an acute psychiatric unit is necessary so
that acute pharmacological treatment can take place. If resistant, the unwell person may need to be
certified under the relevant local mental health legislation.
NEW DEVELOPMENTS
There have been several new developments in the psychological treatment of bipolar disorder in the
past decade. Mindfulness-based cognitive therapy has been shown by recent studies to offer significant
benefits for people with bipolar disorder. The focus is on assisting the patient to manage both anxiety
and depressive symptoms primarily between episodes (Williams et al., 2008). Australian research
suggests that the main benefit of mindfulness-based CBT in bipolar disorder may be for the anxiety
symptoms that are frequently comorbid with this condition (Perich, Manicavasgar, Mitchell, Ball,
& Hadzi-Pavlovic, 2013). In addition, internet-based treatments are being developed and evaluated,
such as the beyondblue-funded self-help program for people with bipolar disorder available at
www.moodswings.net.au (Lauder, Berk, Castle, Dodd, & Chester, 2007). Finally, there is growing
interest in expanding the therapeutic goals of psychological interventions for bipolar disorder, with
calls for approaches that focus on quality of life, especially among people who have a long history of
bipolar disorder (Murray et al., 2017). Consistent with the positive psychology movement, there is
also growing interest in self-management strategies for bipolar disorder, often combined with a focus
on wellness and personal recovery (see www.bdwellness.com).
From a research viewpoint, a key development over recent years has been the active involvement
of consumers in the development of new psychological interventions for bipolar disorder (Michalak
et al., 2016). By involving consumers at every step, the content and style of new therapeutic offerings
will better align with the values and preferences of the end-users. More fundamentally, the expertise
that comes from individuals with a lived experience of bipolar disorder has been used to identify
useful new directions for psychological intervention (Murray et al., 2015).
CASE STUDY: FIRST MANIC EPISODE

Sandra initially presented for therapy sessions with a clinical psychologist under the Medicare Better Access scheme
(which provides subsidies for people to seek professional help for their psychological disorder given that such treatment
is typically expensive). At that time, she was 29 years old and had recently been discharged from an inpatient unit after
her first psychiatric admission.
continued
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Sandra had been hospitalised voluntarily after her colleagues became concerned about her increasingly unusual
behaviour over the preceding few weeks. She works as a nurse and over recent weeks she had been unusually
gregarious and assertive at work, and also on a few occasions became overtly irritable with senior staff in a manner that
was completely out of character. Over the days preceding her inpatient stay, Sandra was working night shifts and had
told colleagues that she was sleeping only two or three hours per day. She nonetheless felt she had plenty of energy
and could concentrate easily at work. She also reported excitement at commencing a new sexual relationship with a
much older man whom she had met on a train. Colleagues also saw this as out of character because Sandra was a
temperamentally quiet and shy young woman who had previously been anxious about pursuing relationships with men.
After Sandra arrived late to a shift, wearing full make-up and moving about the ward in an excited manner and speaking
loudly, a senior nurse took Sandra aside and suggested she see a psychiatrist. The psychiatrist discovered that Sandra
had not slept at all for the past 36 hours, and that Sandra now thought that the child that she would have with her new
partner would be the Messiah. She became teary when the psychiatrist suggested she was showing symptoms of a
manic episode, and agreed to be admitted to the hospital’s psychiatric ward.
Sandra was diagnosed with bipolar I disorder by the psychiatrist on the ward. No comorbid diagnoses were warranted.
The focus of Sandra’s inpatient stay was addressing her acute manic symptoms with antipsychotic medication. She was
also commenced on lithium for the long-term prevention of future episodes of bipolar disorder. As part of the planning for
her treatment after discharge from hospital she was referred to a clinical psychologist.
Her sessions with the clinical psychologist initially focused on building a strong working alliance between the therapist
and Sandra, helping Sandra to process the trauma of her manic episode, and psychoeducation about bipolar disorder.
The assessment acknowledged Sandra’s bipolar disorder, but also her significant strengths as a person, which included
her high levels of conscientiousness, humility, openness and warmth.
Later sessions followed a cognitive-behavioural approach to bipolar disorder (targeting the dysfunctional cognitions
that trigger manic and depressive states) and developed her self-management skills. Elements of social rhythm therapy
were included to stabilise her daily rhythms and sleep. Throughout, the clinical psychologist worked closely with Sandra’s
psychiatrist. As the manic episode resolved, Sandra returned to work.
In the subsequent years, Sandra has maintained a very good quality of life despite three significant manic episodes and
some difficulties with medication side effects. With the long-term support of her treatment team, she continues to progress
her career and actively pursues her interests in yoga and singing. She is currently completing postgraduate studies to
become a maternal and child health nurse, and recently celebrated her 40th birthday with the friends who have been with
her on this journey.
USEFUL RESOURCES
Several self-help books and websites have been developed in Australia and New Zealand in order to provide greater
understanding of bipolar disorders. Examples of these resources are as follows.
SELF-HELP BOOKS
Berk, L., Berk, M., Castle, D., & Lauder, S. (2008). Living with bipolar: A guide to understanding and managing the
disorder. Sydney: Allen & Unwin.
Eyers, K., & Parker, G. (2008). Mastering bipolar disorder: An insider’s guide to managing mood swings and finding
balance. Sydney: Allen & Unwin.
Macneil, C., Hasty, M., Conus, P., Berk, M., & Scott, J. (2010). Bipolar disorder in young people: A psychological
intervention manual. Cambridge: Cambridge University Press.
Tanner, S., & Ball, J. (1991). Beating the blues: A self-help approach to overcoming depression. Sydney: Tower Books.
WEBSITES
beyondblue, the National Depression Initiative: www.beyondblue.org.au
Black Dog Institute: www.blackdoginstitute.org.au
New Zealand Ministry of Health: www.health.govt.nz/your-health/conditions-and-treatments/mental-health/depression
CREST.BD: www.bdwellness.com
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SUMMARY
The bipolar disorders are defined by the occurrence of manic or hypomanic episodes, usually in conjunction with periods of
depression. These episodes are characterised by abnormally elevated or irritable mood and increased activity, with a range
of accompanying symptoms such as inflated self-esteem, a decreased need for sleep, increased talkativeness, and risk-taking
behaviours. While bipolar disorders are less prevalent than depressive disorders, they entail considerable suffering for the
individual, with high rates of comorbid psychological disorders (especially anxiety disorders and substance abuse), social and
economic problems, and suicide.
Over the past decade, substantial progress has been made in developing a better understanding of the biological, psychological
and social factors associated with bipolar disorder. The disorder has a strong genetic component, and is likely to arise from long-
and short-term interplay between numerous genes and life events. Key neurobiological factors for the development of bipolar
disorder include the brain’s reward, circadian and emotion-regulation pathways. In terms of psychosocial factors, increasing
evidence suggests that excessive goal pursuit, and behavioural disturbances such as irregular sleeping patterns are pathways
to mania.
The efficacy of psychological treatments in conjunction with pharmacotherapy has now been established in the treatment of
bipolar disorder. Further psychological research is needed to develop interventions that address both of the major challenges
of bipolar disorder—that is, (1) decreasing symptoms and relapse and (2) maximising quality of life in the context of any ongoing
challenges the individual might experience.
KEY TERMS
amphetamines . . . . . . . . . . . . . . . . . . . 132 diathesis-stress model. . . . . . . . . . . . . 135 mood stabilisers. . . . . . . . . . . . . . . . . . 137
bipolar disorder . . . . . . . . . . . . . . . . . . 126 goal dysregulation model. . . . . . . . . . 135 motivational interviewing . . . . . . . . . . 133
bipolar I disorder . . . . . . . . . . . . . . . . . 128 grandiosity. . . . . . . . . . . . . . . . . . . . . . . 128 psychoeducation. . . . . . . . . . . . . . . . . 137
bipolar II disorder. . . . . . . . . . . . . . . . . 128 hypomanic episodes. . . . . . . . . . . . . . 130 rapid cycling bipolar disorder. . . . . . . 129
circadian system. . . . . . . . . . . . . . . . . . 135 lithium carbonate. . . . . . . . . . . . . . . . . 127 self-efficacy. . . . . . . . . . . . . . . . . . . . . . 138
cyclothymic disorder. . . . . . . . . . . . . . 129 manic episode . . . . . . . . . . . . . . . . . . . 128 temperament. . . . . . . . . . . . . . . . . . . . . 136
REVIEW QUESTIONS
LO 6.1
6.1 What are some of the risk-taking behaviours commonly associated with a manic episode?
6.2 What are the major differences between a manic episode and a hypomanic episode?
LO 6.2
6.3 What is the epidemiological relationship between gender and bipolar disorder diagnosis?
6.4 How common are depressive symptoms in bipolar I disorder? Bipolar II?
LO 6.3
6.5 Describe the diathesis-stress model as it relates to the aetiology of bipolar disorder.
6.6 Which biological system is particularly important in stress-related relapse in bipolar disorder, and what behaviours
are particularly challenging for this system?
6.7 What type of life event seems to be particularly important in triggering hypomanic or manic episodes?
6.8 Describe how cognitive factors and temperament are associated with bipolar disorder.
LO 6.4
6.9 What are the main psychological approaches used in the treatment of bipolar disorder? Which of these is unique
to bipolar disorder?
6.10 What are the core content elements shared across the evidence-based psychological treatments for bipolar
disorder?
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REFERENCES
Akiskal, H. S., Kilzieh, N., Maser, J. D., Clayton, P. J., Schettler, P. Frank, E., Swartz, H. A., & Kupfer, D. J. (2000). Interpersonal and
J., Shea, M. T., . . . Keller, M. B. (2006). The distinct temperament social rhythm therapy: Managing the chaos of bipolar disorder.
profiles of bipolar I, bipolar II and unipolar patients. Journal of Biological Psychiatry, 48, 593–604.
Affective Disorders, 92, 19–33. Gallagher, J. (2013). Stephen Fry: Suicide risk in bipolar disorder.
Alloy, L. B., Reilly-Harrington, N., Fresco, D. M., Whitehouse, W. BBC News Health. 6 June.
G., & Zechmeister, J. S. (1999). Cognitive styles and life-events in Geddes, J. R., & Miklowitz, D. J. (2013). Treatment of bipolar
subsyndromal unipolar and bipolar disorders. Journal of Cognitive disorder. Lancet, 381, 1672–1682.
Psychotherapy, 13, 21–40. Ghaemi, S. N., Ko, J. Y., & Goodwin, F. K. (2002). ‘Cade’s disease’
American Psychiatric Association (2013). Diagnostic and statistical and beyond: Misdiagnosis, antidepressant use, and a proposed
manual of mental disorders (5th ed.). Arlington: Author. definition for bipolar spectrum disorder. Canadian Journal of
Ball, J. R., Mitchell, P. B., Corry, J. C., Skillecorn, A., & Malhi, G. Psychiatry, 47, 125–134.
S. (2006). A randomised controlled trial of cognitive therapy for Gitlin, M. J., Swendsen, J., Heller, T. L., & Hammen, C. (1995).
bipolar disorder: Focus on long-term change. Journal of Clinical Relapse and impairment in bipolar disorder. American Journal of
Psychiatry, 67, 2. Psychiatry, 152, 1635–1640.
Ball, J. R., Mitchell, P., Malhi, G., Skillecorn, A., & Smith, M. (2003). Goodwin, G., & Sachs, G. (2004). Bipolar disorder. Oxford: Fast
Schema-focused cognitive therapy for bipolar disorder: Reducing Facts, Health Press.
vulnerability to relapse through attitudinal change. Australian and Hammen, C., Ellicott, A., & Gitlin, M. J. (1992). Stressors and
New Zealand Journal of Psychiatry, 37, 41–48. sociotropy/autonomy: A longitudinal study of their relationship to
Bauer, M. S., Crits-Christoph, P., Ball, W. A., Dewees, E., the course of bipolar disorder. Cognitive Therapy and Research,
McAllister, T., Alahi, P., . . . Whybrow, P. C. (1991). Independent 16, 409–418.
assessment of manic and depressive symptoms by self-rating: Scale Harris, E. C., & Barraclough, B. (1997). Suicide as an outcome for
characteristics and implications for the study of mania. Archives of mental disorders: A meta-analysis. British Journal of Psychiatry,
General Psychiatry, 48, 807–812. 170, 205–228.
Cade, J. F. J. (1979). Mending the mind: A short history of twentieth Johnson, S. L., Sandrow, D., Meyer, B., Winters, R., Miller, I.,
century psychiatry. Melbourne: Sun Books. Solomon, D., & Keitner, G. (2000). Increases in manic symptoms
Carson, S. H. (2011). Creativity and psychopathology: A shared after life events involving goal attainment. Journal of Abnormal
vulnerability model. Canadian Journal of Psychiatry, 55, Psychology, 109, 721–727.
144–153. Jones, S. (2004). Psychotherapy of bipolar disorder: A review.
Carver, C. S. & White, T. L. (1994). Behavioral inhibition, behavioral Journal of Affective Disorders, 80, 101–114.
activation and affective responses to impending reward and Judd, L. L., Akiskal, H. S., & Schettler, P. J. (2002). The long-term
punishment: The BIS/BAS Scales. Journal of Personality and natural history of the weekly symptomatic status of bipolar I
Social Psychology, 196, 319–333. disorder. Archives of General Psychiatry, 59, 530–537.
Chen, Y. W., & Dilsaver, S. C. (1995). Comorbidity of panic disorder Judd, L. L., Akiskal, H. S., & Schettler, P. J. (2003). A prospective
in bipolar illness: Evidence from the epidemiological catchment investigation of the natural history of the long-term weekly
area survey. American Journal of Psychiatry, 152, 280–282. symptomatic status of bipolar II disorder. Archives of General
Cipriani, A., Barabui, C., Salanti, G., Rendell, J., Brown, J., Psychiatry, 60, 261–269.
Stockton R., . . . Geddes, J. R. (2011). Comparative efficacy and Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas, K. R.,
acceptability of antimanic drugs in acute mania: A multiple- & Walters, E. E. (2005). Lifetime prevalence and age-of-onset
treatments analysis. Lancet, 378, 1306–1315. distributions of DSM-IV disorders in the National Comorbidity
Cochrane, S. D. (1984). Preventing medical non-compliance in the Survey Replication. Archives of General Psychiatry, 62, 593–602.
outpatient treatment of bipolar affective disorders. Journal of Kessler, R. C., Rubinow, D. R., Holmes, C., Abelson, J. M., & Zhao,
Consulting and Clinical Psychology, 52, 873–878. S. (1997). The epidemiology of DSM-III-R bipolar I disorder
Dunner, D. L., & Fieve, R. R. (1974). Clinical factors in lithium in a general population survey. Psychological Medicine, 27,
carbonate prophylaxis failure. Archives of General Psychiatry, 30, 1079–1089.
229–233. Kraepelin, E. (1896). Psychiatrie Auflage. Leipzig: Barth.
Ellicott, A., Hammen, C., Gitlin, M., Brown, G., & Jamison, K. R. Lam, D. H., Hayward, P., Watkins, E. R., Wright, K., & Sham, P.
(1983). Life events and courses of bipolar disorder. American (2005). Relapse prevention in patients with bipolar disorder:
Journal of Psychiatry, 140, 215–217. Cognitive therapy outcome after 2 years. American Journal of
Falret, J. P. (1851). De la folie circulaire ou forme de maladie Psychiatry, 162, 324–329.
mentale caractérisée par l’alternative régulière de la manie et de la Lam, D. H., Jones, S., Haywood, P., & Bright, J. A. (1999). Cognitive
mélancholie. Bulletin de l’Académie Nationale de Médicine. therapy for bipolar disorder: A therapist’s guide to concepts,
Frank, E., Kupfer, D. J., Thase, M. E., Mallinger, A. G., Swartz, A. H., methods and practice. Chichester: John Wiley.
Fagiolini, A. M., . . . Monk, T. (2005). Two-year outcomes for Lam, D. H., Watkins, E. R., Hayward, P., Bright, J., Wright, K.,
interpersonal and social rhythm therapy in individuals with bipolar Kerr, N., . . . Sham, P. (2003). A randomised controlled study
I disorder. Archives of General Psychiatry, 62, 996–1004. of cognitive therapy of relapse prevention for bipolar affective
rie66620_ch06_125-146.indd 144 07/29/17 01:03 PM

disorder: Outcome of the first year. Archives of General Psychiatry, Mortensen, P. B., Pedersen, C. B., & Melbye, M. (2003). Individual
60, 145–152. familial risk factors for bipolar affective disorders in Denmark.
Lauder, S., Berk, M., Castle, D., Dodd, S., & Chester, A. (2007). Archives of General Psychiatry, 60, 1209–1215.
Online psychosocial interventions for bipolar disorder: www. Murray, G., & Johnson, S. L. (2010). The clinical significance of
moodswings.net.au. Australian and New Zealand Journal of creativity in bipolar disorder. Clinical Psychology Review, 30,
Psychiatry, 41 (Supp. 2), A389. 712–732.
Leonhard, K. (1957). The classification of endogenous psychoses. Murray, G., Leitan, N. D., Berk, M., Thomas, N., Michalak, E., Berk,
In E. Robins (Ed.), Aufteilung der endogenen Psychosen (1st ed.). L., . . . Kyrios, M. (2015). Online mindfulness-based intervention
Berlin: Akademic-Verlag. for late-stage bipolar disorder: Pilot evidence for feasibility
Lex, C., Bazner, E., & Meyer, T. D. (2016). Does stress play a and effectiveness. Journal of affective disorders, 178, 46–51.
significant role in bipolar disorder? A meta-analysis. Journal of doi:10.1016/j.jad.2015.02.024
Affective Disorders, 208, 298–308. Murray, G., Leitan, N. D., Neil, T., Michalak, E. E., Johnson, S. L.,
Lichtenstein, P., Yip, B., Björk, C., Pawitan, Y., Cannon, T., Jones, S.,  . 
. . Berk, M. (2017). Towards recovery-oriented
Sullivan, P., & Hultman, C. (2009). Common genetic determinants psychosocial interventions for bipolar disorder: Quality of
of schizophrenia and bipolar disorder in Swedish families: A life outcomes, stage-sensitive treatments, and mindfulness
population-based study. The Lancet, 373, 234–239. mechanisms. Clinical Psychology Review, 52, 148–163.
Lovibond, S. H., & Lovibond, P. F. (1995). Manual for the Depression National Institute of Mental Health (2012). Bipolar disorder.
Anxiety Stress Scales (2nd ed.). Sydney: Psychology Foundation. Maryland: Author.
Malhi, G. S., Bassett, D., Boyce, P., Bryant, R., Fitzgerald, P. B., Fritz, Patelis-Siotis, I., Young, L. T., Robb, J. C., Marriott, M., Bieling, P. J.,
K., . . . Singh, A. B. (2015). Royal Australian and New Zealand Cox, L. C., & Joffe, R. T. (2001). Group cognitive behavioural
College of Psychiatrists clinical practice guidelines for mood therapy for bipolar disorder: A feasibility and effectiveness study.
disorders. Australian and New Zealand Journal of Psychiatry, 49, Journal of Affective Disorders, 65, 145–153.
1087–1206. Pavlova, B., Perlis, R. H., Mantere, O., Isometsa, E., Mitchell, P. B.,
Michalak, E. E., Barnes, S. J., Berk, L., Berk, M., Jones, S., Alda, M., & Uher, R. (2016). Prevalence of anxiety disorders in
Hole, R., . . . Johnson, S. L. (2016). Commentary: Harnessing the people with bipolar disorder during euthymia: A meta-analysis.
potential of community-based participatory research approaches Psychological Medicine. E-pub, December 20, 2016. doi:10.1017/
in bipolar disorder.International Journal of Bipolar Disorders, 4, S0033291716003135
1–9. Perich, T., Manicavasgar, V., Mitchell, P. B., Ball, J. R., & Hadzi-
Miklowitz, D. J., George, E. L., Richards, J. A., Simoneau, T. L., & Pavlovic, D. (2013). A randomized controlled trial of mindfulness-
Suddath, R. L. (2003). A randomised study of family-focused based cognitive therapy for bipolar disorder. Acta Psychiatrica
psychoeducation and pharmacotherapy in the outpatient Scandinavica, 127, 333–343.
management of bipolar disorder. Archives of General Psychiatry, Perry, A., Tarrier, N., Morriss, R., McCarthy, E., & Limb, K. (1999).
60, 904–912. Randomised controlled trial of efficacy of teaching patients with
Miklowitz, D. J., & Goldstein, M. J. (1990). Behavioural family bipolar disorder to identify early symptoms of relapse and obtain
treatment for patients with bipolar affective disorder. Behaviour treatment. British Medical Journal, 16, 149–153.
Modification, 14, 457–489. Perugi, G., Akiskal, H. S., Toni, C., Simonini, E., & Gemignani,
Mitchell, P. B. (2012). Bipolar disorder: The shift to overdiagnosis. A. (2001). The temporal relationship between anxiety disorders
Canadian Journal of Psychiatry, 57, 659–665. and (hypo)mania: A retrospective examination of 63 panic, social
Mitchell, P. B. (2017). The history of bipolar disorder. In C. Zarate phobic and obsessive-compulsive patients with comorbid bipolar
Jr & H. K. Manji (Eds.), Bipolar depression: Molecular disorder. Journal of Affective Disorders, 67, 199–206.
neurobiology, clinical diagnosis and pharmacotherapy (pp. 3–16) Power, M. J., Katz, R., McGuffin, P., Duggan, C. F., Lam, D., Beck,
(2nd ed.). Berlin: Springer-Verlag. A. T. (1994). The Dysfunctional Attitude Scale (DAS). Journal of
Mitchell, P. B., & Hadzi-Pavlovic, D. (1999). John Cade and the Research in Personality, 28, 263–276.
discovery of lithium treatment for manic depressive illness. Psychiatric GWAS Consortium Bipolar Disorder Working Group
Medical Journal of Australia, 171, 262–264. (2011). Large-scale genome-wide association analysis of bipolar
Mitchell, P. B., Hadzi-Pavlovic, D., & Loo, C. K. (2011). Course and disorder identifies a new susceptibility locus near OD24. Nature
outcome of bipolar disorder. In H. K. Manji & C. S. Zarate (Eds.), Genetics, 43, 977–983.
Behavioural neurobiology of bipolar disorder and its treatment Reilly-Harrington, N. A., Alloy, N. B., Fresco, D. M., & Whitehouse,
(pp. 1–18). Berlin: Springer-Verlag. W. G. (1999). Cognitive styles and life events interact to predict
Mitchell, P. B., Johnston, A. K., Corry, J., Ball, J. R., & Malhi, G. S. bipolar disorder and unipolar symptomatology. Journal of
(2009). Characteristics of bipolar disorder in an Australian Abnormal Psychology, 108, 567–578.
specialist outpatient clinic: Comparison across large datasets. Scott, J., Garland, A., & Moorhead, S. (2001). A pilot study of
Australian and New Zealand Journal of Psychiatry, 43, 109–17. cognitive therapy in bipolar disorders. Psychological Medicine, 31,
Mitchell, P. B., Johnston, A. K., Frankland, A., Slade, T., Green, M. J., 459–467.
Roberts, G., . . . Hadzi-Pavlovic, D. (2013). Bipolar disorder in Scott, J., Murray, G., Henry, C., Morken, G., Scott, E., Angst, J.,
a national survey using the World Mental Health Version of the Merikangas, K., & Hickie, I. B. (2016). Activation in bipolar
Composite International Diagnostic Interview. Acta Psychiatrica disorders: a systematic review of existing data. JAMA Psychiatry,
Scandinavica, 127, 281–393. 74, 189–196.
rie66620_ch06_125-146.indd 145 07/29/17 01:03 PM

Solomon, D. A., Leon, A. C., Coryell, W. H., Endicott, J., Li, C., Weissman, A. N. (1979). The Dysfunctional Attitude Scale:
Fiedorowicz, J. G., . . . Keller, M. B. (2010). Longitudinal course A validation study. Dissertation Abstracts International, 40,
of bipolar disorder: Duration of mood episodes. Archives of 1389–1390B.
General Psychiatry, 67, 339–347. Williams, J. M. G., Alatiq, Y., Crane, C., Barnhofer, T., Fennel, M. J. V.,
Sorenson, J., Done, D. J., & Rhodes, J. (2007). A case series Duggan, D. S., . . . Goodwin G. M. (2008). Mindfulness-based
evaluation of a brief, psycho-education approach intended for cognitive therapy (MBCT) in bipolar disorder: Preliminary
the prevention of relapse in bipolar disorder. Behavioural and evaluation of immediate effects on between-episodes functioning.
Cognitive Psychotherapy, 35, 93–107. Journal of Affective Disorders, 107, 275–279.
Thomas, J., & Bentall, R. P. (2002). Hypomanic traits and response Winnicott, D. W. (1971). Playing and reality. London: Tavistock.
styles to depression. British Journal of Clinical Psychology, 41, Winters, K. C., & Neale, J. M. (1985). Mania and low self-esteem.
309–313. Journal of Abnormal Psychology, 94, 282–290.
Todd, F. C., & Sellman, J. D. (2004). Alcohol and drug misuse and Zaretsky, A. E., Segal, Z. V., & Gemar, M. (1999). Cognitive
mood disorders. In P. R. Joyce & P. B. Mitchell (Eds.), Mood therapy for bipolar depression: A pilot study. Canadian Journal of
disorders: Recognition and treatment (pp. 298–311). Sydney: Psychiatry, 44, 491–494.
University of New South Wales Press.
Weisberg, R. W. (1994). Genius and madness?: A quasi-experimental
test of the hypothesis that manic-depression increases creativity.
Psychological Science, 5, 361–367.
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CHAPTER 7
Psychotic disorders
John Gleeson
Sarah Bendall
CHAPTER OUTLINE
● The definition and symptoms of psychosis
● The diagnosis of psychotic disorders: core and associated features
● Historical and current conceptualisations of psychotic disorders
● The epidemiology of psychotic disorders
● The aetiology of psychosis
● The treatment of psychotic disorders
● Summary

7.1 Outline the defining symptoms of psychosis.
7.2 Describe the symptoms of the various DSM-5 psychotic disorders and the problems associated with psychosis.
7.3 Describe the evolution in the diagnostic criteria for schizophrenia and the controversies in the field regarding
this diagnosis.
7.4 Outline the prevalence, age of onset and stages of psychosis.
7.5 Describe the range of factors implicated in the aetiology of psychosis.
7.6 Describe the main treatment priorities in relation to the phases of psychosis and the range of evidence-based
treatment options.
PSYCHOTIC DISORDERS: AN AUSTRALASIAN FOCUS

In 2016 the Royal Australian and New Zealand College of Psychiatrists updated their clinical guidelines to assist mental
health professionals in the optimal treatment of schizophrenia and other psychotic disorders for the first time in 12 years
(Galletly et al., 2016). The changes to these guidelines reflect important changes in the way that psychotic disorders are
conceptualised in Australia and New Zealand. Compared to previous guidelines, they place much greater emphasis
on early intervention, on the addition of psychosocial treatments to augment medication, on improving vocational and
educational outcomes for people with psychosis and on the physical health of people with psychosis.
The guidelines highlight the seriousness of schizophrenia and other psychotic disorders, stating that ‘schizophrenia
is associated with a greater burden of long-term disability than any other mental disorder’ (Galletly et al., p. 415). The
guidelines take the perspective that the social environment of people living with schizophrenia is an important factor
impacting on their ability to function, with the stigma of mental illness and social exclusion being major contributors
to the individual’s disability, low self-esteem and apathy. Helping individuals with schizophrenia to become and stay
socially connected (e.g., through participation in employment) is therefore a key component of support. While describing
the considerable toll that psychotic disorders take on affected individuals, the guidelines also note that the majority of
people with psychosis have good symptomatic recovery between episodes and many experience recovery over the
long term.
continued
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The guidelines emphasise the importance of understanding

the unique social and cultural context of psychotic illness in both
Aboriginal and Torres Strait Islander and Māori people and the
importance of integrating culturally appropriate methods into
their clinical care. For example, the guidelines recommend that
there be mandatory cultural awareness training for all mental
health clinicians working with Aboriginal and Torres Strait
SHUTTERSTOCK.COM
Islander and Māori people who have schizophrenia. Among
the components of such cultural awareness training is the need
to understand the relevance of post-colonial history (with its
collective grief, trauma and loss) and social disadvantage (e.g.,
poor housing, low access to health care, social exclusion and
unemployment) for psychological functioning. The guidelines
The clinical guidelines for the management of
also recommend the inclusion of traditional healers, cultural
schizophrenia state that clinicians need to work
consultants and Aboriginal health workers to contribute to the
closely with members of the Aboriginal and Torres
assessment and treatment process. Since this is an area where
Strait Islander and Māori communities to ensure that
the evidence base is lacking, research into the optimal care of
care is culturally appropriate.
Aboriginal and Torres Strait Islander and Māori people living
with schizophrenia is a priority.
This chapter on psychotic disorders will begin by providing a definition of psychosis in terms of various positive and
negative symptoms, and the types of psychotic conditions, including schizophrenia. Problems associated with these
disorders will be outlined and information provided regarding their prevalence, age of onset and course over time. Some
key findings regarding the aetiology of psychotic conditions, as well as the treatment approaches corresponding to the
various stages of psychosis, will be outlined. Throughout, particular attention will be given to Australasian developments
in the understanding and treatment of psychotic disorders.
LO 7.1 The definition and symptoms of psychosis

positive In spite of more than 100 years of empirical research into schizophrenia and the psychoses, there is
symptoms still no universally agreed-upon definition of psychosis. In the current version of the Diagnostic and
In schizophrenia, Statistical Manual of Mental Disorders (DSM-5) (American Psychiatric Association [APA], 2013),
hallucinations,
psychotic disorders are conceptualised in terms of a spectrum of severity and are characterised by
delusions, and
disorganisation the presence of five diverse symptom dimensions, namely, delusions, hallucinations, disorganised
in thought and thinking (or thought disorder), grossly disorganised or abnormal motor behaviour and so-called
behaviour. negative symptoms.
In clinical practice and in research, symptoms of psychosis are often collapsed into two categories
thought disorder of positive and negative. Positive symptoms include hallucinations (and more subtle perceptual
State of highly
disturbances), delusions, thought disorder and motor disturbances. They are referred to as ‘positive’
disorganised
thinking (also because they entail the addition of disturbance. In contrast, negative symptoms refer to deficits in
known as formal psychological processes including avolition (the loss of drive or motivation), affective flattening
thought disorder (a dampening down in the expression of emotion) and alogia (a lack of unprompted speech, also
or a loosening referred to as ‘poverty of speech’). Although positive and negative symptoms constitute the defining
of associations) symptoms for a diagnosis of a psychotic disorder, researchers have increasingly recognised that other
characteristic of features associated with psychotic disorders, especially problems with social isolation and social
individuals with
participation, may be the most disabling aspects of these conditions. These associated problems are
schizophrenia.
therefore likely to become an important area of increased attention for treatment, including early
intervention and prevention (Insel, 2010).
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Chapter 7 Psychotic disorders 149
Hallucinations motor
disturbance
Hallucinations are arguably the most distressing of the psychotic symptoms. The DSM-5 defines a
Disturbance of
hallucination as ‘a perception-like experience with the clarity and impact of a true perception but bodily movement.
without the external stimulation of the relevant sensory organ’ (APA, 2013, p. 822). Approximately
75 per cent of patients diagnosed with schizophrenia report hallucinations (Bentall, 2006). These negative
are generally auditory hallucinations, with between 60 and 70 per cent of patients diagnosed with symptoms
In schizophrenia,
schizophrenia reporting auditory hallucinations consisting of a voice speaking to them (Sartorius
deficits in
et al., 1986). Such voices are typically critical and hostile, but comforting voices are also reported. functioning such
Command hallucinations, which entail specific instructions to the patient (e.g., to harm him/ as affective
herself), are also described by between 33 and 74 per cent of voice hearers (Braham, Trower, & flattening, alogia
Birchwood, 2004). and avolition.
Hallucinations can occur in sensory modalities other than the aural, including visual avolition
(e.g., seeing the face of a tormentor), olfactory (sensations of smell, such as the experience of a Inability to
rotting odour), gustatory (sensations of taste, such as a metallic taste), tactile (sensations of touch, initiate or persist
such as a hand on one’s shoulder) and somatic (perception of physical experience located within with important
the body) (Assad & Shapiro, 1986). Multimodal hallucinations (e.g., a voice accompanied by the activities; negative
image of a figure) are also reported by patients. Hallucinations can be associated with neurological symptom of
schizophrenia.
conditions including temporal lobe lesions, complex partial seizures, migraine and brain injury.
Intoxication with illicit substances, such as hallucinogens, is associated with alterations in visual affective
perception of the colour, size and shape of objects and the perception of more abstract images flattening
(Assad & Shapiro, 1986). Severe reduction
Interestingly, hallucinations are also known to be experienced by a sizeable minority of people or the complete
absence
in the general population, most of whom do not seek or require assistance, suggesting that the mere of affective
presence of hallucinations does not mark the presence of a mental disorder (Ohayon, 2000). This (emotional)
finding is consistent with a meta-analysis of studies of psychotic symptoms in the general community, responses to the
which found that in approximately 80 per cent of cases, psychotic experiences disappear over time environment;
(Linscott & van Os, 2013). However, the same study showed that in 7.4 per cent of cases, more serious negative symptom
psychosis that warrants treatment can develop over time. of schizophrenia.
Certain features of the hallucinatory experience have been shown to be associated with the degree alogia
of impact of the hallucination upon the sufferer. For example, Birchwood, Iqbal, Chadwick, and
Deficiency in
Trower (2000) found that the beliefs and expectations sufferers hold in relation to their hallucinations, the quantity of
and the strategies they employ to cope with them, may influence the extent of distress associated with speech; negative
symptoms. For example, if the voice hearer assumes that the voice is malevolent or intends harm to symptom of
schizophrenia.
the individual, then distress is more likely than if the voice is assumed to be benevolent (e.g., the
belief that the voice aims to take the individual to a higher spiritual plane) (Birchwood & Chadwick, hallucination
1997). A variety of assumptions may also be held regarding the identity or source of the voice, which Psychotic
may influence the extent of the distress. For example, a belief that the voice is from a convicted high- symptom entailing
profile gangster is likely to be associated with greater distress than if the voice is believed to be that perceptual
experiences
of a close family member.
that are not real,
which can occur
Delusions in any sensory
modality (e.g., the
The DSM-5 defines delusion as ‘a false belief based on incorrect inference about external reality false perception
that is firmly held despite what almost everyone else believes and despite what usually constitutes of sound or sight).
incontrovertible and obvious proof or evidence to the contrary. The belief is not one ordinarily accepted
auditory
by other members of the person’s culture or subculture (i.e., it is not an article of religious faith).
hallucination
When a false belief involves a value judgment, it is regarded as a delusion only when the judgment is
Perception of
so extreme as to defy credibility’ (APA, 2013, p. 819). Researchers have described various features a sound that it
of delusions including their content, bizarreness, degree of complexity and consequences. Content is not real (such as
commonly used as a basis for categorising delusions, although in clinical practice delusions often defy hearing a voice
being placed into a single category. when alone).
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hallucinogens Paranoid delusions (or ‘persecutory delusions’) are those most commonly reported by patients in
Substances clinical settings. These delusions entail a belief that someone, or a force or agency, is seeking to harm
including LSD the patient or his/her interests (e.g., believing that the Australian Security Intelligence Organisation
and MDMA (i.e.,
[ASIO] is tracking the individual’s emails and phone calls). As a consequence, the patient may attempt
‘ecstasy’) that
can produce to avoid the threat, such as minimising contact with strangers or remaining vigilant for possible threats.
perceptual This state of vigilance is also associated with delusions of reference, which comprise a belief that
illusions and messages of a highly personal nature are being conveyed via neutral sources, commonly via electronic
distortions. media (e.g., that advertisements on Facebook contain coded warnings to the individual).
delusion
Somatic delusions, which entail a false belief regarding the appearance or functioning of one’s
Psychotic body (e.g., a belief that one has cancer), are also commonly described by patients in clinical settings.
symptom These beliefs are sometimes accompanied by somatic hallucinations such as the ‘feeling of electricity
entailing a through the body’ or heightened vigilance for internal bodily sensations. They are often highly
strongly held distressing and can lead to the pursuit of multiple medical interventions.
belief that is not Grandiose delusions are primarily associated with, but not restricted to, the manic episodes of
consistent with bipolar disorder, illustrating that psychotic symptoms are not solely experienced in the context of
what almost
everyone else
psychotic disorders. They include ideas that one has acquired special powers, worth, knowledge,
believes and abilities, influence, associations, achievements or even an alternative identity, often entailing power,
despite obvious wealth or fame. Related to this, religious delusions entail religious themes, such as a belief that one
proof to the has acquired the identity of a religious figure—a belief that would not be shared by other members
contrary. of the religious group. The prevalence of religious delusions has been shown to vary considerably
paranoid across studies (with an estimated 20–60% of patients who experience delusions reporting religious
delusion delusions) (Cook, 2015). Those individuals who are more religious have been found to be more prone
False belief to experiencing this type of delusion.
of delusional Nihilistic delusions and delusions of guilt are typically associated with episodes of severe major
intensity that depression, again highlighting that psychotic symptoms are not restricted to psychotic disorders.
someone is Nihilistic delusions include a conviction that one is dead or that parts of one’s body or the environment
seeking to harm have ceased to exist (Debruyne & Audenaert, 2012). On the other hand, delusions of guilt include
the individual or
beliefs of personal responsibility and that punishment is deserved for specific events or outcomes,
his/her interests.
often of catastrophic proportions (such as the 2011 Christchurch earthquake or climate change) or
delusion of sometimes specific negative events in the patient’s personal experience such as the death of someone
reference close to them.

False belief Delusions of jealousy and erotomanic delusions share a focus upon a specific person in the patient’s
strongly held by
life. Jealousy delusions—sometimes referred to as ‘morbid jealousy’ or the ‘Othello syndrome’ after
an individual that
environmental Shakespeare’s character who murdered his wife on the false premise that she had been unfaithful—
stimuli have are usually centred on the patient’s partner and include beliefs of infidelity. Jealousy delusions may
a particular coincidentally be true, but the process through which the patient has arrived at the conviction of his/
significance for her partner’s infidelity is based on an illogical and arbitrary selection of supposed evidence, or actual
him/her. evidence is not available to the patient. For example, a patient may be convinced that his partner is
somatic delusion having an affair based on coded messages received via Twitter (a delusion of reference). Delusions
False belief of jealousy are known to cause significant relationship distress between sufferers and their partners
of delusional and have been known to increase the risk of domestic violence (Smith & Buckley, 2006). Although
intensity these beliefs have been associated with higher levels of danger, they are also relatively rare in patients
regarding the diagnosed with schizophrenia (Soyka & Schmidt, 2011).
appearance or
Erotomanic delusions entail a false belief that the patient’s romantic feelings for another, often a
functioning of
one’s body.
person perceived by the patient to be of significant status or influence, are reciprocated by the other
person. Apparent confirmation of the reciprocal feelings is often received through coded messages or
signals. Beliefs of this kind are known to be highly enduring, even when the other person adamantly
disavows having feelings for the patient. This disavowal might be justified in the patient’s mind
by alternative interpretations, including the conclusion that the person is prevented from directly
expressing his/her love for the patient by other parties. A small proportion of stalkers are known to be
motivated by erotomanic beliefs, but notably there is evidence from Australian researchers suggesting
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that stalkers with a psychotic disorder are less likely to be violent than other stalkers (McEwan, grandiose
Mullen, & Purcell, 2007). One hypothesis that has been put forward to account for this finding is that, delusion
compared with other stalkers, individuals diagnosed with a psychotic disorder may be less likely to False belief
have an actual history of intimacy with their victim. Research suggests that violence by stalkers is of delusional
intensity about
more reliably predicted by the stalker’s previous history of violence than by the presence of delusions the self including
(McEwan, Mullen, MacKenzie, & Ogloff, 2009). ideas of inflated
Delusions which entail a belief that the patient is under the control of some person, force or worth, power,
agency are known as passivity phenomena. Examples include a belief that one’s thoughts are being knowledge,
interfered with in the form of thoughts being implanted (‘thought insertion’) or removed (‘thought ability, identity
withdrawal’) from the patient’s mind, or a belief that one’s actions, impulses or emotions are being or relationships
directly influenced by some external force. Aside from their content, delusions are also categorised with well-known
figures.
into bizarre and non-bizarre on the basis of whether they are considered physically possible within a
person’s culture. For example, delusions of thought broadcasting (the belief that one’s thoughts can
be heard by others) are bizarre, whereas a belief that one’s neighbour has spread malicious gossip is
categorised as non-bizarre.
Another distinction is that between so-called primary and secondary delusions, although this
dichotomy is debated because in practice it may be difficult to make an accurate demarcation (Sims,
1995). Primary delusions are those that have formed without a prior psychopathological event or
process having led to the false conclusion. That is, the belief seems to have appeared de novo or
‘out of the blue’. By contrast, secondary delusions are theoretically secondary to abnormal changes
in mood, memory or perception (especially hallucinations). For example, auditory hallucinations
might form the source of evidence for the patient’s belief that motorcycle criminal gangs are keeping
him/her under surveillance. This distinction may have implications for the role of psychological
treatments for delusions, which in some instances include the patient being encouraged to reflect
with the therapist upon alternative, non-delusional interpretations of the patient’s unusual experience
(e.g., examining any evidence that the hallucinations may be the patient’s own thoughts rather than
the voices of spies) (McGowan, Lavender, & Garety, 2005). This process, at least in theory, is more
difficult in the case of primary delusions where there is no unusual experience upon which the
delusion is based.
Delusions range considerably in their complexity, from simple beliefs regarding specific people or
situations to highly complex belief systems. An example of the former includes a delusion that one’s
boss is conspiring to make life difficult; the latter is illustrated by the belief that one’s peers, family
and government are collaborating in the conspiracy and that information is shared among them for
malicious purposes via email and through thought transmission. Complex delusional belief systems
are highly adaptive to the changing environment. For example, the patient’s treating clinicians might
become incorporated into the belief system, which in turn makes it very difficult for the patient to
obtain help.
Clinical psychologists are interested in understanding the effects of hallucinations and delusions
in order to lessen the impact of these symptoms on the day-to-day life of the sufferer. Haddock,
McCarron, Tarrier, and Faragher (1999) have developed specific inventories for measuring these
effects. The Psychotic Symptom Rating Scales (PSYRATS), for instance, measure the degree of
preoccupation and distress associated with the delusional belief, the level of conviction in the belief
and the disruption to the person’s life caused by the belief. For example, one item rates the patient’s
level of preoccupation with the delusional belief, rated from a score of 0 (‘no delusions, or delusions
that the subject thinks about less than once a week’) to 4 (‘subject thinks about delusions continuously
or almost continuously’).
Clinicians are also mindful of the need to carefully assess the patient’s tendency to act in response
to hallucinations and delusions because this could be associated with potential risks to the patient
or to those around him/her. For example, one patient may be inclined to cope with perceived threats
by withdrawing and avoiding social interaction, whereas another may respond with assertion and
counterthreats that could escalate to conflict.
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Disorganised thinking
In addition to hallucinations and delusions, disorganised thinking (also known as ‘formal thought
disorder’) is frequently categorised as a psychotic symptom. Formal thought disorder refers to
disturbances in the logical sequencing and coherence of thought. In clinical practice and research
on psychosis, the severity of formal thought disorder is inferred through assessments of the person’s
speech, which enables the dimensions of thought sequencing (flow) and form (structure or coherence)
to be identified, as opposed to the content of thought (i.e., delusions). The clinician listens for
disturbances in the coherence of speech, which can range from subtle increases in the use of vague
language to highly incoherent speech in which the individual’s phrases are disjointed and nonsensical.
Disturbances in thought form are common in psychotic disorders, but once again are not restricted to
this group of diagnoses.
Disturbances in thought form can be divided into positive (the addition of disturbed thought
processes) and negative (deficits in thoughts processes) manifestations. Examples of positive thought
disorder include circumstantiality, which describes speech that is very indirect and long-winded in
conveying meaning, although the goal may be eventually reached. Tangentiality describes oblique
or irrelevant responses to questions. This is closely associated with the phenomenon of derailment,
in which the person’s comments slip off one idea onto another, only partially related topic. In more
extreme manifestations of thought disorder, phrases may become linked through sounds rather than
meaning, a phenomenon known as clang associations (e.g., ‘pass me the spoon, moon, I am cocoon’).
During acute phases of psychosis, echolalia may be observed in which the utterances of others around
the patient are repeated. Patients may also use words idiosyncratically (e.g., one patient referred to
his ‘human’ when meaning his physical complaints) or produce false words, known as neologisms
(e.g., ‘it has been creatised by my doctor’). Negative thought disorder refers to a reduced stream of
thought, as evident in a poverty of speech.
Grossly disorganised behaviour

Grossly disorganised or abnormal motor behaviour, including catatonia, is another set of symptoms
in psychosis. These problems may manifest in a variety of ways, including ‘any form of goal-directed
behaviour, leading to difficulties in performing activities of daily living’ (APA, 2013, p. 88). Catatonic
catatonic behaviour is defined as ‘a marked decrease in reactivity to the environment’ (APA, 2013, p. 88). In
behaviour the DSM-5, catatonia is diagnosed as either a feature of a mental disorder (including brief psychotic
Marked motor disorder, schizophreniform disorder, schizophrenia or schizoaffective disorder) or as a catatonic
abnormalities disorder in its own right due to another medical condition. The diagnosis of catatonia requires the
such as adopting
presence of three of the following 12 symptoms:
unusual postures
or engaging ∙ stupor (no psychomotor activity; not actively relating to the environment)
in repetitive ∙ catalepsy (maintaining a rigid body posture or rigidity of the limbs even when this would normally
movements. require some effort to do so)
∙ waxy flexibility (a tendency to remain in a posture even when limbs are moved into place by
another person)
∙ mutism (little or no verbal response)
∙ negativism (opposition or no response to instructions or external stimuli)
∙ posturing (spontaneous and active maintenance of a posture)
∙ mannerism (odd, circumstantial caricature of normal actions)
∙ stereotypy (repetitive, abnormally frequent, non-goal-directed movements such as repeatedly
taking a step back and forth on the spot)
∙ agitation (not influenced by external stimuli)
∙ grimacing (odd facial movements such as baring of the teeth in the absence of provocation)
∙ echolalia (mimicking another’s speech)
∙ echopraxia (mimicking another’s movements).
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Catatonia is less responsive to treatment for schizophrenia, which suggests that it may have an
underlying neurobiological basis separate from other psychotic symptoms (Rosebush & Mazurek,
2010). There is some debate among researchers as to whether catatonic symptoms in schizophrenia
have been decreasing in prevalence over the past 50 years, with some arguing that advances in
treatment with the introduction of certain medications may have led to a reduction in the prevalence of
catatonia. Others, however, argue that the seeming reduction in the occurrence of catatonia is a result
of poor recognition of the problem in clinical practice (Healy, 2013). For instance, Ungvari, Leung,
Ng, Cheung, and Leung (2005) found that 32 per cent of patients in their sample of participants with
chronic schizophrenia in Hong Kong met criteria for catatonia, suggesting that it is far from rare in
this patient population. Their research also supported previous work indicating that the presence of
catatonic symptoms is associated with an earlier age of onset of psychotic illness and poorer overall
functioning.
Negative symptoms
In addition to the positive symptoms of hallucinations, delusions, thought disorder and
disorganised behaviour, deficits in the expression of speech, emotion and spontaneous behaviour
are common in psychosis. One negative symptom is alogia, which refers to a marked reduction
in thoughts as reflected in decreased speech. This might include thought blocking—that is, the
cessation of speech, sometimes mid-sentence. Interestingly, patients can sometimes comment
upon the subjective experience of their thoughts being interrupted and may form secondary
delusional explanations, including beliefs of thought control from external sources, to account
for this experience. Another negative symptom is affective flattening, which entails a lack of
emotional expressiveness that may or may not be accompanied by a subjective loss of emotional
experience. A lack of initiation in activities, known as avolition, also features among the
negative symptoms of psychosis. In more severe cases of avolition, the range of activities and
social interactions becomes extremely restricted, such that the person may spend hours sitting
passively and carers may often feel helpless in trying to motivate their relative. Sometimes these
behaviours can be mistaken for laziness, leading to critical comments from others caring for the
individual. Although these comments are usually derived from a desire to help and influence the
person to work towards goals, such criticism inadvertently increases the risk of an intensification
of positive symptoms (Barrowclough & Hooley, 2003). In clinical practice, negative symptoms are
difficult to distinguish from the adverse effects of medication (Barnes & McPhillips, 1995) as well
as symptoms of depression that are highly prevalent early in the course of psychosis (Birchwood
at al., 2000).
LO 7.2 The diagnosis of psychotic disorders: core

and associated features
Core features
Core features refer to those symptoms that are necessary for a diagnosis. Most mental health
professionals would agree that the diagnosis of a psychotic disorder is warranted when psychotic
symptoms persist for at least one to several weeks and cause significant interference with the person’s
functioning in important domains of his/her life such as vocational, educational and social activities.
Within the DSM-5, psychotic disorders are described in a chapter entitled ‘Schizophrenia Spectrum
and Other Psychotic Disorders’. According to the DSM-5, a diagnosis of a specific psychotic disorder,
such as schizophrenia, is based on the presence of a specific pattern of psychotic symptoms, their
duration and sometimes the precipitating factors or triggers. The full range of DSM-5 psychotic
disorders is listed in Table 7.1.
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TABLE 7.1 DSM-5 types of psychotic disorders
Schizophrenia Lasts at least six months, with at least one month of two or more of
the following: delusions, hallucinations, disorganised speech, grossly
disorganised or catatonic behaviour and/or negative symptoms.
Schizotypal (personality) disorder A pattern of pervasive social and interpersonal deficits and cognitive
or perceptual distortions and eccentricities of behaviour beginning
before early adulthood.
Schizophreniform disorder Equivalent to schizophrenia except the disturbance is of lesser

duration (one to six months).
Schizoaffective disorder The co-occurrence of the symptoms of schizophrenia and a major

mood episode, in addition to at least a two-week period of delusions
or hallucinations without mood disturbance. Mood symptoms are
present for the majority of the total duration of the disorder.
Delusional disorder At least one month of delusions.
Brief psychotic disorder A psychotic disturbance lasting more than one day but less than a
month with eventual return to premorbid level of functioning.
Psychotic disorder due to another Prominent hallucinations or delusions that are the direct
medical condition physiological consequence of another medical condition.
Substance/medication-induced Delusions and/or hallucinations that develop during or soon after

psychotic disorder substance intoxication or withdrawal or after exposure to medication.
Other specified schizophrenia Symptoms of psychosis that cause clinically significant distress or
spectrum and other psychotic impaired functioning but which do not meet full criteria for any other
disorder psychotic disorders. Specific reasons for why the criteria for another
disorder are not met must be specified by the clinician (e.g., persistent
auditory hallucinations in the absence of other psychotic features).
Unspecified schizophrenia Symptoms of psychosis that cause clinically significant distress or

spectrum and other psychotic impaired functioning but which do not meet full criteria for any other
disorder psychotic disorders. The clinician is not required to specify the
reasons why the criteria for this diagnosis are met.
Schizophrenia, the most intensively researched and most prominent psychotic disorder, is
diagnosed according to the DSM-5 when there are two or more of the following symptoms present for
a significant proportion of time during a one-month period:
∙ delusions
∙ hallucinations
∙ disorganised speech
∙ grossly disorganised or catatonic behaviour
∙ negative symptoms.
At least one of these symptoms must be delusions, hallucinations or disorganised speech. In
addition to establishing the presence of these symptoms, the diagnosing clinician must ascertain
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that one or more major areas of the person’s functioning are well below
the level prior to the onset of the active psychotic symptoms (e.g., the
person has withdrawn from social activities and has ceased attending
work or school perhaps in response to suffering hallucinations or
negative symptoms) or there is a failure to achieve expected levels of
functioning in a young person who would have otherwise progressed
in specific domains such as academic achievement. Finally, continuous
signs of schizophrenia must have been consistently present for at
least six months. This six-month period may have entailed a gradual
deterioration in functioning, but must include at least one month of the
psychotic symptoms.
Some changes were made to the diagnostic criteria for schizophrenia
from the DSM-IV-TR (APA, 2000) to the DSM-5. For example, the
DSM-IV-TR specified that only one symptom needed to be present
if it took a specific form (e.g., auditory hallucinations that kept up a
ANTON_IVANOV/SHUTTERSTOCK.COM
running commentary on the person’s behaviour or thoughts or if there
were two or more voices conversing with each other). The DSM-IV-TR
also stipulated some subtypes of schizophrenia that have been dropped
from the DSM-5.
If the criteria for schizophrenia are not fully met, then other diagnoses
may be relevant. For example, if only delusions are present and there
is not a marked impact upon functioning, the diagnosis of delusional
disorder may be applicable. If the duration criterion of six months of
total disturbance is not met, then the diagnosis of schizophreniform In the film A Beautiful Mind, Russell Crowe
disorder may apply. Alternatively, if there is a clear temporal association depicts the life of mathematician John Nash
between the use of, or withdrawal from, substances or medication and and his struggle with schizophrenia.
the onset of psychotic symptoms (and the medication or substance is
capable of producing the psychotic symptoms), then the diagnosis of
substance-induced psychotic disorder can be made, although in clinical practice it can be difficult
to infer a causal relationship in the case of individuals who have engaged in long-term substance
use. In addition, clinicians need to be mindful of distinguishing substance-induced psychosis from

intoxication: the latter may be associated with transient psychotic experiences, which would not
warrant a formal diagnosis of a psychotic disorder.
Although a personality disorder rather than a psychotic disorder, schizotypal personality disorder
is included in the DSM-5 chapter on ‘Schizophrenia Spectrum and Other Psychotic Disorders’ because
it is thought to occur on a continuum of severity of psychotic experiences. It describes a longstanding
pattern of interpersonal, cognitive and perceptual disturbances that do not meet full criteria for a
psychotic disorder.
The DSM-5 also includes two other disorders where full criteria for a specific disorder are
not met, namely, ‘other specified’ and ‘unspecified’ schizophrenia spectrum and other psychotic
disorder. One controversial example was the inclusion of the attenuated psychosis syndrome as
an example of ‘other specified schizophrenia spectrum and other psychotic disorders’. Attenuated
psychosis syndrome includes psychotic symptoms that are less severe and more transient and where
the sufferer has insight into the pathological nature of the symptoms, thus falling below the threshold
for a full psychosis. The controversy has arisen because if symptoms fall below the threshold for a
full psychosis why then is a diagnosis of a psychotic disorder warranted? The syndrome has also
been included in the DSM-5 section on ‘Conditions for Further Study’ to encourage future research
on this topic. As a final point on the diagnostic criteria for the various psychotic disorders, it is
important to note that the core symptoms of psychosis are not solely associated with psychotic
disorders such as schizophrenia but also occur in the context of other mental disorders such as
depressive and bipolar disorders.
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Associated features
Psychotic disorders frequently co-occur with other mental disorders. This is formally recognised in
the diagnosis of schizoaffective disorder, which requires that the criteria for both schizophrenia and a
major depressive, manic or mixed episode (as discussed in Chapters 5 and 6) be present and at least
a two-week period when psychotic symptoms (i.e., hallucinations and delusions) are present in the
absence of prominent mood symptoms.
DEPRESSION
depression Patients with psychotic disorders often suffer from depression, which sometimes precedes or
State marked by appears after the onset of psychosis (Birchwood, Iqbal, Chadwick, & Trower, 2000). The presence
a sad mood and/ of depression is one reason why suicide rates are very high among people diagnosed with a psychotic
or loss of interest
disorder. Specifically, 5–10 per cent of people diagnosed with schizophrenia commit suicide (Palmer,
in one’s usual
activities, as well
Pankratz, & Bostwick, 2005). In addition, there is some recent evidence which suggests that the risk
as feelings of of suicide may have increased significantly for individuals diagnosed with schizophrenia over the
hopelessness, previous 100 years, even though treatments have improved considerably during this period (Healy et
suicidal ideation, al., 2006). This increased risk may in part be the result of deinstitutionalisation (especially the modern
psychomotor trend towards brief hospital admissions as opposed to long-term, even lifelong, hospital admissions
agitation or in the past), unwanted side effects of antipsychotic medications and the effects of withdrawal from
retardation, antipsychotic medications.
appetite
and sleep
ANXIETY AND TRAUMA-RELATED PROBLEMS
disturbances,
fatigue, poor Anxiety and trauma-related problems are also common in individuals with psychotic disorders
concentration and can develop prior to or as a result of psychotic symptoms. These include social phobia and
and a sense of posttraumatic stress disorder (PTSD) (Mueser, Lu, Rosenberg, & Wolfe, 2010; Strakowski, Keck,
worthlessness. McElroy, Lonczak, & West, 1995). Symptoms prior to and as a consequence of psychotic symptoms
can sometimes interact. For example, a proportion of people develop PTSD from the trauma
antipsychotic associated with both the experience of psychosis (e.g., the trauma of persecutory delusions such as
medications believing that one’s life is in imminent danger) and coercive interventions during psychotic episodes
Drugs used to (e.g., involuntary admission to psychiatric inpatient units and seclusion during hospitalisation)
treat psychotic (Chisholm, Freeman, & Cooke, 2006; Morrison, Frame, & Larkin, 2003). However, people are at
symptoms such greater risk of developing PTSD as a consequence of psychotic symptoms or treatment if they also
as delusions and have PTSD from the experience of childhood trauma (Bendall, Alvarez-Jimenez, Hulbert, McGorry,
hallucinations.
& Jackson, 2012). Given the severity of psychotic symptoms, these comorbid anxiety and trauma-
related conditions are often overlooked by clinicians but are known to be associated with significant
disability in their own right.
SUBSTANCE MISUSE
One of the most significant challenges for patients, carers and family members are the well-known
high rates of substance misuse, which exacerbate the symptoms of psychosis and are associated
with health risks. For example, approximately 23 per cent of patients with psychosis report current
cannabis use of cannabis, which has been shown to be a predictor of increased risk of relapse of psychosis
Substance that if cannabis use persists (Green, Young, & Kavanagh, 2005; Hides, Dawe, Kavanagh, & Young,
can produce 2006). Debate continues among researchers as to whether cannabis actually causes psychosis or
feelings of
whether it increases the likelihood of symptoms in individuals with a pre-existing vulnerability to
wellbeing,
perceptual
psychosis (Minozzi et al., 2010; Volkow et al., 2016). A New Zealand study of note has supported
distortions and the theory that the use of cannabis may trigger psychosis in young people with a specific genetic
paranoid thinking. profile (Caspi et al., 2005). This research was conducted as part of the Dunedin Multidisciplinary
Health and Development Study, which enrolled 91 per cent of consecutive births in Dunedin
between April 1972 and March 1973. The sample of 1037 has been regularly assessed on a wide
range of social, psychological and biological variables at 2–3-yearly intervals. When the cohort was
aged 26, researchers were able to examine the relationship between psychosis, use of cannabis in
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the years preceding the onset of psychosis, and variations in a specific gene known as the catechol-
O-methyltransferase (COMT) gene. COMT is an enzyme known to be involved in the breakdown
of dopamine and other neurotransmitters released into the synapses. Some variations of the COMT
gene are thought to result in a slower breakdown of dopamine, which has been linked to the positive
symptoms of psychosis. The researchers found that the risk of psychosis at the age of 26 associated
with the use of cannabis in adolescence was influenced by the presence of a specific form of the
COMT gene. As well as increasing the risk of developing psychosis in genetically vulnerable
individuals, the use of cannabis is associated with earlier onset of psychosis (Large, Sharma,
Compton, Slade, & Nielssen, 2011).
Use of amphetamines, including the drug commonly known as ‘ice’, which some researchers
suggest has been on the rise in Australia in recent years, is known to complicate the course of psychosis
as well as increasing the risk of aggressive behaviour (McKetin et al., 2014; Topp, Degenhardt, Kaye,
& Darke, 2002). Other health problems particularly common in patients with long-term psychotic
disorders include tobacco use as well as obesity and diabetes as a result of antipsychotic medications
(de Leon & Diaz, 2005; Jin, Meyer, & Jeste, 2004).
QUALITY OF LIFE
In addition to mental and physical health complications, mental health clinicians and researchers have
become increasingly focused upon the quality of life across a range of domains for individuals diagnosed
with a psychotic disorder, including their occupational, relationship, social and emotional functioning
(Malla & Payne 2005). Unemployment, for example, has been found to affect approximately 40–50
per cent of individuals with the diagnosis (Killackey, Jackson, Gleeson, Hickie, & McGorry, 2006).
Such findings indicate the need for treatment to focus not only on psychotic symptoms but also on the
individual’s broader functioning.
STIGMA AND SOCIAL ISOLATION

A large proportion of people diagnosed with schizophrenia and other psychotic disorders are also
significantly affected by stigma (Corrigan & Watson, 2002). In comparison with disorders such as
depression, psychosis remains poorly understood in the general community and many myths abound,
often perpetuated by inaccurate, sensationalist and unhelpful stereotyping in the mass media. Myths
include the idea that psychosis is inevitably associated with violence and loss of control, that all
severe mental illness is inevitably associated with intellectual disability, and that schizophrenia is a
‘split personality’. Unfortunately, these myths are damaging to individuals with psychosis because
they maintain a cultural environment that heightens the risk of prejudice and discrimination,
thereby limiting opportunities for recovery. Myths and prejudice also increase the risk of the stigma
being internalised by the individual diagnosed with psychosis, leading to stress, low self-esteem
and despair (Corrigan & Watson, 2002). Given these negative social conditions, individuals may
be reluctant to acknowledge that they have a problem, leading to avoidance or postponement of
treatment, which in turn leads to poorer mental health outcomes. SANE Australia (2011) reported
on the effects of living with stigma in people diagnosed with psychosis. Their research, drawn from
the second national Australian survey of psychosis, revealed that nearly a quarter of people living
with psychosis reported feeling isolated and lonely and 13.3 per cent reported having no friends at
all. For these reasons, organisations such as SANE Australia work to challenge the stereotyping of
psychosis via their long-running ‘stigma watch’ campaign. Other organisations, such as the Early
Psychosis Prevention and Intervention Centre (EPPIC), have also developed a range of educational
materials to provide accurate and accessible information to the general community about psychosis
(as pictured). As well as providing education to the general public, another stigma-reduction strategy
could be changing the terms used regarding psychotic disorders. Researchers have shown that while
the label ‘schizophrenia’ may be associated with increased perceptions of dangerousness among the
general community, using the term ‘medical illness’ does not appear to be associated with increased
stigma (Jorm & Griffiths, 2009).
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LO 7.3 Historical and current conceptualisations

of psychotic disorders
Historical developments
The schizophrenia construct has a history of over 100 years and thus constitutes the most widely
researched of the psychotic disorders and, indeed, of most mental disorders. However, there is a long-
running debate within the scientific community regarding the validity of the diagnosis. This section
will trace the development of the schizophrenia construct from its initial identification in the era
of modern medicine to the present debate regarding its validity, and proposed changes regarding its
diagnosis.
Richard Bentall (2003), in his award-winning book Madness Explained, provides a compelling
history of the schizophrenia concept and its diagnosis. Bentall rightly gives particular prominence to
the roles of Kraepelin, Bleuler and Schneider. Emil Kraepelin, a professor of psychiatry in Munich,
Germany, in the late 1800s, identified the disorder ‘dementia praecox’, the early term for schizophrenia,
literally meaning ‘senility of the young’. The term derived from Kraepelin’s characterisation of
the disorder as one entailing a gradual deterioration of mental functioning with an early onset. He
paranoia differentiated dementia praecox from manic depression and from a separate illness of paranoia.
State The term schizophrenia was subsequently coined by the Swiss psychiatrist Eugen Bleuler,
characterised derived from the words schizein (meaning ‘to split’) and phren (meaning ‘mind’). This term was
by false beliefs
intended to capture what he believed to be the hallmark feature of the disorder: that is, the loosening
that one is
being harassed,
of the connections between thought structures, which he described metaphorically as a ‘breaking
persecuted or of associative threads’. In contrast to Kraepelin, Bleuler conceptualised manic depression and
unfairly treated, schizophrenia as occurring on a continuum rather than arguing for a categorical distinction between
which may these two diagnoses. The legacy of both of these pioneers of empirical research in psychosis can be
reach delusional seen in the modern diagnostic criteria for schizophrenia in the DSM-5, which include thought disorder
intensity. (disorganised speech) and a deterioration in functioning.
schizophrenia Kurt Schneider, another German professor of psychiatry based in Munich from the 1930s to 1950s,
argued that symptoms specific to schizophrenia—the so-called ‘first rank symptoms’—could be
Psychotic
disorder identified, and these symptoms maintained a privileged place up until the DSM-IV-TR. They included
characterised hearing voices arguing, hearing voices commenting on the individual’s actions and bizarre delusions
by two or more including passivity phenomena.
of the following:
delusions,
hallucinations, Ongoing controversies
disorganised
speech, grossly Despite attempts to improve the reliability of the diagnostic criteria for psychotic disorders in successive
disorganised editions of diagnostic systems such as the DSM, considerable scientific debate continues regarding the
or catatonic validity of these constructs. Those who are sceptical regarding these disorders argue that psychotic
behaviour, diagnoses represent arbitrarily defined categories (Bentall, 2003). Large-scale surveys suggest that
and negative psychotic experiences are normally distributed across the general population, with a small proportion
symptoms.
experiencing very severe and enduring symptoms that impact on their functioning in various important
domains of daily living. As such, there is a degree of arbitrariness in determining the cut-off between
those who supposedly have the disorder of schizophrenia (or other psychotic disorders) and those who
do not. Van Os, Linscott, Myin-Germeys, Delespaul, and Krabbendam (2009) reviewed 42 studies
published between 1950 and 2007 that investigated the prevalence of psychotic experiences, psychotic
symptoms and psychotic disorders. The authors concluded that the same demographic, genetic and
other risk factors predicted the occurrence of psychotic features of differing severity. In other words,
there was an aetiological continuity between people with subclinical and clinical manifestations
of psychotic symptoms. This dimensional approach to psychosis challenges the categorical view,
which maintains that a psychotic disorder is an ‘entity’ that ‘people get’ due to specific causes. The
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validity of the schizophrenia construct has also been challenged on the basis of the large overlap
between schizophrenia and other mental disorders, particularly depressive and bipolar disorders. This
suggests that to split depressive, bipolar and psychotic disorders into distinct domains does not fit with
clinical reality. As a result of these concerns, researchers such as Richard Bentall favour abandoning
the diagnosis of schizophrenia and instead adopting a dimensional approach to psychosis, including
a general dimension of psychosis in addition to specific dimensions including positive symptoms,
negative symptoms, disorganisation, mania and depression (Reininghaus, Priebe, & Bentall, 2013).
There is some evidence supporting such an approach (Reininghaus et al., 2016).
Finally, some clinical psychologists and psychiatrists have argued that the stigma associated
with the diagnosis of schizophrenia is associated with considerable emotional harm to the patient
and thus should be abandoned (Read, Haslam, Sayce, & Davies, 2006). However, others have
defended the schizophrenia concept, arguing, for instance, that the real issue related to stigma
is ignorance and fear in the general community rather than the concept of schizophrenia itself
(Lieberman & First, 2007). In Japan, an attempt to solve the stigma problem has been adopted
by replacing the term ‘schizophrenia’, translated as Seishin Bunretsu Byo (‘disease of split and
disorganised mind’), with Togo-Shicchou-Sho (‘a transient state of loosened association’) (Sato et
al., 2002). Unfortunately, a recent survey of media reports suggests this does not appear to have
reduced the prevalence of negative associations with the disorder (Koike, Yamaguchi, Ojio, Ohta,
& Ando, 2016).
LO 7.4 The epidemiology of psychotic disorders

Prevalence and age of onset
In comparison with disorders such as major depressive disorder and generalised anxiety disorder,
psychotic conditions have a relatively low prevalence. For example, the lifetime prevalence of
schizophrenia is approximately 1–2 per cent. Traditionally it was believed that, over the lifetime,
the prevalence of psychotic disorders was equal across genders. However, more recent evidence
suggests that for every three men who develop schizophrenia, two women will develop the disorder
(McGrath, 2007).
Epidemiologists have argued for many years, based on a series of studies conducted around the
world by the World Health Organization, that the prevalence of psychotic disorders is consistent
across Western industrialised and developing nations. This finding would suggest that the primary
causal factors are underlying genetic and biological processes, and that variations in environment play
a much smaller role in the pathway to the disorder. However, there has since been a reconsideration
of the view that psychotic disorders have an equal prevalence rate internationally with the finding
that there is considerable variation across countries and across specific settings within countries.
Specifically, there is now evidence of an increased prevalence rate of psychotic conditions among
migrants and in developed nations compared with developing nations, and a two-fold risk for those
born in urban compared to rural settings (McGrath, 2006).
The peak period of onset for psychotic disorders is during late adolescence and early adulthood.
Unfortunately, this is a period of life that corresponds with a range of developmental and social
challenges (e.g., leaving school and the transition to adulthood), which are substantially complicated
by the onset of symptoms and their associated effects.
The course of psychotic disorders

Psychotic disorders can be described in terms of specific phases, which include the premorbid phase,
the prodromal phase, the acute phase and the recovery phase, with the latter sometimes divided into
early and late recovery. Enduring, treatment-resistant forms of psychotic disorders also occur.
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THE PREMORBID PHASE

It is well known that the presence of risk factors prior to the onset of any mental health symptoms is
a marker of subsequent prognosis after the onset of psychosis. For example, viral infections in utero,
behavioural problems evident to school teachers and poor peer relationships in adolescence may be
subtle markers of risk for psychosis or may indicate a poorer prognosis (Larsen et al., 2004).
THE PRODROMAL PHASE

Researchers have recognised for many decades that the active symptoms of psychosis typically
develop in late adolescence and early adulthood, often following a period of gradual deterioration
in the individual’s mental state and functioning. This preliminary period of change, which precedes
the onset of delusions, hallucinations and other symptoms of psychosis, is often referred to as the
‘prodromal phase’. Researchers at the Personal Assessment and Crisis Evaluation (PACE) clinic in
Melbourne have pioneered a strategy for identifying a group of young people who are known to be
at very high risk of developing psychosis based on their having a close relative who has experienced
psychosis and their own experience of subtle, potentially indicative signs and symptoms (Yung et al.,
prodromal 2003), known as prodromal symptoms. The duration of the prodromal phase is known to be highly
symptoms variable across individual cases, ranging from absent to many years (Yung & McGorry, 1996). During
In schizophrenia, this phase, non-specific changes (i.e., changes that occur across a range of disorders and which are not
milder symptoms specific to psychotic conditions) in the individual’s mental state often emerge, such as depressed mood
prior to an acute
and symptoms of anxiety, which may lead to a deterioration in performance at school and with social
phase of the
disorder during relationships. Brief or attenuated psychotic symptoms are also common, such as very occasional and
which behaviours fleeting auditory hallucinations, or suspicious and paranoid thoughts that might fluctuate in intensity.
are unusual but However, even when these features are evident, the progression to the acute phase of psychosis is not
not yet psychotic. inevitable. While previous editions of the DSM included the diagnosis of ‘prodromal schizophrenia’,
the high prevalence of these features among adolescents led to questions regarding the validity of this
diagnosis and it was excluded from the DSM-IV (APA, 1994; Jackson, McGorry, & McKenzie, 1994).
Contemporary researchers prefer terms such as ‘at-risk mental state’ to reflect this lack of certainty
that the symptoms will necessarily result in schizophrenia.
THE ACUTE PHASE

For those individuals whose symptoms do intensify, the next stage is the ‘acute phase’. Acute psychotic
episodes are characterised by the emergence of persistent positive and negative symptoms that clearly
identify the condition as a psychotic disorder. Unfortunately, young people often suffer very prolonged
periods of acute psychosis without the disorder being accurately diagnosed or treated. Studies in the
1990s highlighted that, on average, there was a one-year delay between the onset of the acute phase
and effective treatment in Western industrialised countries (Loebel et al., 1992). This delay in seeking
treatment seemed to result partly from the individual withdrawing from others and partly from health
professionals failing to accurately diagnose the disorder, despite families often attempting to seek
help for their relative. Such a delay, known as the ‘duration of untreated psychosis’ (DUP), appears
to be related to the time taken to respond to treatment once it commences (Marshall et al., 2005).
That is, the longer the DUP, the longer the patient’s symptoms take to improve with treatment. This
finding has encouraged clinicians and researchers around the world to improve the early detection
and intervention for both acute psychosis and those with an ‘at-risk mental state’, an approach that
has been pioneered at the EPPIC in Melbourne under the leadership of Patrick McGorry (McGorry,
Edwards, Mihalopoulos, Harrigan, & Jackson, 1996). In New Zealand, early psychosis services have
been developed by District Health Boards across both the North and South Islands.
THE EARLY RECOVERY PHASE

Once the acute phase develops, the individual may experience marked fear, confusion and agitation.
In clinical settings it is important to differentiate acute psychosis from other conditions, such as
intoxication. Thus routine medical investigations should be carried out in order to rule out medical
conditions associated with psychotic symptoms. Fortunately, in the majority of cases, symptoms will
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slowly begin to improve over several months once

treatment commences. During this early recovery
phase, problems with depression and social anxiety
may emerge for the first time as the person begins to
reflect on their diagnosis and its significance for their
future (Birchwood, Mason, Macmillan, & Healy,
1993). In addition, some patients will be traumatised
by their experience of psychosis (Morrison, Frame,
& Larkin, 2003; Mueser, Lu, Rosenberg, & Wolfe,
2010). Psychologists and psychiatrists have observed
that as the symptoms improve, patients have a variety
SHUTTERSTOCK.COM
of recovery styles in reaction to the experience
of the disorder (Drayton, Birchwood, & Trower,
1998). For example, some patients appear to respond
defensively to their experience of psychosis and
strive to seal over the details, while others appear The expression of empathy and warmth are particularly important in
to engage in an active effort to make sense of their the acute phase of psychosis since affected individuals frequently
experiences and understand their vulnerability. experience high levels of fear and confusion.
Improved recovery seems to be associated with the
latter style (Thompson, McGorry, & Harrigan, 2003).
The acute phase and the commencement of treatment are often highly distressing for family
members, who may have endured many months of emerging mental health problems in their unwell
relative. Anxiety, stress and a sense of loss are common experiences for family members once
a diagnosis is received and treatment commences. The course of psychosis can be uncertain, so
family members may often remain distressed and worried even when initial treatment is effective.
This highlights the fact that family members can also benefit from education about the disorder and
ongoing support (Jansen, Gleeson, & Cotton, 2015).
THE LATE RECOVERY PHASE

Even when recovery from the acute symptoms progresses well, further challenges arise in the late
recovery phase. These challenges include re-integrating into social, recreational and vocational
pursuits. Unfortunately, high unemployment rates exist for individuals with psychotic disorders
(Killackey, Jackson, Gleeson, Hickie, & McGorry, 2006). In addition, the risk of recurrence in
the form of further episodes of psychosis remains high during the first 2–5 years after treatment
is commenced. In approximately 80–90 per cent of cases, relapse will occur during this period
(Robinson et al., 1999). Recurrence is associated with discontinuation of antipsychotic medication, expressed
the use of cannabis and amphetamines, poorer premorbid adjustment and by conflictual interpersonal emotion (EE)
relationships, referred to by researchers as high expressed emotion (EE) (Alvarez-Jimenez et al., Family interaction
2012). EE is typically measured using standardised methods of observing and rating patterns of style in which
family members
family interactions, and comprises three components—namely, high levels of criticism, hostility and
are overly
emotional over-involvement (i.e., the tendency to be over-concerned, over-protective or overly self- protective and
sacrificing in caring for the individual). self-sacrificing
EE is now a well-established predictor of psychotic relapse. Studies have repeatedly demonstrated towards the
that patients with schizophrenia who return home to high-EE families after hospitalisation for a psychotic person with a
episode are 2–3 times more likely to relapse during the following year compared to patients who return psychological
to low-EE families. Some studies have also found that the adverse impact of high-EE families can disorder while
also expressing
be lowered through medication and a reduction in face-to-face contact between family members. For
high levels of
instance, in a famous study by Vaughn and Leff (1976), which instigated much of the interest in EE in criticism and
schizophrenia, 128 patients with schizophrenia were followed up for a nine-month period after discharge hostility; this may
from hospital. It was found that 51 per cent of patients who returned to high-EE homes relapsed within contribute to the
nine months after discharge compared to 13 per cent of patients who returned to low-EE families. person’s relapse.
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However, the relapse rates of patients in high-EE families were reduced if they had less than 35 hours
per week of face-to-face contact with family members (28% of whom relapsed compared to 69% of
those with more than 35 hours of contact) and if they were on medication. For example, 92 per cent
of patients in high-EE families with high amounts of face-to-face contact and no medication relapsed
compared with 53 per cent of patients in high-EE families with high amounts of face-to-face contact and
who were on medication. The findings of this study (which are displayed in Figure 7.1) highlight that
some families and their relatives may benefit from support in effective ways to communicate.
High EE families
Low EE families
13% 51%
Low contact High contact

28% 69%
Drugs No drugs Drugs No drugs Drugs No drugs

12% 15% 15% 42% 53% 92%
FIGURE 7.1 The percentage of patients with schizophrenia who relapsed in the nine-month period following
their discharge from hospital depending on whether they returned home to high or low expressed emotion
(EE) families, had high or low amounts of contact with family members, and were taking medication or not.
Source: From Vaughn, C., & Leff, J. P. (1976). The influence of family and social factors on the course of psychiatric illness. British Journal of
Psychiatry,129, 125–137, The Royal College of Psychiatrists.
ENDURING PSYCHOSIS
Unfortunately, a sizeable minority of patients will suffer from more severe and enduring psychosis.
The pattern of symptoms varies in this group but can include periods of very acute symptoms that
might require periods of hospitalisation, interspersed by continuing symptoms that do not fully
disappear. Other individuals may gain relief from the positive symptoms of psychosis but suffer from
enduring negative symptoms that can also profoundly inhibit the extent of recovery.
More severe and persisting forms of psychosis are known to be associated with an earlier and
more gradual onset of symptoms. Co-occurring problems such as substance abuse and longstanding
personality traits, which might compromise the individual’s capacity to cope with stress, are also
recognised risk factors for a more complicated course of the disorder. Long-term enduring forms
of psychosis have also been associated with increased problems in cognitive processes, especially
attention, memory and executive functioning (i.e., planning and problem-solving abilities).
This chronic pattern of psychosis can lead to other major problems in living. For example, the
children of individuals with severe enduring or recurring psychosis may be at risk of suffering from
periods of inadvertent neglect as a result of their parents’ inability to effectively care for their material
or emotional wellbeing during periods of active psychosis. Unfortunately, the needs of children in this
predicament have only relatively recently begun to receive adequate attention, so much more research
is needed to develop effective children’s programs (Reupert et al., 2012). Other issues for patients with
a chronic psychosis can include problems with maintaining adequate housing, poverty, physical health
complications and the long-term side effects of antipsychotic medications.
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However, many contemporary researchers have challenged Kraepelin’s assumption that patients
with enduring psychosis follow a dementia-like progressive deterioration (Menezes, Arenovich, &
Zipursky, 2006). For example, Harding, Zubin, and Strauss (1992) conducted a long-term follow-up
study in Vermont, USA, which found that approximately half of the patients significantly improved and/
or recovered from schizophrenia or a first episode of psychosis when followed up over several decades.
LO 7.5 The aetiology of psychosis adoption study

Study of the
heritability of
Despite more than 100 years of research, much remains unknown about the causes of psychosis. a disorder by
There is interest among researchers in a wide variety of possible causal factors for psychotic disorders, finding adopted
ranging from genetic factors to specific environmental problems. This wide array of factors has often people with a
disorder and then
been subsumed under the broad aetiological model known as the diathesis-stress model, which was
determining the
first espoused by Zubin and Spring (1977). The model assumes that a psychotic episode occurs when a prevalence of the
triggering event interacts with an underlying vulnerability and overwhelms the coping resources of the disorder among
individual. Zubin and Spring further maintained that vulnerability to psychosis can include biological their biological
and psychosocial factors. Triggering events can also theoretically be biological or psychosocial. Many and adoptive
of the possible causal factors associated with psychotic disorders identified by research are not specific relatives in order
to psychosis but are instead associated with a broad range of mental health problems. This highlights to separate
contributing
the fact that there remains much that is not understood about the specific pathways to psychosis.
genetic
factors from
Vulnerability factors: biological environmental
factors.
Research aimed at characterising the biological vulnerabilities that place an individual at heightened risk
for psychosis extends across a vast range of risk factors including genetics, prenatal and birth complications, family study
Study of the
a wide variety of biochemical factors and structural brain problems (Lieberman et al., 2001).
heritability of a
disorder involving
GENETIC BASIS
identifying people
A large body of research—including family, twin and adoption studies—supports the existence of a with a particular
genetic basis for schizophrenia (Read, Potter, & Gurling, 1992). Family studies indicate that the risk
disorder and
of developing schizophrenia increases as the degree of genetic relatedness with an affected individual people without
(referred to as the ‘proband’) increases. Thus the percentage of individuals with schizophrenia at differing the disorder and
degrees of relationship with the proband are as follows: 1 per cent for spouses (no genetic relationship), then determining
2.8 per cent for grandchildren, 7.3 per cent for siblings, 9.4 per cent for children with one affected the disorder’s
frequency within
parent and 46.3 per cent for children with both parents affected. In twin studies, the concordance rate
each person’s
for schizophrenia between monozygotic twins (who have the same genes) has been found to be higher family.
than that for dizygotic twins (who, on average, have only 50 per cent of their genes in common), again
supporting a genetic contribution. However, family and twin studies cannot provide definitive evidence concordance rate
of a genetic role since the higher rates of schizophrenia among family members of patients with the Probability that
disorder and the higher number of both twins having the condition among monozygotic compared with both members
of a twin pair will
dizygotic twins may be due to their shared environment. In the case of family studies, for example, an
develop the same
individual who has two parents with schizophrenia may be at heightened risk of developing the disorder disorder.
compared with an individual who has only one affected parent, since s/he is likely to have experienced a
more disturbed upbringing. In twin studies, monozygotic twins may be treated by others more similarly monozygotic
than dizygotic twins due to their greater similarity. twins
Adoption studies offer the strongest support for familial genetic factors because with this approach genes Identical twins
who share 100
and the environment are more clearly separated than in family and twin studies. In these studies, children
per cent of their
whose parents had schizophrenia but who were reared by parents without schizophrenia from infancy are genes because
compared with adopted children who have no biological parents with schizophrenia. It has been found that they developed
adopted children who had a biological parent (mother or father) with schizophrenia have a higher rate of from a single
the disorder than adopted children whose biological parents did not have the disorder (Read et al., 1992). fertilised egg.
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dizygotic twins Geneticists have also investigated the possibility that rare and genetic structural variations that
Non-identical arise in individual cases de novo, or that have arisen recently in individual families, may increase the
twins who share risk for schizophrenia (Levinson et al., 2011). Rare microdeletions (i.e., the loss of a very small piece
with each other,
of a chromosome), or replications of genes that are known to play a role in neurodevelopment, have
on average,
50 per cent been shown to occur at significantly higher rates in individuals diagnosed with psychosis compared to
of their genes a control group matched in terms of racial ancestry (Levinson et al., 2011; Walsh et al., 2008).
because they Researchers continue to identity new possible alleles (i.e., a specific variant of a gene at a particular
developed from location on a chromosome) that contribute to the risk of schizophrenia. One genome-wide study
two separate found 83 sites that had not been previously identified (Ripke et al., 2014). The establishment of new
fertilised eggs methods to identify the role of candidate genes in the development of schizophrenia has progressed at
(comparable to
a rapid pace in recent years. One such example has been the discovery by researchers of the specific
non-twin siblings).
role of a gene on chromosome 6 previously known to express a molecule known as complement
component 4, which is known to be important to the immune system. In a recent landmark study,
scientists showed through a novel genetic method that this molecule is also important in reducing
neural connections (so-called neural pruning) in adolescence, which is known to be associated with
the onset of schizophrenia when this process of pruning goes awry (Sekar et al., 2016).
GENE–ENVIRONMENT INTERACTIONS
Critics of traditional genetics research in psychosis have argued that the interaction between genes and
exposure to environmental factors has been given insufficient prominence in the research (Bentall,
2003). Indeed, in recent years increased attention has been given by researchers to investigating how
environmental factors can increase the risk that a genetic vulnerability for psychosis will actually
be expressed (van Os, Rutten, & Poulton, 2008). In other words, schizophrenia may develop when
specific genes are activated through exposure to certain environments. This research has focused
on specific environmental exposure during certain phases of development—including during foetal
development (e.g., exposure to maternal infection), early childhood (e.g., exposure to trauma), middle
childhood and adolescence (e.g., exposure to illicit substances)—and wider social and environment
factors (e.g., living in an urban environment).
One factor that might be influenced by gene–environment interactions is a high level of reactivity
to stress in daily life, detected by intensive repeated measurements of psychological and physiological
changes over the course of hours or days. Although reactivity to stress is not a symptom of psychosis,
it is known to increase the risk for the subsequent onset of psychosis. Thus, certain gene–environment
interactions may give rise to an increased risk for psychosis but not necessarily to specific symptoms
or diagnoses (van Os, Kenis, & Rutten, 2010).
NEUROTRANSMITTERS
neurotransmitters Much research has focused on abnormalities in certain neurotransmitters, such as dopamine, noradrenaline
Biochemicals and serotonin, as contributing to psychosis. The dopamine hypothesis of schizophrenia states that the
released from a disorder is associated with excessive dopaminergic function in the central nervous system. This hypothesis
sending neuron evolved from two main sources of evidence: (a) drugs that reduce dopamine activity were found to be
to a receiving effective in treating the symptoms of schizophrenia, and (b) amphetamines, which cause the release of
neuron so as
dopamine, can produce symptoms of schizophrenia (Leuner & Muller, 2006). While researchers initially
to transmit
messages in the postulated that individuals with schizophrenia have excessively high levels of dopamine, several findings
brain and nervous failed to support this contention. For instance, homovanillic acid, the major metabolite (breakdown product)
system. of dopamine, is not found in greater amounts in individuals with schizophrenia compared to healthy
individuals (Sumiyoshi et al., 1999). Thus, the dopamine hypothesis was revised such that schizophrenia
was proposed to be associated with excessive numbers of or oversensitive dopamine receptors, rather than
high levels of dopamine. Subsequent work suggests that excessive dopaminergic activity is more related to
the positive symptoms of schizophrenia (e.g., antipsychotics that reduce dopamine activity lessen positive
symptoms but have little or no effect on negative symptoms). Thus, while dopamine has been the most
widely investigated neurotransmitter in schizophrenia research, it is likely that multiple neurotransmitters
are involved given the complex array of disturbances associated with schizophrenia.
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BRAIN STRUCTURE enlarged

Numerous abnormalities in brain structure have also been investigated as possibly contributing to ventricles
psychotic symptoms. The most consistent finding has been that of enlarged ventricles (the spaces Fluid-filled spaces
in the brain
containing cerebrospinal fluid), which indicates a loss of brain tissue (Pantelis et al., 2005). Researchers
that are larger
have turned their attention to investigating possible tissue loss in specific brain regions. For example, than normal
researchers have found evidence that negative symptoms (e.g., a lack of speech, affect and behaviour) and suggest a
are closely associated with a loss of grey and white matter in the brain, including a loss of tissue deterioration in
within regions of the pre-frontal cortex (Stahl & Buckley, 2007). The finding that regions of the pre- brain tissue.
frontal cortex are relevant for negative symptoms is perhaps not surprising given that this part of the
pre-frontal cortex
brain is associated with executive functioning—that is, cognitive abilities related to the planning, Region at the
initiation and monitoring of goal-directed behaviour. front of the
Christos Pantelis at the Melbourne Neuropsychiatry Centre and his team have led research brain important
examining structural brain abnormalities in psychosis using magnetic resonance imaging (MRI) in language,
(Pantelis et al., 2005). These studies typically include patients at ultra-high risk of developing emotional
psychosis, patients experiencing first acute episodes, patients with longer-term forms of psychosis and expression, the
healthy control groups matched on variables such as age and gender. By including a group of ultra- planning and
production of
high-risk individuals, this research enables the identification of factors that characterise those who
new ideas, and
go on to develop psychosis versus those who do not and thus highlights factors that may be specific the mediation
to the development of schizophrenia rather than general psychological disturbance. The comparison of social
between patients experiencing first acute episodes and those with longer-term psychosis helps in the interactions.
identification of factors that may be associated with vulnerability to the disorder versus those that
magnetic
may be associated with the disorder’s progression and/or its treatment with medication. Among this
resonance
research group’s findings is evidence of certain non-genetic structural brain abnormalities. Specifically,
imaging (MRI)
compared with the ultra-high-risk group who have a family history of schizophrenia, those without Method of
a family history were found to have significantly smaller volumes of the left hippocampus (Wood et measuring both
al., 2008). Thus, early neurodevelopmental damage (occurring during pregnancy, for example) may brain structure
be a key vulnerability factor for these individuals rather than a genetic predisposition. Patients at high and function
risk for psychosis who subsequently suffered a first episode of psychosis have also been found to have through the
significantly smaller hippocampal volumes (Pantelis et al., 2005). In summary, structural changes construction of a
in the hippocampus appear to predate the onset of psychosis (at least among those without a family magnetic field that
affects hydrogen
history of psychosis) and may worsen over the course of the illness.
atoms in the brain,
emitting signals
NEUROENDOCRINE FUNCTIONING that a computer
Another biological abnormality relevant to psychosis is the hypothalamic-pituitary-adrenal (HPA) then records and
axis. The HPA axis is an important biological system in the physiological response to stress. The uses to produce a
three-dimensional
hypothalamus receives neural signals related to stress, and in response releases stress hormones
image of the
(including corticotropin), which communicate with the pituitary gland. This triggers the release of the brain.
andrenocorticotropin hormone, which then enters the bloodstream. In turn, this triggers the release
of glucocorticoids from the adrenal gland, which enables the body to mount a physiological reaction hypothalamic-
in order to cope with stress—a useful and adaptive response in the short term (Phillips et al., 2006). pituitary-adrenal
However, over the long term, over-activation of this stress response is known to lead to negative (HPA) axis
impacts upon the central nervous system including the hippocampus. Three
components
It has been hypothesised that psychosis is related to disturbances in the HPA axis, although these
of the
are not clearly understood. Two major hypotheses have been put forward to explain these changes in neuroendocrine
the function of the HPA axis: (1) that environmental factors (such as exposure to cannabis or high system that work
levels of conflict in relationships) affect the HPA axis; or (2) that the genes associated with the risk together in a
for schizophrenia contribute to dysfunctional HPA axis activity (Aiello, Horowitz, Hepgul, Pariante, feedback system
& Mondelli, 2012). A related puzzle for researchers is how HPA axis dysfunction leads to the onset interconnected
of psychosis. Perhaps altered HPA axis activity triggers the expression of genes affecting brain with the brain’s
limbic system and
development, or perhaps exposure to stress (and hence altered HPA axis activity) changes the activity
cerebral cortex.
of brain neurotransmitters such as dopamine (Aiello et al., 2012).
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Vulnerability factors: psychosocial

Researchers have become increasingly interested in the role of psychosocial factors in increasing the
vulnerability for psychosis. Social factors include residing in an urban environment, migration, being
socially excluded and experiences of childhood abuse (McGrath, 2007; Read, van Os, Morrison, &
Ross, 2005; van Os, Hanssen, Bak, Bijl, & Vollebergh, 2003). Further evidence supporting the view that
environmental factors can influence the development of psychosis can be gleaned from data on the rates of
psychosis in the Māori population and in Indigenous Australians. In New Zealand, Kake, Arnold, and Ellis
(2008) reported that the annual prevalence rates of schizophrenia for Māori individuals were approximately
three times the non-Māori rate (with the latter similar to rates found in the general Australian population).
This finding is consistent with the role of accumulated adverse social and environmental circumstances,
such as racial discrimination, in substantially increasing the risk of psychosis. In the Indigenous Australian
population, very high levels of psychological distress related to marginalisation, dispossession, exposure to
violence, racism and other forms of chronic stress pose a major risk to health and wellbeing (Cunningham
& Paradies, 2012). In line with the New Zealand data, the rates of hospitalisation for schizophrenia
spectrum disorders among Indigenous Australians in 2005–2006 were 2.7 times higher for males and 2.5
times higher for females than expected, based on data from the rest of the Australian population (Australian
Bureau of Statistics & Australian Institute of Health and Welfare, 2008). Research on how exposure to
adverse social factors early in life may increase the risk of psychosis later in life is in its infancy, but
evidence is accumulating that stress has long-term impacts on biological systems, such as the HPA
axis discussed above, which are important in the pathway to psychosis (Holtzman et al., 2013).
Cognitive models propose that these early experiences (such as exposure to stress and trauma) result
in the formation of dysfunctional cognitions, which in turn trigger psychotic symptoms (Bentall, 2006;
Morrison, 2001). These approaches highlight the role of cognitive factors in increasing vulnerability to
psychosis. Morrison (2001) has proposed a cognitive model in understanding the development of
positive psychotic symptoms such as delusions and hallucinations. At the core of this model is the
notion that psychosis entails culturally unacceptable interpretations of ‘intrusions into awareness’, which
are defined as thoughts, images or impulses that intrude upon the individual’s consciousness and are
uncontrollable. Intrusions into awareness are potentially experienced by anyone and are themselves not an
indication of psychosis. For instance, one study found that 82 per cent of bereaved older adults experienced
hallucinations (e.g., hearing the deceased’s voice) in the month following bereavement. According to
Morrison (2001), it is the manner in which such intrusions into awareness are interpreted that is central
in the development of psychosis. Examples of culturally unacceptable interpretations of intrusions into
awareness include a woman interpreting intrusive thoughts (e.g., ‘I hate my child’) as evidence that
thoughts are being inserted into her mind by an evil force; interpreting intrusive impulses (e.g., the impulse
to hit one’s child) as evidence of external control over her body; and interpreting auditory hallucinations
(e.g., a voice saying ‘hit her’) as evidence that the devil is trying to make her hurt her child. In contrast,
a non-psychotic interpretation of such intrusions into awareness would be ‘That was a strange thought/
impulse/image. I must be over-tired.’ While other psychological disorders entail distorted interpretations,
it is the culturally unacceptable nature of these distortions that is characteristic of psychosis. For example,
an individual with obsessive-compulsive disorder might experience the obsessional thought ‘I hate my
child’ and interpret this as a need to engage in some kind of ritual to prevent harm coming to his/her child
but would not interpret the thought as a sign of thought insertion by an evil force.
Morrison (2001) proposes that these culturally unacceptable interpretations are a result of faulty
knowledge about the self (e.g., ‘I am a bad person if I have thoughts of hating my child’, which makes
the person prone to misattributing the thought to an external force rather than seeing it as a product of
her own mind), and faulty knowledge about others (e.g., ‘Adults cannot be trusted around children’).
Such faulty knowledge is in turn theorised to be the product of life experiences (e.g., having been
sexually, physically or emotionally abused as a child).
The final aspect of Morrison’s (2001) model asserts that interpreting intrusions into awareness in
a culturally unacceptable and typically distressing manner triggers responses that serve to increase the
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likelihood of further intrusions into awareness. These counterproductive responses include disturbances
in mood (e.g., anxiety) and physiological arousal (e.g., a lack of sleep), which research suggests can
intensify intrusive thoughts, images and impulses. These responses also include behaviours such as
those designed to keep the individual or others safe (e.g., a mother avoiding being alone with her child
so that she fails to disconfirm the false belief that she might hurt her child). Other unhelpful responses
include a range of cognitive changes such as selective attention (e.g., the mother might constantly
be on the lookout for any negative thoughts regarding her child, thereby increasing the likelihood of
noticing such thoughts) and attempting to suppress intrusive thoughts, images and impulses by pushing
them out of one’s mind. Thought suppression, however, is known to actually increase the frequency of
intrusive thoughts—as demonstrated in the exercise developed by Salkovskis and Kirk (1989) in which
the individual is asked to not think about a pink rabbit, which results in the individual immediately
thinking about a pink rabbit. The full model proposed by Morrison (2001) is shown in Figure 7.2.
Intrusions into awareness

(intrusive thoughts, images or impulses)
the intrusive thought ‘I hate my child’
intrusive auditory imagery of a voice saying
‘hit her’
the intrusive impulse to hit one’s child
Culturally unacceptable interpretations of intrusions

into awareness
‘The devil is putting thoughts into my mind’
‘The devil is telling me to hurt my child’
‘The devil is trying to take control of my body’
Mood and physiological Cognitive and

disturbance behavioural responses
anxiety, guilt, arousal, safety behaviours such

poor sleep as not being alone with
child, selective attention
to unwanted thoughts,
thought suppression
Faulty knowledge regarding the self and others

the self: ‘I am a bad person if I have thoughts of hating
my child’
the world: ‘Adults cannot be trusted around children’
Life experiences
childhood sexual abuse
strict religious upbringing
FIGURE 7.2 The cognitive model of psychosis developed by Morrison (2001) using as an example the case
of a mother distressed by fears of hurting her child
Source: From Morrison, A. P. (2001). The interpretation of intrusions in psychosis: An integrative approach to hallucinations and delusions.
Behavioural and Cognitive Psychotherapy, 29, 257–276, Cambridge University Press.
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Triggering factors
Among vulnerable individuals, the occurrence of certain events will trigger psychosis. Triggering
events can entail biological processes (e.g., using illicit substances such as cannabis), psychosocial
processes (e.g., stressful life events) or an interaction between the two (e.g., disturbances in hormonal
functioning induced by stress) (Nuechterlein et al., 1992; Tarrier & Turpin, 1992). In support of the
latter, Pantelis and colleagues (2005) found that patients assessed as being at high risk of developing
psychosis who later in fact did go on to develop psychosis had significantly larger volumes of the
pituitary pituitary (indicating higher levels of stress hormones) compared with high-risk patients who did not
Major endocrine go on to develop psychosis.
gland that In terms of psychosocial factors, both retrospective and prospective studies have found that stressful
produces the
life events (such as exposure to negative interpersonal dynamics as characterised by the expressed
largest number
of different
emotion construct, financial strain or health problems) occur significantly more often in the weeks
hormones and preceding the onset of psychotic episodes. In one such prospective study, Ventura, Nuechterlein,
controls the Lukoff, and Hardesty (1989) asked patients with schizophrenia to record any life events at monthly
secretions of intervals for one year. It was found that the number of life events in the month preceding the onset of
other endocrine a psychotic episode was significantly higher than in the other months, as well as being significantly
glands. higher than the number of life events experienced by patients who did not relapse. More recent
studies have found more complex relationships between triggering factors and genetic predisposition
(Walder, Faraone, Glatt, Tsuang, & Seidman, 2014).
CASE STUDY: THE ROLE OF STRESS AND TRAUMA IN PSYCHOSIS ONSET

Amanda, a 28-year-old single woman, reported a two-year history of persistent, daily auditory hallucinations, which had
a sudden onset when she discovered that her close friend had been seriously physically assaulted by her husband. She
lived with her mother and received a government sickness benefit due to her psychotic illness. Amanda was referred to a
psychologist by her case worker as her hallucinations had not resolved even though she had been taking her medication
and had experienced a gradual improvement in her social functioning. Her hallucinations were the primary barrier to her
returning to work in the hospitality industry.
At the psychological assessment, Amanda reported that her persistent auditory hallucinations consisted of her mother
screaming. Amanda reported no mental health problems prior to being told of the assault on her friend. She described the
acute phase of her psychotic episode in which she believed that her mother, who was travelling overseas at the time, was
being tortured and her screams were being telepathically communicated to her. Amanda had been extremely distressed
for her mother, believing that her mother was being coerced by her torturers into acting normally when she spoke to her
by telephone. Her mother’s return from overseas reduced her distress regarding her mother’s safety but, despite gaining
good insight into her psychosis, her auditory hallucinations continued to occur for periods of several hours per day.
Amanda also reported to the psychologist that she had witnessed her mother being severely physically abused by her
father on many occasions until her parents separated when Amanda was eight years old. Amanda had regular contact
with her father after the separation and she described a warm, loving relationship with him throughout her childhood.
Amanda showed little emotion when reporting the violence towards her mother and was eager to move on to other topics.
Cognitive behavioural theories of both posttraumatic stress disorder and psychosis were used to build a shared
understanding between Amanda and her psychologist of the development and maintenance of Amanda’s hallucinations.
This began with a gentle challenge to Amanda’s psychological avoidance of the memories of the violence from her
father by discussing her feelings regarding the assault on her friend and comparing these feelings to how she felt as a
child. In particular, Amanda described feelings of powerlessness in her lack of ability to help her friend and, also, anger
towards the perpetrator, her friend’s husband. Amanda and her psychologist agreed that the hallucinations were similar
to posttraumatic flashbacks of the sounds she heard when her father was abusing her mother. She had not previously
connected her current hallucinations with her memories from the past. Amanda’s limited emotional connection with the
abuse she witnessed as a child was seen as a way of protecting herself from these painful feelings: she loved her father
but had to witness him assaulting her mother, so she disconnected her emotions around the abuse from conscious
awareness (a process called dissociation).
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Cognitive restructuring was used to assist her to change her view of her hallucinations from signs of ‘madness’ to a
normal response to trauma and as a manifestation of distress for her mother and friend. This was done via psychoeducation
about posttraumatic flashbacks and delays in response to trauma. Treatment also entailed techniques developed in the
psychosis field. These included experimenting with white noise as a way to start and stop hallucinations. Many people
who suffer from hallucinations find that their hallucination can be triggered by white noise such as a vacuum cleaner.
Conversely, when the white noise is turned off the hallucinations often stop. Amanda found her hallucinations could be
‘turned on’ and ‘turned off’ by turning on and off white noise and this enabled her to discover she had some control
over her hallucinations. Use of these approaches resulted in a marked reduction in the frequency and intensity of
the hallucinations. By the end of treatment, the distress caused by her hallucinations was reported to be minimal and
Amanda began preparations to return to work.
Symptom-specific aetiological factors: hallucinations

Doubts concerning the validity of diagnoses such as schizophrenia have provided impetus for
researchers to focus their investigations at the level of individual symptoms (rather than disorders),
with the aim of understanding biological and psychological processes that might account for their
aetiology and persistence (Bentall, 2006). Hallucinations research is one example, in which patients
with hallucinations are compared with non-hallucinating patients with psychosis, and other comparison
groups such as depressed patients and healthy controls who are usually matched on demographic
variables (e.g., age and gender) with the target group.
This extensive field of psychological research has produced several theories concerning the
aetiology of hallucinations, which were reviewed by Seal, Aleman, and McGuire (2004) with
reference to auditory hallucinations (the most common among patients with schizophrenia). These
theories attempt to account for the process by which self-generated mental events are transformed into
the experience of perceived sound, usually speech.
The first and oldest theory—the dysfunction in auditory imagery theory—states that individuals
prone to auditory hallucinations are able to imagine particularly vivid sounds. This auditory imagery
is so lifelike that the individual mistakes it for an actual sound. Yet research testing this theory has
been generally unsupportive, with one study finding that hallucinating patients with schizophrenia
actually experienced less vivid imagery than non-hallucinating patients. This led to the refined
auditory imagery theory, which suggests that hallucinating individuals typically experience deficits
in the vividness of their auditory imagery so that when they do experience unusually vivid auditory
imagery, this is more likely to be confused for the actual perception of sound. Again, however, this
theory has received minimal support.
In contrast, Seal et al. (2004) report evidence to support a second theory, which proposes that
auditory hallucinations involve a dysfunction in verbal self-monitoring. According to this theory,
auditory hallucinations stem from a breakdown in the individual’s ability to notice his/her intentions
to act (e.g., the intention to make internal speech). As a result, the individual confuses internally
generated actions (e.g., making internal speech) with externally generated actions (e.g., someone else
speaking). In support of this theory, research has found that hallucinating patients are more likely than
non-hallucinating patients to misattribute their own speech to an external source when their speech
is distorted in some way (e.g., the pitch is altered), suggesting that they are failing to notice their
intention to speak.
Bentall and Fernyhough (2008) developed a model of hallucinations that integrates cognitive
deficits (such as poor verbal self-monitoring) with dysfunctional beliefs (of the type identified in
Morrison’s [2001] model described in Figure 7.2) and environmental adversity (specifically,
childhood trauma). More specifically, this model proposes that trauma, such as early childhood
adversity, may lead to increased susceptibility to intrusive and unwanted cognitive activity and that
poor self-monitoring ability may result in these trauma-related cognitions being misattributed to an
external source, giving rise to the subjective experience of a voice. The individual may use unhelpful
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strategies, such as thought suppression, in an attempt to reduce the hallucinatory experience, which,
however, inadvertently maintains the experience.
Symptom-specific aetiological factors: delusions

Psychological processes in delusions have also been extensively investigated. Garety and colleagues
(2005), for example, have studied the tendency of patients with delusions to make cognitive errors
(such as a tendency to rapidly jump to a conclusion based on relatively small amounts of information)
in tasks of general reasoning. In one of these tasks, participants were shown the images of two jars
containing yellow and black beads on a computer screen. In one jar the number of black beads
outweighed the number of yellow beads, while in the second jar this ratio was reversed. The jars were
then hidden from view and participants were permitted to request as many beads as they required in
order to complete their task of deciding from which of the two jars the beads were drawn. Patients
with delusions, and those recently recovered from delusions, were found to jump to a conclusion
regarding the jar from which the beads were drawn based on relatively few beads compared with
healthy controls. In other words, they drew conclusions with far less available information compared
to others. Emotional states can also contribute to the tendency to make cognitive errors, with anxiety
found to be associated with a higher degree of certainty regarding the validity of delusional beliefs
(Garety et al., 2005).
In another line of investigation, Bentall, Corcoran, Howard, Blackwood, and Kinderman (2001)
have led research focusing on the explanations or attributions formed by people prone to delusions when
they are faced with negative life events. Results from this research demonstrate that individuals prone
to delusions tend to blame other people, rather than themselves or random misfortune, in explaining
the causes of negative events (e.g., attributing failure on an exam to someone trying to prevent the
individual from succeeding rather than a lack of preparation). While this style of attribution assists
people to protect their self-esteem by avoiding self-blame, it may contribute to delusional thinking
because it creates a bias towards suspiciousness of others.
Memory may also play a role in delusions. For example, when patients with a diagnosis of
schizophrenia with current delusions were compared on a word memory task with patients without
current delusions, the delusions group were found to recall twice as many false memories (words that
were never presented), known as false positives. There were no differences on correct words recalled
by the two groups. This higher rate of false positives has been explained by the so-called ‘spreading
activation’ hypothesis, which predicts that in delusion-prone individuals there is a greater spread of
activation in cognitive association networks in response to stimuli. This broader activation creates a
greater likelihood of false positives in the recall process (Bhatt, Laws, & McKenna, 2010). Delusions
may therefore be reinforced by memories of experiences that never actually occurred.
Symptom-specific aetiological factors: thought disorder

For many years, psychologists have been developing theoretical models and researching factors
associated with thought disorder. Researchers have found associations between the severity of
thought disorder (as reflected in disordered speech) and deficits in certain cognitive processes.
More specifically, there is evidence of problems in the storage of information among patients with
schizophrenia, which may in turn give rise to disordered speech (Leeson, Laws, & McKenna, 2006).
Rossell and David (2006) conducted a study that provided evidence of a deficit in the information-
storage system of patients with schizophrenia. They recruited 32 patients who had been diagnosed
with schizophrenia and 32 healthy controls who were matched with the patient group by age and
years of education. The participants were given a word-association task that consisted of a key word
(e.g., ‘fog’) presented with four other words: a word related in meaning to the key word (e.g., ‘mist’),
a word similar but unrelated in meaning to the key word (e.g., ‘steam’) and two words related to each
other but unrelated to the key word (e.g., ‘bolt’ and ‘lock’). The participant’s task was to identify
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the word related in meaning to the key word. Thirty key words were presented in total, consisting of
15 words that are in frequent use in the English language and 15 low-frequency words. It was found
that the control group made a significantly higher number of accurate responses compared to the
patients with schizophrenia. In addition, both groups provided significantly more accurate responses
to the high-frequency words compared with the low-frequency words. However, the main finding
was that the poorer performance on low-frequency versus high-frequency words was more evident
in the patient group compared to the control group. Rossell and David (2006) interpreted this finding
as evidence of dysfunction in the information-storage system among patients with schizophrenia. In
other words, the normal connections between related terms that are stored closely together in memory
were somehow impaired in the patient group, leading to retrieval problems. This is based on the idea
that damage to the information-storage system will affect those terms with weaker connections first
(i.e., the low-frequency items).
Other investigators have suggested that thought disorder is more apparent in patients with
schizophrenia during speech regarding topics of heightened emotional salience compared with
discussions on more neutral topics. This finding suggests that emotional distress may contribute to
disrupted thought processes, similar to the research on delusional thinking (Haddock, Wolfenden,
Lowens, Tarrier, & Bentall, 1995).
LO 7.6 The treatment of psychotic disorders

The emergence of the diathesis-stress model of psychosis in the late 1970s has shaped treatment
frameworks towards a biopsychosocial or integrated approach, involving assessment and intervention
across biological, psychological and social domains (Zubin & Spring, 1977). The influence of this model
is reflected in expert guidelines for the treatment of psychotic disorders such as the ‘Royal Australian
and New Zealand College of Psychiatrists (RANZCP) clinical practice guidelines for the treatment of
schizophrenia and related disorders’ (McGorry, 2005). Treatment guidelines are
developed by panels of experts in the field who review the evidence for
the effectiveness of specific treatments and then reach a consensus on
recommended best practice. The guidelines are organised with reference

to the specific phases of psychosis and outline the optimal combination of
biological, psychological and social interventions corresponding to each
stage of the disorder.
Prodromal phase interventions

Within Australia and internationally there is a growing emphasis upon
COURTESY OF PROFESSOR PATRICK MCGORRY

early detection of individuals at risk of developing psychosis and offering
them intensive interventions in order to prevent progression to more severe
and enduring psychological disturbance. Researchers at the Personal
Assessment and Crisis Evaluation (PACE) clinic in Melbourne have
pioneered the development of criteria for identifying individuals at high
risk for psychosis. These criteria include less severe features of psychosis
(e.g., an increase in suspicious thinking), transient psychotic symptoms
(e.g., auditory hallucinations that might appear intermittently for very
brief periods of time), a substantial deterioration in general psychological
functioning, and a family history of psychosis in a first-degree relative.
Research has found that 40 per cent of individuals defined as being at risk Australian of the Year (2010) Professor Patrick
for psychosis using these criteria go on to develop psychosis over a nine- McGorry is a leading researcher in the area
month period (Yung et al., 1998). of psychosis.
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Researchers led by Patrick McGorry and Alison Yung at the PACE clinic have also conducted
interventions targeting high-risk individuals. This team has reported promising results for the early use
of antipsychotic medication combined with cognitive behaviour therapy (CBT) with a group of young
people at high risk of developing psychosis (McGorry et al., 2002). Specifically, the researchers found
that this combined treatment seemed to delay the proportion of young people who developed an acute
episode of psychosis. In other words, in the short term, there were fewer young people developing
full-threshold psychosis but this difference was unfortunately not sustained over the longer term. This
finding indicates the need for more research to identify strategies for maintaining wellbeing.
Subsequent research has found that CBT alone is successful in reducing the transition to psychosis
for individuals at high risk of developing a first episode of psychosis (Morrison et al., 2004). In this
study, 58 high-risk patients were randomly allocated to receive either six months of CBT or regular
monitoring of symptoms. The CBT intervention was based on Morrison’s (2001) cognitive model of
psychosis (see Figure 7.2) and aimed to challenge patients’ culturally unacceptable interpretations
of their intrusions into awareness, to correct faulty knowledge regarding the self and others, and to
alter responses (disturbances in mood, arousal, behaviours and cognition) that intensify intrusive
thoughts, images and impulses. For example, one patient had the thought that people were looking at
him while he was driving (intrusion into awareness), which he interpreted as evidence that his family
was arranging for him to be followed (culturally unacceptable interpretation) (French, Morrison,
Walford, Knight, & Bentall, 2003). The therapist helped the patient to challenge this interpretation by
questioning the patient regarding how many people would be required for this surveillance operation
to succeed and the cost involved, which would be beyond his family’s means. The results of the study
are displayed in Figure 7.3. One year after treatment commenced it was found that significantly fewer
patients in the CBT group had developed psychosis (6%) compared to those in the monitoring group
(22%). In addition, significantly fewer CBT patients had been prescribed antipsychotic medication
(6%) compared to the monitoring group (30%). Importantly, the significant advantage of the CBT
group over the monitoring group was sustained at a three-year follow-up (Morrison et al., 2007). One
notable advantage of CBT as an intervention for high-risk individuals is that it avoids prescribing
antipsychotic medication (with its potentially serious side effects) to individuals who may not even
have a developing psychosis.
35
30
25 CBT
20 Monitoring
15
10
0
Psychosis Medication
FIGURE 7.3 The percentage of high-risk patients developing psychosis and being prescribed antipsychotic
medication one year after commencing CBT or regular symptom monitoring
Source: From Morrison et al. (2004). Cognitive therapy for the prevention of psychosis in people at ultra-high risk: Randomised controlled
trial. British Journal of Psychiatry, 185, 291–297, The Royal College of Psychiatrists.
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The scientific community is in agreement that further research is needed before these interventions
can be recommended in routine clinical practice. For instance, it is not clear whether the beneficial
effects reported by Morrison and colleagues (2004) were specifically due to the CBT techniques
that were used or stemmed from the support patients obtained by meeting regularly with a therapist.
However, it does appear that CBT offers a specific benefit to patients at risk for psychosis, especially
in relation to their positive symptoms (French, Shryane, Bentall, Lewis, & Morrison, 2007). These
preliminary results are promising and highlight the importance of ongoing efforts to improve the early
identification of individuals who will develop psychosis and to provide preventative interventions for
this high-risk group.
Acute phase interventions

Compared to the relatively recent focus on interventions at the prodromal stage, interventions for
acute psychosis have been more thoroughly researched and are more firmly established in routine
clinical practice. Given the finding that a greater delay in obtaining treatment after the development of
psychosis is associated with a longer time before the patient responds to treatment, there is a growing
international trend towards encouraging timely access to expert assessment and acute treatment
facilities (Marshall et al., 2005). Specialist early psychosis intervention programs within mental health
services have become increasingly common in Australia over the past 10 years, strongly influenced
by the development of the EPPIC program. The dissemination of the early intervention model across
Australia is currently being supported via the establishment of the headspace Youth Early Psychosis
Programs (hYEPPS) across Australia, a federal government initiative to support the distribution of
evidence-based early psychosis services (McGorry et al., 2007).
In the case of first-episode psychosis, the initial priority once contact is made with specialist
mental health services is the comprehensive assessment of the person’s mental state along with an
assessment of his/her physical health and an understanding of his/her individual and family history,
including any previous mental health problems. If an episode of psychosis is diagnosed, then
treatment should preferably be commenced in the person’s home and the patient and family members
should have 24-hour access to mobile treatment teams who can come to the patient’s home. However,
often the severity of symptoms and associated risks to the person, combined with the stress upon the
family attempting to care for the individual at home, necessitates a period of hospitalisation. If this
is required, it should ideally be provided within units specifically designed for young people in the
early stages of the disorder, because adult inpatient units with patients whose psychosis is chronic may
inadvertently provide a pessimistic message to the young person regarding his/her own likely mental
health outcome.
Psychological support and the provision of basic psychoeducation about the disorder and its
treatment are critical in order to engage the young person and his/her family at the commencement of
treatment. Social needs also often require immediate attention, including accommodation and financial
problems, and communicating appropriately with the patient’s employer or educational institution.
Pharmacological approaches are at the centre of care for the treatment of acute psychosis. These
include antipsychotic medication (also known as neuroleptics) for the active symptoms, often in
combination with the brief use of benzodiazapines to assist the person to regulate their sleep and
to reduce the severe anxiety associated with the acute phase. Commonly prescribed antipsychotics
in Australia include the newer so-called ‘atypical antipsychotics’ such as risperidone, olanzapine,
quetiapine and clozapine, and the older ‘typical neuroleptics’ including haloperidol (Mond, Morice,
Owen, & Korten, 2003). Pharmacologists agree that antipsychotics should be used at the lowest
effective dose for the treatment of first-episode psychosis in order to minimise the adverse side effects
of medication, such as weight gain, and in order to reduce the long-term health risks associated
with antipsychotic medications (McGorry, 2005). Although the extent and timing of the response
to antipsychotic medication varies between patients, it is known that the majority of first-episode
patients will experience significant reductions in acute symptoms over the early months of treatment
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in response to these medications (Emsley, Rabinowitz, & Medori, 2007). Trials have shown that a
shorter duration of untreated psychosis and an early response to medication in the first six weeks of
treatment predict a greater chance of reaching a remission from the acute symptoms.
tardive One side effect that is of greatest concern is tardive dyskinesia, which occurs in approximately
dyskinesia 10 per cent of patients treated with neuroleptics for more than a year and is perhaps the most serious
Neurological limitation associated with the long-term use of neuroleptics. This condition consists of a range of
disorder abnormal body movements such as lip smacking, facial grimacing, piano player-like movements of
characterised
the fingers and toes, and writhing movements of the trunk.
by involuntary
movements Some researchers, such as Loren Mosher and colleagues, have evaluated the effectiveness of
of the tongue, alternative approaches, including the Soteria model, first developed in California in the early 1970s,
face, mouth or which includes a high level of 24-hour support in a home-like setting, usually without medication
jaw, which may (Bola & Mosher, 2003). The outcomes from the program have been found to be comparable with
result from taking standard care within a state hospital in terms of symptom recovery and return to the community
neuroleptic (Mosher, 1999). Interest in effective medication-free interventions for psychosis continues today. For
drugs.
instance, Anthony Morrison and his colleagues in the United Kingdom developed and evaluated a
form of CBT for patients who either refuse or discontinue taking antipsychotic medications and they
found that compared to patients randomised to treatment as usual without CBT, the CBT patients did
significantly better in terms of the severity of their symptoms 18 months after treatment had ended
(Morrison et al., 2014).
Once the most severe psychotic symptoms begin to improve, the priorities shift towards addressing
other psychological problems such as anxiety and depression through both psychological interventions
and appropriate medication. Comorbid substance abuse is highly prevalent in people with psychosis.
So-called ‘dual-diagnosis’ services have been established in an attempt to treat both the psychosis and
substance abuse problems simultaneously, in recognition that the two disorders influence one another.
For example, Jane Edwards at EPPIC has led a team of researchers evaluating the effectiveness of
careful education and psychological treatments for young people experiencing both psychosis and
cannabis abuse problems (Edwards et al., 2006). Findings from various treatment trials combined into
a meta-analysis show that interventions for cannabis use in patients with psychosis have an effect in
reducing both the quantity of cannabis consumed by patients and their positive symptoms of psychosis
(Hjorthoj, Baker, Fohlmann, & Nordentoft, 2014).
Psychosocial approaches also target social and occupational functioning once the most
severe psychotic symptoms begin to improve, especially since these aspects of functioning may
be less responsive to medication. That is, while positive symptoms are often eliminated by
drug treatment, the negative symptoms may be only moderately improved and thus continue to
impair the individual’s social and occupational functioning. Group-based interventions are often
available in early psychosis programs to foster social support and social confidence, and encourage
reintegration into recreational, vocational and educational activities. Symptomatic recovery is
not always necessary or sufficient for reintegration into vocational and educational activities.
Individual support programs that encourage people back to work and continue to support them once
employment is obtained have been shown to be effective for people diagnosed with schizophrenia.
Associate Professor Eóin Killackey from Orygen, The National Centre of Excellence in Youth
Mental Health, together with Professor Henry Jackson from the University of Melbourne, have been
leading a team of researchers in evaluating ways to support young people in gaining employment or
returning to study after a first episode of psychosis (Killackey et al., 2006). Their trial involved the
provision of one-on-one employment or educational support as a component of a comprehensive
program of mental health care to assist young people to either enter or return to employment or
education. This research, which built upon work undertaken with older people with a longer-term
form of psychosis (Cook et al., 2005), showed that those who received the additional support had
significantly better outcomes in their level of employment, hours worked per week, jobs acquired
and longevity of employment compared with those receiving treatment-as-usual within a specialist
first-episode psychosis program (Killackey, Jackson, & McGorry, 2008).
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Interventions to prevent relapse

Relapse is a major risk once symptoms have remitted. As with interventions for acute psychotic episodes,
medication is essential in reducing the risk of relapse, with an estimated relapse rate of 65 per cent one
year after hospitalisation among those who have discontinued their medication (Hogarty & Ulrich,
1998). However, even with ongoing medication, relapse rates are still high, with approximately 40 per
cent of patients on medication relapsing within one year. These findings highlight the importance of
adding psychosocial interventions to medication, with a combined treatment approach found to halve
the relapse rates associated with medication alone.
Effective preventive treatments have included both individual and family approaches. Examining an
individual approach, Gumley and colleagues (2003) randomly allocated 144 patients with schizophrenia
to receive either standard treatment alone (medication and regular symptom review) or CBT plus standard
treatment. In the CBT intervention, patients were introduced to a cognitive model of relapse, which states
that early signs of relapse (e.g., racing thoughts) trigger negative beliefs (e.g., ‘I have no control over
what is happening to me and am going to end up in hospital’), which in turn trigger negative emotions
(e.g., anxiety) and behaviours (e.g., substance use, withdrawal and avoidance of mental health services)
that can intensify psychotic symptoms. Given this model, treatment aimed to help patients develop more
optimistic beliefs regarding symptoms (e.g., ‘I can learn skills to manage my thoughts’). The results
revealed that, one year after commencing treatment, fewer patients in the CBT group had relapsed
(18.1%) compared to those receiving standard treatment (34.7%). The percentage of patients who relapsed
across the 12 months of the study is shown in Figure 7.4. In addition, significantly fewer patients in the
CBT group were admitted to hospital (15.3%) compared to the standard group (26.4%). CBT was also
significantly more effective than standard treatment in reducing positive and negative psychotic symptoms
and increasing social functioning. A subsequent study by Gumley and colleagues (2015) provided support
for this theory that fear of relapse itself is a stressor that contributes to the risk of relapse.
40
35
30
Relapse rate (%)
25
Standard
20 CBT
15
10
0
0 1 2 3 4 5 6 7 8 9 10 11 12
Month in the study
FIGURE 7.4 The percentage of CBT and standard treatment patients who relapsed over the 12 months of
the study
Source: From Gumley et al. (2003). Early intervention for relapse in schizophrenia: Results of a 12-month randomised controlled trial of
cognitive behavioural therapy. Psychological Medicine, 33, 419–431, Cambridge University Press.
The association between high expressed emotion (EE) and relapse in schizophrenia has provided
the impetus for the development of family interventions, which have also been found to be effective
in reducing relapse rates (Kavanagh, 1992; McFarlane, Dixon, Lukens, & Lucksted, 2003; Pilling
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et al., 2002). Family interventions usually entail a combination of joint sessions with the patient
and the family, and individual sessions with the patient alone. The core components of CBT family
interventions include: providing education about schizophrenia (especially emphasising the biological
vulnerability to developing the illness in an attempt to decrease any tendency of family members
to blame themselves or each other) and its treatment (especially the importance of medication and
monitoring early signs of relapse); aid in setting positive yet realistic goals (to increase a sense of hope
of what can be achieved while minimising excessive pressure to reach goals that are unlikely to be
achieved); communication training (especially targeting the expression of concerns in a constructive,
empathic and non-demanding manner rather than a critical or overprotective manner); training in the
skills of problem solving as a method of managing conflict; and encouraging the establishment of
wider social supports as an effective strategy for coping with stress. The effectiveness of this form
of therapy for the prevention of relapse after the first episode, which may in turn reduce the long-
term severity of the disorder, has recently been evaluated in a randomised controlled trial at EPPIC.
Standard treatment after the first episode of psychosis was compared with standard treatment plus
CBT for the individual patient and his/her family (Gleeson et al., 2009; 2010). The addition of CBT
to standard treatment resulted in improvement in the experience of caregiving for family members,
which was sustained at follow-up 2.5 years after the family CBT program was completed.
One current limitation of early intervention services is that they have not been shown to have a
sustained benefit compared to usual treatments beyond the period of exposure to the specialist treatment
program, indicating that improved treatments are needed to achieve better long-term outcomes.
Researchers from Orygen, The National Centre of Excellence in Youth Mental Health, Australian
Catholic University and Computer Science and Information Systems at the University of Melbourne
are currently testing within a randomised controlled trial a moderated online social networking program
that includes interactive online education to maintain support and engagement over the longer term, with
a view to improving social functioning and preventing relapse (Alvarez-Jimenez et al., 2013; Gleeson,
Alvarez-Jimenez, & Lederman, 2012).
Interventions for enduring psychosis

For sufferers of long-term psychosis who experience persistent positive symptoms, alternative
antipsychotic medications such as clozapine are often prescribed based on favourable reviews of the
evidence (Wahlbeck, Cheine, Essali, & Adams, 1999). The addition of CBT to pharmacotherapy has
been shown in several trials to be effective for reducing the impact of delusions and hallucinations
(Garety, Fowler, & Kuipers, 2000). An example is a controlled treatment study conducted by Tarrier
and colleagues (1998). In this study, 87 patients with schizophrenia who continued to experience
hallucinations or delusions despite taking medication were randomly allocated to one of three conditions:
standard treatment (i.e., maintenance medication and routine outpatient review), standard treatment
plus supportive counselling (i.e., 20 sessions of one hour twice a week aimed at providing emotional
support to the patient through the development of a supportive relationship with the therapist), and
standard treatment plus CBT (i.e., 20 sessions of one hour twice a week aimed at teaching effective
coping strategies for managing symptoms and problem-solving skills for managing life stressors).
Patients in the CBT group experienced a significantly greater reduction in the number and severity
of psychotic symptoms from pre- to post-treatment compared with the supportive counselling group,
while patients in the standard treatment group actually demonstrated a slight deterioration. Specifically,
33 per cent of patients in the CBT group achieved a 50 per cent reduction in psychotic symptoms
compared to 15.4 per cent in the supportive counselling group, and 10.7 per cent in the routine care
group. Despite the brevity of the intervention, a follow-up study conducted two years later continued
to find that patients in the standard treatment group did significantly worse in terms of the severity
of both positive and negative symptoms compared to those in the CBT and supportive counselling
groups (which did not differ significantly from each other) (Tarrier et al., 2000). Thus, psychosocial
approaches are an effective additional intervention for at least a proportion of patients with entrenched
psychotic symptoms (i.e., those that persist despite adequate medication).
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The consumer recovery model

Survivors of psychosis and serious mental illness have espoused their own consumer recovery model, using
the word ‘consumer’ rather than ‘patient’ because it highlights a shift in values away from a paternalistic
model of care (in which the doctor makes decisions about treatment for the patient) to one that raises
awareness of the importance of civil rights and personal choice (Bellack, 2006). The consumer recovery
model highlights the principles of hope, personal responsibility, empowerment, respect from the broader
community, the resilience of the consumer (i.e., his/her specific strengths or abilities) and the importance
of peer support for the consumer in the recovery process. The Australian Government, which sets the
policy framework for the delivery of mental health services in Australia, launched the national standards
for mental health services in 1996 (Australian Government Department of Health and Family Services,
1996). These standards require participation by consumers and carers in the planning, implementation and
evaluation of mental health services. As a result, many Australian mental health services employ carer and
consumer advocates who participate in staff training, and in service planning and evaluation activities.
Limitations of current treatment approaches

Despite all of the developments in biological, psychological and social interventions for psychosis,
there are significant gaps in the delivery of mental health services across nearly all states and territories
within Australia. A report published in 2005 by the Mental Health Council of Australia, entitled ‘Not
for Service’, highlighted that more needs to be done to improve access to services. Data from New
South Wales indicated that a significant proportion of people diagnosed with a mental illness are
incarcerated within prisons (rather than being located within the mental health system), and that there
are no systematic efforts to prevent this outcome (Butler, Allnutt, Cain, Owens, & Muller, 2005).
SANE Australia’s 2011 report found that 90 per cent of people with a psychotic disorder reported a
deterioration in their ability to function in daily life.
In addition to poor access to mental health services, those treatments that are offered are often limited
in scope. Although treatment guidelines espouse a biopsychosocial framework, treatments received
are often overly narrow, and psychological interventions (such as CBT) may be extremely difficult to
access. Family interventions have also repeatedly been shown to be effective in reducing the rates of
relapse, but once again are rarely available (Fadden, 2006). A national prevalence survey of people
diagnosed with psychotic disorders revealed that less than 40 per cent of Australians with psychotic
disorders reported receiving any psychosocial intervention over the previous year (Jablensky et al.,
2000). A target of Australia’s fourth national mental health plan is the implementation of evidence-
based and cost-effective models of intervention for early psychosis (which include psychosocial
treatments) to provide broader national coverage (Australian Health Ministers, 2009).
The development of improved treatments for psychosis also needs to incorporate cultural values and
perspectives. Given the accumulation of trauma, distress and dispossession in Indigenous Australians,
there is an urgent need to improve their mental health outcomes, which include high rates of hospital
admission for psychosis. As reported by Dudgeon and Calma (2013), Aboriginal and Torres Strait
Islander peoples have consistently asserted that mental health should be considered holistically with
physical health and guided by a positive focus on social and emotional wellbeing. This positive state
incorporates healthy relationships between the individual, family, kin, community, traditional lands and
ancestors. The most effective models of mental health service delivery are those designed and led by
Indigenous health workers at the community level with support from Australian governments. In New
Zealand, mental health services have been significantly transformed by Māori cultural values, with Māori
psychological perspectives informing the assessment, treatment and care of patients (Durie, 2011).
In terms of research priorities, more needs to be done to evaluate effective interventions for comorbid
substance use disorders, depression, trauma and stressor-related disorders and other problems that
impede full recovery from psychosis. Finally, too many people diagnosed with psychosis in Australia
continue to suffer from stigma and have limited access to appropriate housing, employment and
educational support.
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To improve the outcomes for individuals with psychotic disorders, a number of information sources
may benefit patients, their family and friends, mental health professionals and the wider community.
Some helpful organisations and online resources regarding psychosis and severe mental illness are
listed below.
USEFUL RESOURCES WEBSITES

Early Psychosis Prevention and Intervention Centre: www.eppic.org.au
Like Minds, Like Mine: www.likeminds.org.nz/about/
Mental Health Australia: www.mhaustralia.org
Mental Health Foundation of New Zealand: www.mentalhealth.org.nz
Mental Illness Fellowship of Australia: www.mifa.org.au
MIND Australia: www.mindaustralia.org.au/
International Early Psychosis Association: www.iepa.org.au
SANE Australia: www.sane.org
CASE STUDY: FROM PRODROMAL PHASE TO EARLY RECOVERY

Sam was 19 years of age when he first had contact with a mental health service after being referred by the family GP.
In the initial weeks of his enrolment at university he was actively involved in campus social life. He was relieved to
commence university after an extremely stressful Year 12 when his closest friend was killed in a car accident and when he
suffered from a prolonged bout of glandular fever. Sam’s family were very supportive of him but his mother, Eva, suffered
from longstanding depression and anxiety, leaving Sam with a heavy sense of responsibility towards supporting her.
Sam’s father, Ian, was extremely busy running a small accountancy business and often had to work weekends to keep
on top of the load.
In his early years of secondary school, Sam experienced persistent bullying from a group of older boys. As a result of
his mother’s mental health problems, Sam believed that he had to cope with these problems on his own.
As Sam’s first year at university progressed his father became increasingly concerned for his wellbeing. Ian noticed
Sam was skipping classes, disengaging from social life and spending more and more time isolating himself in his room.
His sleep was becoming increasingly unsettled over a three-month period. Sam started to miss meals with the family
and without warning started to accuse his mother of poisoning him. Ian observed that Sam was mumbling and laughing
to himself and was becoming increasingly difficult to follow in conversation. Sam’s friend telephoned Ian to express his
concerns that Sam was posting accusations about his best friends on Facebook and claiming to have discovered the
secret to ‘the afterlife’. As a result of his increasing concerns about Sam, Ian spoke with the family GP, who encouraged
Ian to accompany Sam to an appointment. Sam reluctantly agreed to attend but was very guarded and refused to answer
some of the doctor’s questions. The GP noticed that Sam appeared highly distracted throughout the appointment and
speculated that he was hearing voices. The GP advised Ian and Sam that it would be important to meet with the local
mental health team.
Because Sam refused to attend the local mental health clinic, the crisis assessment team arranged to meet with Sam,
Eva and Ian at the family home. A psychiatric nurse from the team talked separately with Sam with the aim of building
rapport and gaining an understanding of Sam’s concerns. Sam appeared perplexed, anxious and guarded, and the nurse
noted that he was slow to respond to questions and that his answers to questions were frequently off track. However,
Sam did confide to the nurse that he believed his family were poisoning him because they had been brainwashed by
an international businessman. Sam also expressed a belief that he was developing special insights into ‘how everything
worked’. He seemed unable to answer questions about whether he was experiencing any unusual auditory phenomena.
A clinical psychologist met with Eva and Ian to discuss Sam’s functioning. Eva was very distressed throughout the
interview and divulged that she was exhausted from Sam’s intermittent sleeping pattern. She expressed significant
fears for his wellbeing. Ian believed that Sam was definitely not his usual self and this was taking a toll on the whole
household—he was unsure how much longer they could hold out.
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The mental health team, including a psychiatrist, continued to visit the family home each day with the aim of completing
the assessment, providing support to Sam and his family and commencing acute phase treatment. However, over the
next 48 hours it became clear that Sam required an admission to a psychiatric hospital because he was becoming
agitated at home and the family were becoming increasingly distressed.
Sam agreed to the hospital admission to have a break from the stress at home. The assessment, including physical
investigations and examinations, was completed in hospital to rule out any medical cause for these symptoms. He was
commenced on short-term benzodiazepines to help him sleep and to reduce the immediate anxiety and agitation. He
was then commenced on a low dose of an antipsychotic medication and there was an additional improvement over a
two-week period, although he continued to harbour some concerns about his family. In hospital he acknowledged that
he was hearing voices that advised him about conspiracies. After three weeks in hospital, he started to spend some
time at home and he was discharged soon after back to his family. During this period, his family were supported through
separate family meetings with the treating team and they had the opportunity to meet with other families who were
caring for a young person with psychosis.
Following discharge from hospital, Sam was offered ongoing support from a case manager and psychiatrist and was
invited to participate in a group program. He suffered from depression, social anxiety and loneliness, and wondered
if he would be able to return to university. His case manager worked with him to achieve this goal over the next 6–8
months. The following year he returned to a modified program of study, with specialist support from his treating team.
However, Sam gained significant weight from the antipsychotic medication, even though he was previously a lean and
fit young man. He was introduced to a dietitian and encouraged to resume an active life. Sam continued to meet with
his treating team and slowly developed an understanding of his experience. He was eager to learn more about why this
had happened to him. He remained somewhat ambivalent about continuing with medication and battled with persistent
social anxiety. But he still managed to reconnect with old friends from school and university.
SUMMARY
Psychotic disorders are among the most distressing and severe forms of mental disorder. The core symptoms include positive
symptoms (i.e., hallucinations, delusions, thought disorder and disorganised behaviour) and negative symptoms (i.e., alogia,
avolition and blunted affect). The diagnosis of a specific psychotic disorder (such as schizophrenia) is based on the range of
symptoms present, the duration of the symptoms, the precipitating factors and the impact upon the person’s functioning. Debate
continues in the scientific community regarding the validity and merits of specific diagnoses such as schizophrenia, which were first
defined for the purpose of a modern classification system 100 years ago.
Psychotic disorders are commonly associated with secondary problems, including substance use disorders, depression and
anxiety. In addition, sufferers often experience significant interruptions to their lives, including problems with unemployment and
the stigma associated with mental illness.
Compared with mental disorders such as major depressive disorders, psychotic disorders are relatively rare. They are more
common in men than in women, and appear at higher rates in migrants, in developed nations and in people born and residing in
urban areas.
Psychosis typically develops for the first time in late adolescence and early adulthood, often with many months of non-specific
changes in mental state preceding the onset of acute psychotic symptoms. A longer duration of untreated psychosis is associated
with a longer length of time to respond to treatment. For this reason, early intervention programs around the world aim to identify
and treat psychosis as soon as possible.
A wide range of factors have been examined as possible causes of psychosis under the framework of the diathesis-stress
model of psychosis. Contributors to vulnerability appear to include biological factors (e.g., genes and changes in brain structures)
and psychosocial factors (e.g., exposure to trauma, adversity and abuse, and dysfunctional cognitions). Precipitating factors that
interact with vulnerability include illicit substances, stressful life events and exposure to hostility and criticism in relationships.
Researchers have also identified various psychological factors in the pathway to the development and maintenance of specific
symptoms. For example, psychologists have found that proneness to delusions is associated with a greater tendency to ‘jump to
conclusions’ based on relatively small amounts of information.
Once a comprehensive assessment has been completed and psychosis is accurately diagnosed, acute phase treatments
focus upon the immediate reduction of symptoms and associated distress, while longer-term recovery requires a broad array of
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psychological, social and biological interventions. Comprehensive treatments include a focus on staying well after psychosis and
achieving a satisfying quality of life. Researchers are also beginning to report that some treatments may be effective in preventing
or postponing the onset of psychosis in young people who have been identified as being at ‘ultra-high risk’ of psychosis. In addition
to the work of researchers and clinicians, consumers of psychiatric services have developed their own empowering consumer
recovery model of psychosis, with a strong emphasis upon recovery, the strengths of the individual and the reduction of stigma.
Despite many discoveries and improvements in the available treatments for psychosis, there are unfortunately significant gaps
for sufferers of psychosis, especially in relation to access to psychosocial treatments. Hence, considerably more needs to be done
to improve treatment access and to enhance the quality of life for many people diagnosed with psychosis.
KEY TERMS
adoption study. . . . . . . . . . . . . . . . . . . 163 enlarged ventricles . . . . . . . . . . . . . . . 165 neurotransmitters. . . . . . . . . . . . . . . . . 164
affective flattening. . . . . . . . . . . . . . . . 149 expressed emotion (EE) . . . . . . . . . . . 161 paranoia. . . . . . . . . . . . . . . . . . . . . . . . . 158
alogia. . . . . . . . . . . . . . . . . . . . . . . . . . . 149 family study. . . . . . . . . . . . . . . . . . . . . . 163 paranoid delusion . . . . . . . . . . . . . . . . 150
antipsychotic medications . . . . . . . . . 156 grandiose delusion . . . . . . . . . . . . . . . 151 pituitary . . . . . . . . . . . . . . . . . . . . . . . . . 168
auditory hallucinations . . . . . . . . . . . . 149 hallucinations . . . . . . . . . . . . . . . . . . . . 149 positive symptoms. . . . . . . . . . . . . . . . 160
avolition. . . . . . . . . . . . . . . . . . . . . . . . . 149 hallucinogens. . . . . . . . . . . . . . . . . . . . 149 pre-frontal cortex. . . . . . . . . . . . . . . . . 165
cannabis. . . . . . . . . . . . . . . . . . . . . . . . . 156 hypothalamic-pituitary-adrenal prodromal symptoms. . . . . . . . . . . . . . 148
catatonic behaviour. . . . . . . . . . . . . . . 152 (HPA) axis. . . . . . . . . . . . . . . . . . . . . . . . 165 schizophrenia. . . . . . . . . . . . . . . . . . . . 158
concordance rate. . . . . . . . . . . . . . . . . 163 magnetic resonance somatic delusion . . . . . . . . . . . . . . . . . 150
delusion. . . . . . . . . . . . . . . . . . . . . . . . . 150 imaging (MRI) . . . . . . . . . . . . . . . . . . . . 165 tardive dyskinesia . . . . . . . . . . . . . . . . 174
delusion of reference . . . . . . . . . . . . . 150 monozygotic twins. . . . . . . . . . . . . . . . 163 thought disorder. . . . . . . . . . . . . . . . . . 148
depression. . . . . . . . . . . . . . . . . . . . . . . 156 motor disturbance. . . . . . . . . . . . . . . . 149
dizygotic twins . . . . . . . . . . . . . . . . . . . 164 negative symptoms. . . . . . . . . . . . . . . 149
REVIEW QUESTIONS
LO 7.1
7.1 What are the positive symptoms of psychosis?
7.2 What is the definition of a delusion and what are some examples of delusions?
LO 7.2
7.3 According to the DSM-5, what are the criteria for a diagnosis of schizophrenia?
LO 7.3
7.4 What have been some concerns raised by researchers regarding the diagnosis of schizophrenia?
LO 7.4
7.5 At what stage of life does psychosis most commonly develop?
7.6 Why is early detection of psychosis an important aim?
LO 7.5
7.7 Do you need to have a relative with psychosis in order to develop the disorder?
7.8 Can either stress or cannabis use cause psychosis?
LO 7.6
7.9 Can psychosis be prevented?
7.10 What are the potential benefits and problems of antipsychotic medications?
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REFERENCES
Aiello, G., Horowitz, M., Hepgul, N., Pariante, C. M., & Mondelli, Bhatt, R., Laws, K. R., & McKenna, P. J. (2010). False memory in
V. (2012). Stress abnormalities in individuals at risk for psychosis: schizophrenia patients with and without delusions. Psychiatry
A review of studies in subjects with familial risk or with at risk Research, 178, 260–265.
mental state. Psychoneuroendocrinology, 37, 1600–1613. Birchwood, M., & Chadwick, P. (1997). The omnipotence of voices:
Alvarez-Jimenez, M., Bendall, S., Lederman, R., Wadley, G., Chinnery, Testing the validity of a cognitive model. Psychological Medicine,
G., Vargas, S., . . . Gleeson, J. F. (2013). On the HORYZON: 27, 1345–1353.
Moderated online social therapy for long-term recovery in first Birchwood, M., Iqbal, Z., Chadwick, P., & Trower, P. (2000).
episode psychosis. Schizophrenia Research, 143, 143–149. Cognitive approach to depression and suicidal thinking in psychosis
Alvarez-Jimenez, M., Priede, A., Hetrick, S. E., Bendall, S., Killackey, I: Ontogeny of post-psychotic depression. British Journal of
E., Parker, A. G., . . . Gleeson, J. F. (2012). Risk factors for relapse Psychiatry, 177, 516–521.
following treatment for first episode psychosis: A systematic Birchwood, M., Mason, R., Macmillan, F., & Healy, J. (1993).
review and meta-analysis of longitudinal studies. Schizophrenia Depression, demoralisation, and control over psychotic illness: A
Research, 139, 116–128. comparison of depressed and non-depressed patients with a chronic
American Psychiatric Association (1994). Diagnostic and statistical psychosis. Psychological Medicine, 23, 387–395.
manual of mental disorders (4th ed.). Washington, DC: Author. Bola, J. R., & Mosher, L. R. (2003). Treatment of acute psychosis
American Psychiatric Association (2000). Diagnostic and statistical without neuroleptics: Two-year outcomes from the Soteria project.
manual of mental disorders (4th ed., text revision). Washington, Journal of Nervous and Mental Disease, 191, 219–229.
DC: Author. Braham, L. G., Trower, P., & Birchwood, M. (2004). Acting on command
American Psychiatric Association (2013). Diagnostic and statistical hallucinations and dangerous behavior: A critique of the major findings
manual of mental disorders (5th ed.). Arlington: Author. in the last decade. Clinical Psychology Review, 24, 513–528.
Assad, G., & Shapiro, B. (1986). Hallucinations: Theoretical and Butler, T., Allnutt, S., Cain, D., Owens, D., & Muller, C. (2005).
clinical overview. American Journal of Psychiatry, 143, 1088–1097. Mental disorder in the New South Wales prisoner population.
Australian Bureau of Statistics & Australian Institute of Health and Australian and New Zealand Journal of Psychiatry, 39, 407–413.
Welfare (2008). The health and welfare of Australias Aboriginal Caspi, A., Moffitt, T. E., Cannon, M., McClay, J., Murray, R.,
and Torres Strait Islander Peoples. Canberra: Author. Harrington, H., . . . Craig, I. W. (2005). Moderation of the
Australian Government Department of Health and Family Services effect of adolescent-onset cannabis use on adult psychosis by a
(1996). National mental health standards. Canberra: Author. functional polymorphism in the catechol-O-methyltransferase
Australian Health Ministers (2009). Fourth national mental health gene: Longitudinal evidence of a gene X environment interaction.
plan: An agenda for collaborative government action in mental Biological Psychiatry, 57, 1117–1127.
health 2009–2014. Canberra: Commonwealth of Australia. Chisholm, B., Freeman, D., & Cooke, A. (2006). Identifying potential
Barnes, T. R. E., & McPhillips, M. A. (1995). How to distinguish predictors of traumatic reactions to psychotic episodes. British
between the neuroleptic-induced deficit syndrome, depression and Journal of Clinical Psychology, 45, 545–559.
disease-related negative symptoms in schizophrenia. International Cook, C. C. H. (2015). Religious psychopathology: The prevalence
Clinical Psychopharmacology, 10, 115–121. of religious content of delusions and hallucinations in mental
Barrowclough, C., & Hooley, J. M. (2003). Attributions and expressed disorder. International Journal of Social Psychiatry, 61, 404–425.
emotion: A review. Clinical Psychology Review, 23, 849–880. Cook, J. A., Leff, H. S., Blyler, C. R., Gold, P. B., Goldberg,
Bellack, A. S. (2006). Scientific and consumer models of recovery R. W., Mueser, K. T., . . . Burke-Miller, J. (2005). Results of a
in schizophrenia: Concordance, contrasts, and implications. multisite randomized trial of supported employment interventions
Schizophrenia Bulletin, 32, 432–442. for individuals with severe mental illness. Archives of General
Bendall, S., Alvarez-Jimenez, M., Hulbert, C. A., McGorry, P. D., & Psychiatry, 62, 505–512.
Jackson, H. J. (2012). Childhood trauma increases the risk of post- Corrigan, P. W., & Watson, A. C. (2002). The paradox of self-stigma
traumatic stress disorder in response to first episode psychosis. and mental illness. Clinical Psychology: Science and Practice, 9,
Australian and New Zealand Journal of Psychiatry, 46, 35–39. 35–53.
Bentall, R. (2003). Madness explained: Psychosis and human nature. Cunningham, J., & Paradies, Y. C. (2012). Socio-demographic factors
London: Penguin Books. and psychological distress in Indigenous and non-Indigenous
Bentall, R. (2006). Madness explained: Why we must reject the Australian adults aged 18–64 years: Analysis of national survey
Kraepelinian paradigm and replace it with a complaint-orientated data. BMC Public Health, 12, 95.
approach to understanding mental illness. Medical Hypotheses, 66, Debruyne, H., & Audenaert, K. (2012). Towards understanding
220–233. Cotards syndrome: An overview. Neuropsychiatry, 2, 481–486.
Bentall, R. P., Corcoran, R., Howard, R., Blackwood, N., & de Leon, J., & Diaz, F. J. (2005). A meta-analysis of worldwide
Kinderman, P. (2001). Persecutory delusions: A review and studies demonstrates an association between schizophrenia and
theoretical integration. Clinical Psychology Review, 21, 1143–1192. tobacco smoking behaviors. Schizophrenia Research, 76, 135–157.
Bentall, R. P., & Fernyhough, C. (2008). Social predictors of Drayton, M., Birchwood, M., & Trower, P. (1998). Early attachment
psychotic experiences: Specificity and psychological mechanisms. experience and recovery from psychosis. British Journal of
Schizophrenia Bulletin, 34, 1012–1020. Clinical Psychology, 37, 269–284.
rie66620_ch07_147-186.indd 181 07/29/17 02:14 PM

Dudgeon, P., & Calma, T. (2013). The social and emotional wellbeing of a randomized trial of relapse detection in schizophrenia. British
of Aboriginal and Torres Strait Islander Peoples. In Mental Journal of Clinical Psychology, 54, 49–62. doi: 10.1111/bjc.12060
Health Council of Australia (Ed.), Perspectives: Mental health Gumley, A., O’Grady, M., McNay, L., Reilly, J., Power, K., & Norrie,
& wellbeing in Australia (pp. 36–42). Canberra: Mental Health J. (2003). Early intervention for relapse in schizophrenia: Results
Council of Australia. of a 12-month randomised controlled trial of cognitive behavioural
Durie, M. (2011). Indigenizing mental health services: New Zealand therapy. Psychological Medicine, 33, 419–431.
experience. Transcultural Psychiatry, 48, 24–36. Haddock, G., McCarron, J., Tarrier, N., & Faragher, E. B. (1999).
Edwards, J., Elkins, K., Hinton, M., Harrigan, S. M., Donovan, Scales to measure dimensions of hallucinations and delusions:
K., Athanasopoulos, O., & McGorry, P. D. (2006). Randomised The psychotic symptom rating scales (PSYRATS). Psychological
controlled trial of a cannabis-focused intervention for young people Medicine, 29, 879–889.
with first-episode psychosis. Acta Psychiatrica Scandinavica, 114, Haddock, G., Wolfenden, M., Lowens, I., Tarrier, N., & Bentall, R. P.
109–117. (1995). Effect of emotional salience on thought-disorder in patients
Egerton, A., & Stone, J. M. (2012). The glutamate hypothesis of with schizophrenia. British Journal of Psychiatry, 167, 618–620.
schizophrenia: Neuroimaging and drug development. Current Harding, C. M., Zubin, J., & Strauss, J. S. (1992). Chronicity
Pharmaceutical Biotechnology, 13, 1500–1512. in schizophrenia: Revisited. British Journal of Psychiatry,
Emsley, R., Rabinowitz, J., & Medori, R. (2007). Remission in early 161, 27–37.
psychosis: Rates, predictors, and clinical and functional outcome Healy, D. (2013). Catatonia from Kahlbaum to DSM-5. Australian
correlates. Schizophrenia Research, 89, 129–139. and New Zealand Journal of Psychiatry, 47, 412–416.
Fadden, G. I. (2006). Training and disseminating family interventions Healy, D., Harris, M., Tranter, R., Gutting, P., Austin, R., Jones-
for schizophrenia: Developing family intervention skills with Edwards, G., & Roberts, A. P. (2006). Lifetime suicide rates
multi-disciplinary groups. Journal of Family Therapy, 28, 23–38. in treated schizophrenia: 1875–1924 and 1994–1998 cohorts
French, P., Morrison, A. P., Walford, L., Knight, A., & Bentall, R. P. compared. British Journal of Psychiatry, 188, 223–228.
(2003). Cognitive therapy for preventing transition to psychosis in Hides, L., Dawe, S., Kavanagh, D. J., & Young, R. M. (2006).
high risk individuals. Behavioural and Cognitive Psychotherapy, Psychotic symptom and cannabis relapse in recent-onset psychosis:
31, 53–67. Prospective study. British Journal of Psychiatry, 189, 137–143.
French, P., Shryane, N., Bentall, R. P., Lewis, S. W., & Morrison, Hjorthoj, C. R., Baker, A., Fohlmann, A., & Nordentoft, M. (2014).
A. P. (2007). Effects of cognitive therapy on the longitudinal Intervention efficacy in trials targeting cannabis use disorders in
development of psychotic experiences in people at high risk patients with comorbid psychosis: Systematic review and meta-
of developing psychosis. British Journal of Psychiatry, 191, analysis. Current Pharmaceutical Design, 20, 2205–2211.
S82–S87. Hogarty, G., & Ulrich, R. (1998). The limitations of antipsychotic
Galletly, C., Castle, D., Dark, F., Humberstone, V., Jablensky, A., medication on schizophrenia relapse and adjustment and the
Killackey, E., . . . Tran, N. (2016). Royal Australian and New contributions of psychosocial treatment. Journal of Psychiatric
Zealand College of psychiatrists clinical practice guidelines for the Research, 32, 243–250.
management of schizophrenia and related disorders. Australian & Holtzman, C. W., Trotman, H. D., Goulding, S. M., Ryan, A. T.,
New Zealand Journal of Psychiatry, 50, 410–472. Macdonald, A. N., Shapiro, D. I., . . . Walker, E. F. (2013). Stress
Garety, P., Fowler, D., & Kuipers, E. (2000). Cognitive behavioural and neurodevelopmental processes in the emergence of psychosis.
therapy for medication-resistant symptoms. Schizophrenia Bulletin, Neuroscience, 249, 172–191.
26, 73–86. Insel, T. R. (2010). Rethinking schizophrenia. Nature, 468, 187–193.
Garety, P. A., Freeman, D., Jolley, S., Dunn, G., Bebbington, P. Jablensky, A., McGrath, J., Herrman, H., Castle, D., Gureje, O.,
E., Fowler, D. G., . . . Dudley, R. (2005). Reasoning, emotions, Evans, M., . . . Harvey, C. (2000). Psychotic disorders in urban
and delusional conviction in psychosis. Journal of Abnormal areas: An overview of the study on low prevalence disorders.
Psychology, 114, 373–384. Australian and New Zealand Journal of Psychiatry, 34, 221–236.
Gleeson, J. F. M., Alvarez-Jimenez, M., & Lederman, R. (2012). Jackson, H. J., McGorry, P. D., & McKenzie, D. (1994). The
Moderated online social therapy for recovery from early psychosis. reliability of DSM-III prodromal symptoms in first-episode
Psychiatric Services, 63, 719–719. psychotic patients. Acta Psychiatrica Scandinavica, 90,
Gleeson, J. F. M., Cotton, S. M., Alvarez-Jimenez, M., Wade, D., 375–378.
Gee, D., Crisp, K., . . . McGorry, P. D. (2009). A randomised Jansen, J. E., Gleeson, J., & Cotton, S. (2015). Towards a better
controlled trial of relapse prevention therapy for first-episode understanding of caregiver distress in early psychosis: A systematic
psychosis patients. Journal of Clinical Psychiatry, 70, 477–486. review of the psychological factors involved. Clinical Psychology
Gleeson, J. F., Cotton, S., Alvarez-Jimenez, M., Wade, D., Gee, Review, 35, 59–66.
D., Crisp, K., . . . McGorry, P. D. (2010). Family outcomes from Jin, H., Meyer, J. M., & Jeste, D. V. (2004). Atypical antipsychotics
an RCT of relapse prevention therapy in first-episode psychosis. and glucose dysregulation: A systematic review. Schizophrenia
Journal of Clinical Psychiatry, 71, 475–483. Research, 71, 195–212.
Green, B., Young, R., & Kavanagh, D. (2005). Cannabis use and Jorm, A. F., & Griffiths, K. M. (2009). The need to rely on evidence
misuse prevalence among people with psychosis. British Journal not ideology in stigma research: Reply. Acta Psychiatrica
of Psychiatry, 187, 306–313. Scandinavica, 119, 413.
Gumley, A. I., MacBeth, A., Reilly, J. D., O’Grady, M., White, R. G., Kake, T. R., Arnold, R., & Ellis, P. (2008). Estimating the prevalence
McLeod, H., . . . Power, K. G. (2015). Fear of recurrence: Results of schizophrenia amongst New Zealand Maori: A capture-recapture
rie66620_ch07_147-186.indd 182 07/29/17 02:14 PM

approach. Australian and New Zealand Journal of Psychiatry, 42, psychosis and outcome in cohorts of first-episode outcome patients:
941–949. A systematic review. Archives of General Psychiatry, 62, 975–983.
Kavanagh, D. J. (1992). Family interventions for schizophrenia. In McEwan, T. E., Mullen, P. E., MacKenzie, R. D., & Ogloff, J. R.
D. J. Kavanagh (Ed.), Schizophrenia: An overview and practical P. (2009). Violence in stalking situations. Psychological Medicine,
handbook (pp. 407–423). Melbourne: Chapman & Hall. 39, 1469–1478.
Killackey, E. J., Jackson, H. J., Gleeson, J., Hickie, I. B., & McEwan, T., Mullen, P. E., & Purcell, R. (2007). Identifying risk
McGorry, P. D. (2006). Exciting career opportunity beckons! factors in stalking: A review of current research. International
Early intervention and vocational rehabilitation in first-episode Journal of Law and Psychiatry, 30, 1–9.
psychosis: Employing cautious optimism. Australian and New McFarlane, W. R., Dixon, L., Lukens, E., & Lucksted, A. (2003).
Zealand Journal of Psychiatry, 40, 951–962. Family psychoeducation and schizophrenia: A review of the
Killackey, E., Jackson, H. J., & McGorry, P. D. (2008). Vocational literature. Journal of Marital and Family Therapy, 29, 223–245.
intervention in first-episode psychosis: Individual placement and McGorry, P. (2005). Royal Australian and New Zealand College
support v. treatment as usual. British Journal of Psychiatry, 193, of Psychiatrists clinical practice guidelines for the treatment of
114–120. schizophrenia and related disorders. Australian and New Zealand
Koike, S., Yamaguchi, S., Ojio, Y., Ohta, K., & Ando, S. (2016). Journal of Psychiatry, 39, 1–30.
Effect of name change of schizophrenia on mass media between McGorry, P. D., Edwards, J., Mihalopoulos, C., Harrigan, S. M., &
1985 and 2013 in Japan: A text data mining analysis. Schizophrenia Jackson, H. J. (1996). EPPIC: An evolving system of early detection
Bulletin, 42, 552–559. and optimal management. Schizophrenia Bulletin, 22, 305–326.
Large, M., Sharma, S., Compton, M. T., Slade, T., & Nielssen, O. McGorry, P. D., Tanti, C., Stokes, R., Hickie, I. B., Carnell, K.,
(2011). Cannabis use and earlier onset of psychosis. Archives of Littlefield, L. K., & Moran, J. (2007). Headspace: Australias
General Psychiatry, 68, 555–561. National Youth Mental Health Foundation—where young minds
Larsen, T. K., Friis, S., Haahr, U., Johannessen, J. O., Melle, I., come first. Medical Journal of Australia, 187, S68–S70.
Opjordsmoen, S., . . . McGlashan, T. H. (2004). Premorbid McGorry, P. D., Yung, A. R., Phillips, L. J., Yuen, H. P., Francey, S.,
adjustment in first-episode non-affective psychosis: Distinct Cosgrave, E. M., . . . Jackson, H. (2002). Randomised controlled
patterns of pre-onset course. British Journal of Psychiatry, 185, trial of interventions designed to reduce the risk of progression
108–115. to first-episode psychosis in a clinical sample with subthreshold
Leeson, V. C., Laws, K. R., & McKenna, P. J. (2006). Formal thought symptoms. Archives of General Psychiatry, 59, 921–928.
disorder is characterised by impaired lexical access. Schizophrenia McGowan, J. F., Lavender, T., & Garety, P. A. (2005). Factors in
Research, 88, 161–168. outcome of cognitive-behavioural therapy for psychosis: Users and
Leuner, K., & Muller, W. E. (2006). The complexity of clinicians views. Psychology and Psychotherapy: Theory, Research
dopaminergic synapses and their modulation by antipsychotics. and Practice, 78, 513–529.
Pharmacopsychiatry, 39 (Supp. 1), S15–S20. McGrath, J. J. (2006). Variations in the incidence of schizophrenia:
Levinson, D. F., Duan, J. B., Oh, S., Wang, K., Sanders, A. R., Data versus dogma. Schizophrenia Bulletin, 32, 195–197.
Shi, J. X., . . . Gejman, P. V. (2011). Copy number variants in McGrath, J. J. (2007). The surprisingly rich contours of schizophrenia
schizophrenia: Confirmation of five previous findings and new epidemiology. Archives of General Psychiatry, 64, 14–16.
evidence for 3q29 microdeletions and VIPR2 duplications. McKetin, R., Lubman, D. I., Najman, J. M., Dawe, S., Butterworth,
American Journal of Psychiatry, 168, 302–316. P., & Baker, A. L. (2014). Does methamphetamine use increase
Lieberman, J. A., & First, M. B. (2007). Renaming schizophrenia: violent behaviour? Evidence from a prospective longitudinal study.
Diagnosis and treatment are more important than semantics. Addiction, 109, 798–806.
British Medical Journal, 334, 108. Menezes, N. M., Arenovich, T., & Zipursky, R. B. (2006). A
Lieberman, J. A., Perkins, D., Belger, A., Chakos, M., Jarskog, F., systematic review of longitudinal outcome studies of first-episode
Boteva, K., & Gilmore, J. (2001). The early stages of schizophrenia: psychosis. Psychological Medicine, 36, 1349–1362.
Speculations on pathogenesis, pathophysiology, and therapeutic Mental Health Council of Australia. (2005). Not for service:
approaches. Biological Psychiatry, 50, 884–897. Experiences of injustice and despair in mental health care in
Linscott, R. J., & van Os, J. (2013). An updated and conservative Australia. Canberra: Author.
systematic review and meta-analysis of epidemiological evidence Minozzi, S., Davoli, M., Bargagli, A. M., Amato, L., Vecchi, S.,
on psychotic experiences in children and adults: On the pathway & Perucci, C. A. (2010). An overview of systematic reviews on
from proneness to persistence to dimensional expression across cannabis and psychosis: Discussing apparently conflicting results.
mental disorders. Psychological Medicine, 43, 1133–1149. Drug and Alcohol Review, 29, 304–317.
Loebel, A. D., Lieberman, J. A., Alvir, J. M. J., Mayerhoff, D. I., Mond, J., Morice, R., Owen, C., & Korten, A. (2003). Use of antipsychotic
Geisler, S. H., & Szymanski, S. R. (1992). Duration of psychosis medications in Australia between July 1995 and December 2001.
and outcome in first episode schizophrenia. American Journal of Australian and New Zealand Journal of Psychiatry, 37, 55–61.
Psychiatry, 149, 1183–1188. Morrison, A. P. (2001). The interpretation of intrusions in psychosis:
Malla, A., & Payne, J. (2005). First-episode psychosis: An integrative approach to hallucinations and delusions.
Psychopathology, quality of life, and functional outcome. Behavioural and Cognitive Psychotherapy, 29, 257–276.
Schizophrenia Bulletin, 31, 650–671. Morrison, A. P., Frame, L., & Larkin, W. (2003). Relationships
Marshall, M., Lewis, S., Lockwood, A., Drake, R., Jones, P., & between trauma and psychosis: A review and integration. British
Croudace, T. (2005). Association between duration of untreated Journal of Clinical Psychology, 42, 331–353.
rie66620_ch07_147-186.indd 183 07/29/17 02:14 PM

Morrison, A. P., French, P., Parker, S., Roberts, M., Stevens, H., schizophrenia and bipolar disorder. British Journal of Psychiatry,
Bentall, R. P., & Lewis, S. W. (2007). Three-year follow-up of a 209, 107–113.
randomised controlled trial of cognitive therapy for the prevention Reininghaus, U., Priebe, S., & Bentall, R. P. (2013). Testing the
of psychosis in people at ultrahigh risk. Schizophrenia Bulletin, 33, psychopathology of psychosis: Evidence for a general psychosis
682–687. dimension. Schizophrenia Bulletin, 39, 884–895.
Morrison, A. P., French, P., Walford, L., Lewis, S. W., Kilcommons, Reupert, A. E., Cuff, R., Drost, L., Foster, K., van Doesum, K. T.
A., Green, J., . . . Bentall, R. P. (2004). Cognitive therapy for the M., & van Santvoort, F. (2012). Intervention programs for children
prevention of psychosis in people at ultra-high risk: Randomised whose parents have a mental illness: A review. Medical Journal of
controlled trial. British Journal of Psychiatry, 185, 291–297. Australia, 1 (1) 18–22.
Morrison, A. P., Turkington, D., Pyle, M., Spencer, H., Brabban, A., Ripke, S., Neale, B. M., Corvin, A., Walters, J. T. R., Farh, K. H.,
Dunn, G., . . . Hutton, P. (2014). Cognitive therapy for people with Holmans, P. A., . . . ODonovan, M. C. (2014). Biological insights
schizophrenia spectrum disorders not taking antipsychotic drugs: A from 108 schizophrenia-associated genetic loci. Nature, 511,
single-blind randomised controlled trial. Lancet, 383, 1395–1403. 421–427.
Mosher, L. R. (1999). Soteria and other alternatives to acute Robinson, D. G., Woerner, M. G., Alvir, J. M. J., Bilder, R.,
psychiatric hospitalization: A personal and professional review. Goldman, R., Geisler, S., . . . Lieberman, J. A. (1999). Predictors
Journal of Nervous and Mental Disease, 187, 142–149. of relapse following response from a first episode of schizophrenia
Mueser, K. T., Lu, W. L., Rosenberg, S. D., & Wolfe, R. (2010). The or schizoaffective disorder. Archives of General Psychiatry, 56,
trauma of psychosis: Posttraumatic stress disorder and recent onset 241–247.
psychosis. Schizophrenia Research, 116, 217–227. Rosebush, P. I., & Mazurek, M. F. (2010). Catatonia and its treatment.
Nuechterlein, K. H., Dawson, M. E., Gitlin, M., Ventura, J., Goldstein, Schizophrenia Bulletin, 36, 239–242.
M. J., Snyder, K. S., . . . Mintz, J. (1992). Developmental processes Rossell, S. L., & David, A. S. (2006). Are semantic deficits
in schizophrenic disorders: Longitudinal studies of vulnerability in schizophrenia due to problems with access or storage?
and stress. Schizophrenia Bulletin, 18, 387–424. Schizophrenia Research, 82, 121–134.
Ohayon, M. M. (2000). Prevalence of hallucinations and their Salkovskis, P. M., & Kirk, J. (1989). Obsessional disorders. In K.
pathological associations in the general population. Psychiatry Hawton, P. Salkovskis, J. Kirk, & D. Clark (Eds.), Cognitive
Research, 97, 153–164. behaviour therapy for psychiatric problems: A practical guide
Palmer, B. A., Pankratz, V. S., & Bostwick, J. M. (2005). The lifetime (pp. 129–168). Oxford: Oxford University Press.
risk of suicide in schizophrenia: A reexamination. Archives of SANE Australia (2011). People living with psychotic illness: A SANE
General Psychiatry, 62, 247–253. response. Retrieved from www.sane.org/images/PDFs/1111_
Pantelis, C., Yucel, M., Wood, S. J., Velakoulis, D., Sun, D. Q., info_A-SANE-response.pdf.
Berger, G., . . . McGorry, P. D. (2005). Structural brain imaging Sartorius, N., Jablensky, A., Korten, A., Ernberg, G., Anker,
evidence for multiple pathological processes at different stages of M., Cooper, J. E., & Day, R. (1986). Early manifestations and
brain development in schizophrenia. Schizophrenia Bulletin, 31, first-contact incidence of schizophrenia in different cultures.
672–696. Psychological Medicine, 16, 909–928.
Phillips, L. J., McGorry, P. D., Garner, B., Thompson, K. N., Pantelis, Sato, M. (2006). Renaming schizophrenia: A Japanese perspective.
C., Wood, S. J., & Berger, G. (2006). Stress, the hippocampus World Psychiatry, 5(1), 53-55.
and the hypothalamic-pituitary-adrenal axis: Implications for Seal, M. L., Aleman, A., & McGuire, P. K. (2004). Compelling
the development of psychotic disorders. Australian and New imagery, unanticipated speech and deceptive memory:
Zealand Journal of Psychiatry, 40, 725–741. doi: 10.1080/j.1440- Neurocognitive models of auditory verbal hallucinations in
1614.2006.01877.x schizophrenia. Cognitive Neuropsychiatry, 9, 43–72.
Pilling, S., Bebbington, P., Kuipers, E., Garety, P., Geddes, J., Sekar, A., Bialas, A. R., de Rivera, H., Davis, A., Hammond, T.
Orbach, G., & Morgan, C. (2002). Psychological treatments in R., Kamitaki, N., . . . Schizophrenia Working Group (2016).
schizophrenia I: Meta-analysis of family intervention and cognitive Schizophrenia risk from complex variation of complement
behaviour therapy. Psychological Medicine, 32, 763–782. component 4. Nature, 530, 177–183. doi:10.1038/nature16549
Read, J., Haslam, N., Sayce, L., & Davies, E. (2006). Prejudice and Sims, A. (1995). Symptoms in the mind: An introduction to descriptive
schizophrenia: A review of the mental illness is an illness like any psychopathology (2nd ed.). London: Saunders.
other approach. Acta Psychiatrica Scandinavica, 114, 303–318. Smith, D. A., & Buckley, P. F. (2006). Pharmacotherapy of
Read, T., Potter, M., & Gurling, H. (1992). The genetics of delusional disorders in the context of offending and the potential
schizophrenia. In D. J. Kavanagh (Ed.), Schizophrenia: An for compulsory treatment. Behavioral Sciences & the Law, 24,
overview and practical handbook (pp. 109–125). Melbourne: 351–367.
Chapman & Hall. Soyka, M., & Schmidt, P. (2011). Prevalence of delusional jealousy in
Read, J., van Os, J., Morrison, A. P., & Ross, C. A. (2005). psychiatric disorders. Journal of Forensic Sciences, 56, 450–452.
Childhood trauma, psychosis and schizophrenia: A literature Stahl, S. M., & Buckley, P. F. (2007). Negative symptoms of
review with theoretical and clinical implications. Acta Psychiatrica schizophrenia: A problem that will not go away. Acta Psychiatrica
Scandinavica, 112, 330–350. Scandinavica, 115, 4–11.
Reininghaus, U., Bohnke, J. R., Hosang, G., Farmer, A., Burns, T., Stone, J. M., Morrison, P. D., & Pilowsky, L. S. (2007). Glutamate
McGuffin, P., & Bentall, R. P. (2016). Evaluation of the validity and dopamine dysregulation in schizophrenia: A synthesis and
and utility of a transdiagnostic psychosis dimension encompassing selective review. Journal of Psychopharmacology, 21, 440–452.
rie66620_ch07_147-186.indd 184 07/29/17 02:14 PM

Strakowski, S. M., Keck, P. E., McElroy, S. L., Lonczak, H. S., & Vaughn, C., & Leff, J. P. (1976). The influence of family and social
West, S. A. (1995). Chronology of comorbid and principal factors on the course of psychiatric illness. British Journal of
syndromes in first-episode psychosis. Comprehensive Psychiatry, Psychiatry, 129, 125–137.
36, 106–112. Ventura, J., Nuechterlein, K. H., Lukoff, D., & Hardesty, J. P. (1989).
Sumiyoshi, T., Saitoh, O., Yotsutsuji, T., Itoh, H., Kurokawa, K., A prospective study of stressful life events and schizophrenic
& Kurachi, M. (1999). Differential effects of mental stress on relapse. Journal of Abnormal Psychology, 98, 407–411.
plasma homovanillic acid in schizophrenia and normal controls. Volkow, N. D., Swanson, J. M., Evins, A. E., DeLisi, L. E., Meier, M.
Neuropsychopharmacology, 20, 365–369. H., Gonzalez, R., . . . Baler, R. (2016). Effects of cannabis use on
Tarrier, N., Kinney, C., McCarthy, E., Humphreys, L., Wittkowski, A., human behavior, including cognition, motivation, and psychosis: A
& Morris, J. (2000). Two-year follow-up of cognitive-behavioural review. JAMA Psychiatry, 73, 292–297.
therapy and supportive counselling in the treatment of persistent Wahlbeck, K., Cheine, M., Essali, A., & Adams, C. (1999). Evidence
symptoms in chronic schizophrenia. Journal of Consulting and of clozapines effectiveness in schizophrenia: A systematic review
Clinical Psychology, 68, 917–922. and meta-analysis of randomized trials. American Journal of
Tarrier, N., & Turpin, G. (1992). Psychosocial factors, arousal and Psychiatry, 156, 990–999.
schizophrenic relapse: The psychophysiological data. British Walder, D. J., Faraone, S. V., Glatt, S. J., Tsuang, M. T., & Seidman,
Journal of Psychiatry, 161, 3–11. L. J. (2014). Genetic liability, prenatal health, stress and family
Tarrier, N., Yusupoff, L., Kinney, C., McCarthy, E., Gledhill, A., environment: Risk factors in the Harvard adolescent family
Haddock, G., & Morris, J. (1998). Randomised controlled trial high risk for schizophrenia study. Schizophrenia Research, 157,
of intensive cognitive behaviour therapy for patients with chronic 142–148.
schizophrenia. British Medical Journal, 317, 303–307. Walsh, T., McClellan, J. M., McCarthy, S. E., Addington, A. M.,
Thompson, K. N., McGorry, P. D., & Harrigan, S. M. (2003). Pierce, S. B., Cooper, G. M., . . . Sebat, J. (2008). Rare structural
Recovery style and outcome in first-episode psychosis. variants disrupt multiple genes in neurodevelopmental pathways in
Schizophrenia Research, 62, 31–36. schizophrenia. Science, 320, 539–543.
Topp, L., Degenhardt, L., Kaye, S., & Darke, S. (2002). The Wood, S. J., Pantelis, C., Velakoulis, D., Yucel, M., Fornito, A., &
emergence of potent forms of methamphetamine in Sydney, McGorry, P. D. (2008). Progressive changes in the development
Australia: A case study of the IDRS as a strategic early warning toward schizophrenia: Studies in subjects at increased symptomatic
system. Drug & Alcohol Review, 21, 341–348. risk. Schizophrenia Bulletin, 34, 322–329. doi: 10.1093/schbul/
Ungvari, G. S., Leung, S. K., Ng, F. S., Cheung, H. K., & Leung, sbm149
T. (2005). Schizophrenia with prominent catatonic features Yung, A. R., & McGorry, P. D. (1996). The prodromal phase of
(catatonic schizophrenia) I: Demographic and clinical correlates first-episode psychosis: Past and current conceptualisations.
in the chronic phase. Progress in Neuro-Psychopharmacology & Schizophrenia Bulletin, 22, 353–370.
Biological Psychiatry, 29, 27–38. Yung, A., Phillips, L., McGorry, P., McFarlane, C., Francey, S.,
van Os, J., Hanssen, M., Bak, M., Bijl, R. V., & Vollebergh, W. Harrrigan, S., . . . Jackson, H. (1998). A step towards indicated
(2003). Do urbanicity and familial liability coparticipate in causing prevention of schizophrenia. British Journal of Psychiatry, 172
psychosis? American Journal of Psychiatry, 160, 477–482. (Supp. 33), 14–20.

van Os, J., Kenis, G., & Rutten, B. P. F. (2010). The environment and Yung, A. R., Phillips, L. J., Yuen, H. P., Francey, S. M., McFarlane,
schizophrenia. Nature, 468, 203–212. C. A., Hallgren, M., & McGorry, P. D. (2003). Psychosis
van Os, J., Linscott, R. J., Myin-Germeys, I., Delespaul, P., & prediction: 12-month follow up of a high-risk (prodromal) group.
Krabbendam, L. (2009). A systematic review and meta-analysis Schizophrenia Research, 60, 21–32.
of the psychosis continuum: Evidence for a psychosis proneness- Zubin, J., & Spring, B. (1977). Vulnerability: A new view of
persistence-impairment model of psychotic disorder. Psychological schizophrenia. Journal of Abnormal Psychology, 86, 103–126.
Medicine, 39, 179–195.
van Os, J., Rutten, B. P. F., & Poulton, R. (2008). Gene–environment
interactions in schizophrenia: Review of epidemiological findings
and future directions. Schizophrenia Bulletin, 34, 1066–1082.
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CHAPTER 9
Eating disorders
Stephen Touyz
Phillipa Hay
Elizabeth Rieger
CHAPTER OUTLINE
● Historical and current approaches to the diagnosis of eating disorders
● Anorexia nervosa
● Bulimia nervosa
● Binge eating disorder
● General topics in eating disorders
● Summary

9.1 Describe the diagnostic features of eating disorders.
9.2 Describe current understandings regarding the epidemiology, aetiology and treatment of anorexia nervosa.
9.3 Describe current understandings regarding the epidemiology, aetiology and treatment of bulimia nervosa.
9.4 Describe current understandings regarding the epidemiology, aetiology and treatment of binge eating disorder.
9.5 Understand key challenges facing the eating disorders field and evaluate the various responses to these
challenges.
EATING DISORDERS: AN AUSTRALASIAN FOCUS

The Butterfly Foundation is a national organisation supporting the needs of people affected by eating disorders and poor
body image. In 2016, the Mental Health Commission of NSW commissioned the Butterfly Foundation to conduct a research
project entitled, ‘Insights in Recovery’. The project sought to obtain the views of people with eating disorders regarding
the effective ingredients that have helped their journey of recovery. The insights gained from these participants were
then used to develop guidelines for health professionals working to help people recover from these serious conditions.
The first guideline encourages people with eating disorders and those who care for them to develop a mutual
understanding of the recovery process. This means understanding that recovery includes not just improved eating habits
and weight control behaviours, but broader issues such as self-acceptance, having a fulfilling social life, and being able
to express and manage emotions. Recovery is also often a lengthy process with many ups and downs. As one participant
stated, ‘Unrealistic expectations of recovery (that it is quick, easy or predictable) make you feel as if you are failing at
recovery and are de-motivating’ (p. 21). At the same time, it is essential to understand that recovery is achievable: ‘I also
needed to have hope. It gave me hope to have someone help me believe that recovery was possible for me no matter
what diagnosis or how long (or short) I have been unwell’ (p. 21).
Another guideline for health professionals is to support individuals in disclosing their eating disorder and obtaining
help. In the words of one participant, ‘I felt deeply ashamed about what was going on for me and that made it very
difficult for me to talk about my eating disorder’ (p. 23).
continued
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A related guideline is the importance of health

professionals helping the person with an eating disorder to
feel safe: ‘I don’t think that everyone gets how low your self-
esteem goes with an eating disorder . . . I needed people
who were gentle with me and nurtured me. People who
made me feel valued, welcome and safe. But I also needed
firm, clear boundaries to help me feel safe’ (p. 28).
Part of providing safety is encompassed in the guideline
for health professionals to be careful with the language
they use when communicating with someone with an
eating disorder. As just one example, referring to ‘a person
struggling with anorexia nervosa’ rather than ‘an anorexic’
demonstrates that the person is first and foremost a human
being; a unique individual who is more than their eating
DAL
disorder.
Eating disorders are serious conditions that cause
A key guideline for health professionals in supporting
significant distress both to the individuals with these
recovery is to help the person develop a sense of self-
conditions and to their family members and friends.
identity. As one participant said, ‘It helps when you see me
Recovery, however, can be achieved.
as a person even when I can’t see myself as anything other
than my eating disorder’ (p. 36). Developing a sense of
identify other than the eating disorder helps people to envisage a valuable self and life beyond their condition.
Another guideline refers to the importance of people with eating disorders being provided with choice in the recovery
process: ‘It helps me when you are open to learning about eating disorders in partnership with me and work with me to
frame treatment goals that have meaning for me. So please help me to take ownership of my recovery’ (p. 40).
An additional guideline refers to helping people with eating disorders find healthy supports, whether among
health professionals, family members or peers. Healthy support is characterised by a sense of trust and connection,
and is needed over the long term and during all stages of recovery. As one participant noted, ‘You need a social
support team. It doesn’t have to be immediate family; it can be friends or peers. You need someone there with you for
the long term. You don’t get over an eating disorder by yourself’ (p. 44).
The final guideline emphasises the importance of gaining insights regarding the recovery process from those
who have experienced recovery, or who are in the process of recovering, just as the ‘Insights in Recovery’ project
sought to do. In the words of one of the participants, ‘It really helps when my health professionals have an up-to-
date knowledge of eating disorders. That doesn’t mean they have to know it all from the start. Sometimes the most
helpful professionals are the ones who admit they don’t know and are prepared to learn about eating disorders in
partnership with me’ (p. 47).
Eating disorders are the focus of this chapter. Following a brief overview of the historical approaches to understanding
these disorders and the current classification system, the eating disorders of anorexia nervosa, bulimia nervosa and
binge eating disorder will be dealt with in turn. For each of these conditions, a description of the disorder’s prevalence,
age of onset, course, associated problems, aetiology and main treatment approaches will be provided. Finally, some
key challenges and controversies in the eating disorders field will be highlighted, including limitations of the available
treatment approaches, the clinical and ethical issues associated with involuntary treatment, the categorisation of muscle
dysmorphia as an eating disorder and efforts to prevent the development of these serious and often chronic conditions.

to the diagnosis of eating disorders
The current, fifth edition of the American Psychiatric Association’s Diagnostic and Statistical Manual
of Mental Disorders (DSM-5) (American Psychiatric Association [APA], 2013) includes a chapter on
‘Feeding and Eating Disorders’, which refers to conditions that entail ‘a persistent disturbance in
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Chapter 9 Eating disorders 237
eating or eating-related behaviour that results in the altered consumption or absorption of food and
that significantly impairs physical health or psychosocial functioning’ (p. 329). While each of these
conditions will be briefly described, the focus of this chapter is on anorexia nervosa, bulimia nervosa
and binge eating disorder.
Anorexia nervosa
Anorexia nervosa was the first eating disorder to be recognised. Conditions resembling anorexia
nervosa can be found among accounts of fasting female saints during the medieval period (Bell,
1985). However, definitive clinical descriptions of the disorder did not appear until the 1870s,
when the British physician William Gull (1874) and the French neuropsychiatrist Charles
Lasègue (1873) provided detailed accounts of a condition whose essential features have remained
unchanged to this day. Gull (1874) proposed the term anorexia nervosa, which referred to a loss anorexia nervosa
of appetite (anorexia) as a result of a nervous (nervosa) or mental rather than a biological cause. Eating disorder
For a period in the first half of the twentieth century, biological approaches to anorexia nervosa in which the
individual is
became dominant, when the disorder was thought to result from dysfunction of the pituitary gland
significantly
(Simmonds, 1914). Yet a careful review by Sheehan and Summers (1948) demonstrated that the below a body
clinical features of anorexia nervosa and pituitary disease were in fact distinct. Psychological weight that is
understandings of the disorder again became predominant, largely through the influential work of normal for his/her
Hilde Bruch beginning in the 1960s. Diagnostic criteria used in this period were, however, loosely age and height
defined and the term ‘anorexia nervosa’ tended to be used to embrace all forms of weight loss and suffers from
without a biological basis. a fear of gaining
The British psychiatrist Gerald Russell (1970) was the first to propose formal diagnostic criteria for weight and from
body image
anorexia nervosa. These criteria were a landmark in the history of eating disorders. They distinguished
disturbance.
anorexia nervosa from other forms of weight loss not attributable to a medical cause (e.g., major
depression). The criteria included characteristic attitudes and behaviours, their effect on weight, and
symptoms of the hormonal disturbance associated with weight loss.
Russell’s (1970) criteria are reflected in what are currently the most widely used diagnostic criteria
for defining cases of anorexia nervosa, namely, those from the DSM-5 (APA, 2013). According to
the DSM-5, patients with anorexia nervosa are primarily characterised by a relentless pursuit of
thinness resulting in weight loss substantially below a normal body weight (e.g., a weight less than
85 per cent of that expected given the individual’s age and height). The criteria further specify several
characteristic cognitive distortions, including various manifestations of a body image disturbance
(e.g., that the individual’s sense of self-worth is based excessively on his/her shape/weight or that the
individual denies the seriousness of his/her low weight). In addition, there is a criterion that refers to
an intense fear of gaining weight or engaging in persistent behaviour to avoid gaining weight. The bulimia nervosa
phrase ‘engaging in persistent behaviour to avoid gaining weight’ indicates that a significant minority Eating disorder
of individuals with anorexia nervosa state that they do not fear weight gain, even though they engage in which the
in strong efforts to prevent it. individual
engages in
The DSM-5 specifies two subtypes of anorexia nervosa: a restricting and a binge eating/purging
recurrent
type. In the second subtype, the person regularly engages in binge eating or purging behaviour (e.g., binge eating
self-induced vomiting or the misuse of laxatives). This subtype is nevertheless distinct from bulimia episodes and
nervosa in that patients with bulimia nervosa are not underweight. Partial and full remission subtypes compensatory
are also specified. behaviours (such
The DSM-5 also includes severity specifiers for anorexia nervosa based on body weight or body as self-induced
mass index (BMI = kg/m2). For adults, mild anorexia nervosa is a BMI > 17, moderate 16–16.99, vomiting, abuse
of laxatives
severe 15–15.9 and extreme < 15 (or equivalent percentiles for children and adolescents). These levels
and excessive
can be revised to also take into consideration the individual’s clinical symptoms, level of functional exercise)
disability and/or need for supervision. In line with this, Maguire, Touyz, Surgenor, Lacey, and Le designed to
Grange (2011) proposed that a staging system based on the severity of symptoms (similar to the prevent
staging system used for categorising cancer of different levels of severity) be used for anorexia weight gain.
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nervosa. Such a staging system would help clinicians to take into account the severity of the patient’s
condition in terms of treatment planning, and would also allow for clearer descriptions of the patients
included in studies, which is essential when comparing the findings obtained in different studies.
An instrument for staging anorexia nervosa based on symptomatic severity has been developed: the
Clinician Administered Staging Instrument for Anorexia Nervosa. This instrument derives an illness
severity score and on this basis classifies patients as having stage 1 anorexia nervosa (mild illness
pathology), stage 2 (moderate illness pathology), stage 3 (moderate to severe illness pathology) or
stage 4 (extremely severe illness pathology).
Bulimia nervosa
Stunkard (1993), in his writings on the history of binge eating, points out that physicians in the
Graeco-Roman classical world already made reference to pathological forms of hunger and overeating,
commonly associated with faintness. In the contemporary era, clinical descriptions of ‘boulimie’ or
‘bulimia’ (stemming from the Greek term for ‘ox appetite’) appeared in the nineteenth century. In
these clinical accounts, food was a major preoccupation and enormous quantities were consumed. By
the end of the nineteenth century, references to bulimia were found in Osler’s (1892) medical textbook.
Bulimia received very little further attention in the first half of the twentieth century. Clinical
interest in overeating syndromes was then stimulated from studies of individuals with obesity and the
forms of overeating found in newly described neurological disorders such as Klüver-Bucy syndrome
(Stunkard, 1993). During this period, studies of the central nervous system identified the neurological
mechanisms of satiety (fullness) regulation. A failure to register fullness after eating was thought
to lead to forms of obesity and the syndrome of ‘night-eating’, which was described by Stunkard
and colleagues in 1955. This was a syndrome found in obese individuals that primarily consisted of
overeating in the evening and seemed to be precipitated by stress. Stunkard termed the uncontrolled
overeating of large amounts of food ‘binge eating’, based on its similarity to a drinking binge by
someone with an alcohol problem.
The next development occurred with the identification of overeating in normal-weight individuals,
including the accounts of binge eating followed by vomiting in college women termed ‘bulimarexia’
(Boskind-Lodahl & White, 1978). In 1979, Gerald Russell published another landmark paper titled
‘Bulimia nervosa: An ominous variant of anorexia nervosa’. In this paper, Russell distinguished
bulimia nervosa from anorexia nervosa by the patients’ strong urges to overeat and the fact that patients
were not required to be underweight. The following year, the American Psychiatric Association, in the
DSM-III, also recognised bulimia as a new eating disorder characterised by overeating (APA, 1980).
Thus, by 1980 two eating disorders were recognised: anorexia nervosa and bulimia (later termed
bulimia nervosa).
However, there were several major problems with the DSM-III diagnostic criteria of bulimia.
First, they were too broad and thereby over-inclusive. For example, patients with overeating as part
of a depressive disorder could meet the criteria for bulimia. Second, there was an overemphasis on
binge eating a single behaviour (i.e., binge eating episodes) being sufficient for the diagnosis, while other eating
episode disorder symptoms of importance (such as extreme weight-control behaviours) were not an essential
An instance of requirement. Third, the criteria also caused confusion in their use of the term ‘bulimia’ to denote both
disordered eating the disorder as well as the behaviour of overeating.
characterised Russell’s criteria (1979; 1983) were reflected in the major revision of the DSM-III (APA, 1987).
by eating an Bulimia was renamed and Russell’s term ‘bulimia nervosa’ adopted. The DSM-III-R criteria, like
excessive
Russell’s criteria (1983), incorporated both inappropriate weight-control behaviours (e.g., self-induced
amount of food,
accompanied by vomiting) and the presence of a characteristic attitudinal disturbance (namely, the over-importance of
a sense of lack shape and weight in determining the individual’s sense of self-worth) as necessary diagnostic features,
of control over together with binge eating. Episodes of binge eating were defined in terms of two characteristics:
eating. (a) eating an amount of food that is definitely larger than most people would eat in the same amount of
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time, and (b) a sense of lack of control over eating during the episode (a feeling that one cannot stop
eating or control what or how much one is eating).
The DSM-IV (APA, 1994; 2000) and current DSM-5 (APA, 2013) systems have made few
alterations to the criteria for bulimia nervosa except to further specify the frequency and duration of
behaviours (with both the binge eating and weight-control behaviours needing to occur, on average,
at least once a week for three months in the DSM-5). In addition, it is specified that bulimia nervosa
cannot occur at the same time as anorexia nervosa: individuals who meet all of the criteria for
bulimia nervosa but are significantly underweight will be diagnosed solely with anorexia nervosa.
Inappropriate, compensatory weight-control behaviours can include fasting or excessive exercise
or purging behaviours (i.e., self-induced vomiting or the misuse of laxatives, diuretics or enemas).
There are diagnostic specifiers for partial and full remission and severity based on weekly frequency
of episodes of inappropriate compensatory behaviours: mild bulimia nervosa is 1–3, moderate 4–7,
severe 8–13 and extreme > 14 episodes per week.
Binge eating disorder binge eating

disorder
In 1992, Spitzer and colleagues suggested that another eating disorder, termed binge eating disorder, Eating disorder
be recognised; it is characterised by the occurrence of binge eating episodes but without the weight- in which the
control behaviours (e.g., vomiting) characteristic of those with bulimia nervosa. The DSM-5 included individual
binge eating disorder in its own right (in contrast to the DSM-IV, where it was listed in a residual engages in
recurrent binge
category of ‘eating disorders not otherwise specified’). In order to meet the criteria for binge eating
eating episodes
disorder, the individual must engage in binge eating episodes at least once weekly for at least three but does not
months (comparable to the frequency criteria for bulimia nervosa), but not regularly engage in the engage in
inappropriate weight-control behaviours (e.g., purging) that are characteristic of bulimia nervosa. compensatory
In addition, the binge eating is required to be associated with marked distress and three of five behaviours
descriptors, namely eating more rapidly than normal, eating until uncomfortably full, eating when (such as self-
not hungry, eating alone because of embarrassment, or feeling disgusted, guilty or depressed after induced vomiting)
eating. Like bulimia nervosa, there are diagnostic specifiers for partial and full remission and designed to
counteract the
severity based on weekly frequency of binge eating episodes: mild binge eating disorder is 1–3,
caloric intake.
moderate 4–7, severe 8–13 and extreme > 14 episodes per week. It is important to note that to be
diagnosed with binge eating disorder the individual does not meet criteria for anorexia nervosa or tube feeding
bulimia nervosa. In addition, unlike anorexia nervosa and bulimia nervosa, there is no requirement Practice of
feeding a patient
for a disturbance of body image or overvaluation of weight or shape in the diagnosis of binge
via a tube in the
eating disorder. case of patients
who are unable
or refuse to
Other DSM-5 feeding or eating disorders obtain nutrition
Another diagnostic category listed among the feeding and eating disorders of the DSM-5 is avoidant/ by swallowing;
in the case
restrictive food intake disorder (ARFID). This is a heterogeneous syndrome, which can occur in
of severely
people ranging from children with autistic spectrum disorder to adults with food or swallowing malnourished
phobias. Common to all cases is a persistent eating disturbance such that energy and/or nutritional patients with
needs are not met. Subsequently, the person becomes either underweight or fails to gain weight anorexia nervosa,
expected for age, is deficient in essential nutrients, is dependent on enteral nutrition (i.e., tube a nasogastric
feeding in which liquid food is administered through a tube into the stomach or small intestine) tube may be
or medically prescribed oral supplementary feeding and/or is impaired in his/her psychosocial used, which
entails a plastic
functioning. There is no disturbance of body image or weight/shape concern and the disturbance is
tube being
not better explained by another eating, mental health or physical health disorder, cultural practices or inserted through
food being unavailable. the nose and
The DSM-5 provides two residual categories for disturbances not meeting the full diagnostic throat into the
criteria for anorexia nervosa, bulimia nervosa, binge eating disorder or avoidant/restrictive food stomach.
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CASE STUDY: AVOIDANT/RESTRICTIVE FOOD INTAKE DISORDER (ARFID)

Rachel is a 32-year-old woman who was admitted to a general medical hospital ward after she presented to the
Emergency Department. She was referred to the Emergency Department by her family doctor, who was concerned
about her low weight (a BMI of 16) and very low blood pressure during a routine yearly consultation to renew her oral
contraceptive pill prescription and for a ‘pap smear’. Blood tests taken in the Emergency Department found that she had
severe anaemia and she reported that she had lost an extreme amount of weight (30 kg) during the past year.
Rachel said her weight loss started when she choked while eating a beef steak about a year previously. She was eating
dinner in a restaurant when this occurred and she became very distressed, both because of the physical discomfort of
coughing and gagging for several minutes and the intense embarrassment she felt for causing a scene in public. Since
this event she had avoided eating in public and had become very restrictive in her eating habits. Initially she cut out
all red meat, then all meat. Over time, she eventually eliminated all solid foods so that she consumed only liquid dairy
products or vegetables (e.g., carrot juice).
While Rachel accepted that she was now underweight, was unhappy with her appearance at such a low weight and
was no longer losing weight, she reported a terror of eating solid foods and that she struggled to drink enough to regain
weight. So she agreed to nasogastric tube feeding in the hospital.
Rachel has no past history of an eating disorder or major mental illness. She described being anxious as a child,
beginning when she experienced high distress during her first weeks at school as a result of being separated from
her mother. Due to this anxiety, her school entry was delayed for six months and she was eventually enrolled in an
alternate school where her mother could join her each day at school during her first year. Rachel has been otherwise
well and, even though she was previously moderately well-built (she described herself as ‘chubby’), she has not dieted
or restricted her food intake in the past as a way to reduce her weight.
A psychiatrist at the hospital diagnosed Rachel as having ARFID. A barium swallow test revealed no physical
impediments to swallowing. As a result of finding no physical obstructions, Rachel was commenced on a ‘swallowing’
rehabilitation program, with swallowing exercises, anxiety management training and gradual increases in the consistency
of her oral intake, starting with semi-solids such as baked custard and iron supplements given for anaemia. She made a
good recovery over the next three months, by which time she had resumed a solid diet with the exception of red meat,
which she did not want to eat ever again. She had also regained a healthy amount of weight and was no longer anxious
about eating in public.
barium swallow intake disorder, namely, ‘other specified feeding or eating disorder’ and ‘unspecified feeding or eating
A test that is used disorder’. Compared to the DSM-IV, the DSM-5 entails using less strict criteria for anorexia nervosa
to determine the and bulimia nervosa and includes binge eating disorder in its own right. These changes reduce the
cause of difficulty
number of people who are likely to fall into the residual eating/feeding disorder categories. This
with swallowing.
The patient drinks is an important development as the former residual DSM-IV category was relatively neglected by
a preparation researchers despite evidence from many studies that between a third and a half of individuals with
containing barium disturbances regarding their eating, shape and weight did not meet the DSM-IV criteria for anorexia
sulphate, which nervosa or bulimia nervosa and thus fell into the residual category (Fairburn & Harrison, 2003). In
is a metallic other words, a substantial number of people with significant eating and body image disturbances were
compound that being neglected.
shows up on
There are five ‘other specified feeding or eating disorder’ (OSFED) types described in the
X-rays and is
used to see
DSM-5. These are atypical anorexia nervosa (where all criteria are met for anorexia nervosa, except
abnormalities in low weight); bulimia nervosa and binge eating disorder of low (less than weekly) frequency and/or
the oesophagus duration of binge eating/compensatory episodes; purging disorder (purging behaviours in the absence
and stomach. of binge eating); and night eating syndrome (excessive eating after the evening meal or eating at
night after awakening from sleep). The ‘unspecified feeding or eating disorder’ category is to be
used when the feeding or eating disorder causes significant distress and/or impaired psychosocial
functioning but there is insufficient information to specify the type of disorder (e.g., in emergency
hospital settings).
Two final conditions are listed among the DSM-5’s feeding and eating disorders, that is, pica
and rumination disorder. Pica refers to the eating of one or more non-food substances (e.g., soap,
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hair or soil) on a persistent basis for at least one month. Rumination disorder refers to the repeated
regurgitation of food (which may be re-chewed, re-swallowed or spat out) for a period of at least one
month but does not occur in the context of anorexia nervosa, bulimia nervosa, binge eating disorder
or avoidant/restrictive food intake disorder. The range of feeding and eating disorders contained in the
DSM-5 is shown in Table 9.1.
TABLE 9.1 Summary of the feeding and eating disorders contained in the DSM-5
Anorexia nervosa • Significantly underweight
• Fears gaining weight and/or engages in behaviours to prevent weight gain
• Body image disturbance (e.g., self-worth is excessively influenced by shape/weight, lack
of recognition of the seriousness of the current low weight)
Bulimia nervosa • Binge eating episodes
• Inappropriate weight-control behaviours (e.g., self-induced vomiting)
• Self-worth is excessively influenced by shape/weight
Binge eating disorder • Binge eating episodes
• Marked distress regarding the binge eating
• No current regular inappropriate weight-control behaviours (e.g., self-induced vomiting)
Avoidant/restrictive food intake • A persistent eating disturbance associated with failure to meet nutritional/energy needs
disorder (ARFID) • The eating disturbance cannot be explained by cultural practices, another eating
disorder, body image disturbance and/or another medical or mental health condition
Other specified feeding or • Disturbances of eating that do not meet criteria for anorexia nervosa, bulimia nervosa,
eating disorder (OSFED) binge eating disorder or avoidant/restrictive food intake disorder. Types include:
1. atypical anorexia nervosa where all of the criteria for anorexia nervosa are met
except for current underweight
2. bulimia nervosa of low frequency and/or limited duration where all criteria are met
except that the binge eating or weight-control behaviours occur less than once a
week and/or for less than 3 months
3. binge eating disorder of low frequency and/or limited duration where all criteria are
met except frequency and/or duration of binge eating episodes
4. purging disorder (recurrent purging to influence weight or shape)
5. night eating syndrome (recurrent eating in the evening or after awakening from sleep
that is excessive and causes distress)
Unspecified feeding or eating • Symptoms characteristic of an eating disorder causing significant impairment or distress
disorder that do not meet full criteria for another eating disorder
Pica • Persistent eating of non-food substances
Rumination disorder • Repeated regurgitation of food, which may then be re-chewed, re-swallowed or spat out
Source: Adapted from the Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Copyright 2013, American Psychiatric Association.
LO 9.2 Anorexia nervosa

The first of the major eating disorders to be addressed is anorexia nervosa, a disorder characterised by
emaciation; a fear of gaining weight or engaging in behaviours to prevent weight gain; and body image
disturbance (e.g., self-worth based excessively on shape/weight).
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The epidemiology of anorexia nervosa

Anorexia nervosa primarily affects females, with an age of onset that is generally younger than other
eating disorders. Sufferers experience a number of associated psychological and medical problems.
PREVALENCE
Anorexia nervosa affects mainly adolescent girls and young women. National surveys conducted
in the United States and New Zealand found that 0.9 per cent of women had experienced anorexia
nervosa at some point in their lifetime (Hudson, Hiripi, Pope, & Kessler, 2007) and less than one per
cent currently had anorexia nervosa (Oakley Browne, Wells, & Scott, 2006). The disorder is usually
estimated to be 10 times more common in females than in males. The condition appears to have
become more common over the second half of the twentieth century (Pawluck & Gorey, 1998).
AGE OF ONSET AND COURSE OF THE DISORDER
The age of onset for anorexia nervosa is generally younger than other eating disorders, and is
most usually in early to late adolescence (Hudson et al., 2007). However, pre-pubertal onset is not
uncommon. The mortality rate for anorexia nervosa (5–10 per cent of patients die per decade of illness)
is among the highest of all psychiatric disorders, with most deaths due to the medical complications of
starvation or suicide (Arcelus, Mitchell, Wales, & Nielsen, 2011).
Recovery from anorexia nervosa is typically a lengthy process, and a substantial proportion of
patients will fail to make a full recovery. In a review of outcome studies by Steinhausen (2002),
47 per cent of patients with anorexia nervosa had recovered after 4–10 years of illness, 32.4 per cent
had improved but still experienced some symptoms, and 19.7 per cent remained chronically ill.
Young girls with a brief history of illness tend to experience a better outcome. In contrast, patients
who engage in binge eating and purging behaviours, have been ill for a longer period of time or
have symptoms of obsessive-compulsive personality disorder tend to have a poorer outcome. About
50 per cent of patients with anorexia nervosa go on to develop bulimia nervosa, binge eating disorder
or ‘other specified feeding or eating disorder’ (OSFED).
ASSOCIATED PSYCHOLOGICAL AND MEDICAL PROBLEMS
Since anorexia nervosa is by definition a syndrome of self-starvation, individuals suffer from the
medical and psychological complications of starvation. A classic study of human starvation by Keys,
Brozek, Henschel, Mickelsen, and Taylor (1950) reported the striking psychological and physical
consequences of starvation. Participants were 36 healthy young men who took part in the study as an
alternative to military service. For three months they ate normally while their behaviour, personality
and eating patterns were assessed. This was followed by a six-month period during which they were
restricted to about half their normal food intake and lost on average about 25 per cent of their body
weight. The psychological effects that the men experienced included severe depression, mood swings,
irritability and outbursts of anger, compulsive behaviours, self-harming behaviours (e.g., one man cut
off three fingers), obsessional thoughts of food and eating, hoarding of food, changes in eating habits
(e.g., increased use of spices and salt) and serious binge eating that persisted for about five months
after re-feeding. In addition, the men became isolated and withdrawn, with food and eating taking
amphetamines precedence over their interest in relationships and other social activities.
Stimulant drugs For many individuals with anorexia nervosa, their psychological problems may also be severe
that can produce enough to warrant a diagnosis of a psychological disorder. Common psychological comorbidities
symptoms of in those with anorexia nervosa include mood disorders (e.g., major depression), anxiety disorders
euphoria, self- (e.g., social phobia), substance use disorders (the most common being alcohol but can also include
confidence, amphetamines and similar substances that are used for their weight-losing properties) and personality
alertness,
disorders (e.g., obsessive-compulsive personality disorder) (Steinhausen, 2002).
agitation,
paranoia, Self-starvation is also associated with a range of medical problems, with the process of starvation
perceptual potentially affecting every organ system of the body. Irregular heartbeats, heart failure and severe
illusions and metabolic disturbance (e.g., low potassium levels and dehydration) are of major concern and a potential
depression. cause of death. Some of the main medical complications of anorexia nervosa are listed in Table 9.2.
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TABLE 9.2 Medical features and physical effects of anorexia nervosa
BODY SYSTEM MEDICAL FEATURES
Face, skin, bone and limbs • Parotid and salivary gland enlargement (‘chubby cheeks’) from vomiting
• Low body temperature (hypothermia)
• Dental decay (from exposure to acidic stomach juices when vomiting and over-brushing)
• Brittle hair/hair loss/lanugo (baby-like/downy) hair over the body
• Pale skin from anaemia
• Osteopenia (loss of bone density) and fractures
• Calluses on back of fingers from fingers scraping on teeth when inducing vomiting
• Muscle weakness
• Ankle swelling (fluid rebound after dehydration)
Endocrine/hormonal • Low sex steroid hormones, leading to amenorrhoea (absent periods) in women
• Decreased libido and low testosterone in men
• Altered thyroid hormone metabolism
• Low blood glucose and poor control of diabetes
• Increased cortisol and growth hormone
Fluids and electrolytes • Dehydration (especially if purging)

(blood chemistry) • Low potassium (from vomiting)
• Low phosphate (especially with rapid re-feeding)
• Kidney failure
Cardiac (heart) • Slow heartbeat and/or irregular rhythm

• Heart failure
• Small, weak heart
Nutritional/gastric • Low levels of essential minerals and vitamins (e.g., magnesium, calcium, thiamine)
• Acute inflammation of the pancreas
• Slow stomach emptying (leading to fullness after meals)
•
Constipation (especially after ceasing laxative abuse)
•
Diarrhoea (from laxative abuse, can cause dehydration and, in the long term, bowel damage)
•
Inflammation, ulceration, tearing and scarring of the oesophagus (from exposure to acidic
stomach juices when vomiting)
• Stomach rupture (after binge eating)
• Inflammation of the liver
Immune system • Low white cell count

• Susceptibility to overwhelming bacterial infection
Reproductive system • Increased risk of miscarriage, premature delivery and death of baby
• Low-weight baby and increased risk of malformations
Source: Adapted from Diagnostic and Statistical Manual of Mental Disorders (5th ed.), Copyright 2013, American Psychiatric Association.
The aetiology of anorexia nervosa

While the causes of anorexia nervosa and other eating disorders are not fully understood, there is heritability
general consensus that multiple biological, psychological and social factors are involved. Percentage
indicating the
degree to
BIOLOGICAL FACTORS which genes
Biological factors are insufficient to account for the development of anorexia nervosa in any one contribute to the
person, but they are important in increasing the risk of the disorder in otherwise vulnerable people development of a
(Jacobi, Hayward, de Zwaan, Kraemer, & Agras, 2004). In particular, it is known that the heritability disorder.
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(a percentage that indicates how much genes contribute to the development of a disorder) for eating
concordance rate disorders is moderate, as suggested by higher concordance rates for monozygotic versus dizygotic
Probability that twins. A familial predisposition to leanness and family histories of obsessive-compulsive personality
both members and mood disorders are common in anorexia nervosa patients.
of a twin pair will
Research has highlighted the interplay between genetic factors and the environment for anorexia
develop the same
disorder.
nervosa. Bulik, Sullivan, Wade, and Kendler (2000) used data from the Australian Twin Registry and
the Virginia Twin Registry to examine a variety of questions relating to genes, the environment and
monozygotic eating disorders. Genetic factors were estimated to make a strong contribution to anorexia nervosa,
twins
an eating disorder defined by weight, behaviours and attitudes. However, when just the attitudinal
Identical twins
who share
components of eating disorders were examined, such as body dissatisfaction, these were shown to
100 per cent be completely influenced by the environment and had no genetic contribution (Wade, Bulik, Heath,
of their genes Martin, & Eaves, 2001). Thus genetic and environmental factors may have a different causal role for
because they the different aspects of the disorder.
developed from a An increasing number of molecular genetics studies in eating disorders have focused on candidate
single genes that could be involved in neurotransmitter pathways regulating weight, feeding and energy
fertilised egg. expenditure (Gorwood, Bouvard, Mouren-Simeoni, Kipman, & Ades, 1998). Studies have focused
dizygotic twins mainly on serotonin-linked genes based on the involvement of the serotonin neurotransmitter system
Non-identical in the control of appetite and other aspects relevant to anorexia nervosa, such as impulse control
twins who share
(Kaye, Frank, Bailer, & Henry, 2005). For example, reduced serotonin activity has been found to be
with each other,
on average,
associated with increased appetite and decreased impulse control. In research on weight-recovered
50 per cent individuals with anorexia nervosa, serotonin activity in the brain has been found to be unusually high
of their genes (Kaye et al., 2005). It is therefore possible that patients with anorexia nervosa have abnormally high
because they levels of serotonin activity that contribute to the development of the illness by promoting undereating
developed from and over-control.
two separate A number of the neuroendocrine (hormonal) systems involved in the regulation of hunger and
fertilised eggs fullness have been found to be abnormal in anorexia nervosa. However, most of these alterations are
(comparable to
considered to be consequences of the starvation state and disordered eating rather than causal factors.
non-twin siblings).
For example, much research focus has been on the possible role of leptin (a hormone that results
in decreased food intake and weight) in anorexia nervosa. However, the abnormal levels of leptin
in anorexia nervosa patients have been found to normalise with weight gain (Eckert, Pomeroy, &
Raymond, 1998). Moreover, leptin levels have consistently been found to be significantly lower in
anorexia nervosa patients (which should increase food intake and hence weight gain) compared to
normal-weight controls. These lowered leptin levels are probably the result of reduced body fat, since
leptin is secreted by fat cells. In sum, the findings indicate that leptin abnormalities are likely to be a
consequence of the disorder.
Research has also investigated possible abnormalities in the structure and function of the brain
neuroimaging that may contribute to the development of anorexia nervosa. Structural neuroimaging studies in
Range of anorexia nervosa have reported decreased brain volume, most of which again is a likely consequence
techniques used of starvation since it has been found to reverse with weight gain (Frank, Bailer, Henry, Wagner, &
to image the
Kaye, 2004). However, some recent evidence has emerged from functional neuroimaging studies in
structure and/
or function of
patients with anorexia nervosa that raises the possibility of a predisposing biological abnormality.
the brain such These studies have found abnormal functioning in the temporal lobe and limbic system that may
as computerised persist after recovery (Hay & Sachdev, 2011).
tomography (CT), Overall, biological research in anorexia nervosa is a rapidly moving area and it is likely that a
positron emission much greater understanding of the biological determinants of anorexia nervosa and other eating
tomography (PET) disorders will emerge over time. The future likely lies in the area of epigenetics, which refers to
and magnetic mechanisms that affect the expression of genes independently of the underlying DNA sequence
resonance
(Campbell, Mill, Uher, & Schmidt, 2011). For example, exposure to maternal stress or poor
imaging (MRI)
scans. nutrition in utero may modify the foetal DNA in a way that places the individual at increased risk
of anorexia nervosa.
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Research suggests that a range of psychological influences are involved in the development of anorexia
nervosa. Many of these psychological constructs are contained in the third revision of the Eating
Disorders Inventory (EDI-3; Garner, 2004), a common self-report questionnaire used for patients with
an eating disorder. The 12 subscales of the EDI-3 and example items are presented in Table 9.3.
TABLE 9.3 The subscales and example items of the Eating Disorder Inventory-3 (EDI-3)
SUBSCALE DESCRIPTION
Drive for thinness 7 items assessing the desire to be thinner and fears regarding weight gain
Bulimia 8 items assessing binge eating tendencies
Body dissatisfaction 10 items assessing dissatisfaction with the whole body and body parts relevant to those with an
eating disorder
Low self-esteem 6 items assessing a sense of low self-worth
Personal alienation 7 items assessing a sense of emptiness, lack of control and poor self-understanding
Interpersonal insecurity 7 items assessing discomfort in social situations
Interpersonal alienation 7 items assessing difficulties in relating to others
Interoceptive deficits 9 items assessing difficulty identifying and coping with emotions
Emotional dysregulation 8 items assessing mood instability and impulsivity
Perfectionism 6 items assessing the tendency to strive for high standards of performance
Asceticism 7 items assessing the tendency to pursue virtue through self-deprivation and discipline
Maturity fears 8 items assessing the desire to avoid adult roles and return to the security of childhood
Note: Each item is rated on a six-point scale ranging from ‘never’ to ‘always’.
Source: Reproduced by special permission of the Publisher, Psychological Assessment Resources Inc. (PAR), 16204 North Florida Avenue, Lutz, Florida 33549, from the
Eating Disorder Inventory-3 by David M. Garner, PhD, Copyright 1984, 1991, 2004, by PAR. Further reproduction is prohibited without permission of PAR.
In an early and influential account of the disorder, Hilde Bruch (1973) highlighted the role of
low self-esteem in describing anorexia nervosa as ‘a desperate struggle for a self-respecting identity’
(p. 250). According to this view, individuals seek to overcome a sense of low self-worth through the
attainment of extreme thinness. As one young woman describes her experience of anorexia nervosa: ‘It’s
like I never knew what self-respect was all about until now. The thinner I get, the better I feel . . . This
has become the most important thing I have ever done’ (in Ciseaux, 1980, p. 1468). Supporting the role
of low self-esteem in the development of anorexia nervosa, a prospective study involving 11–12-year-
old schoolgirls found that those with lower levels of self-esteem at baseline were significantly more
likely to manifest eating disorder symptoms at the age of 15–16 years compared to those with high
self-esteem at the commencement of the study (Button, Sonuga-Barke, Davies, & Thompson, 1996).
Negative affect (e.g., anxiety, guilt, anger and shame) may also contribute to the development of
anorexia nervosa in that the individual may attempt to avoid emotional distress by refocusing attention
solely on eating, shape and weight rather than broader life concerns such as interpersonal or academic
problems (Polivy & Herman, 2002). Bodily control can provide an enhanced sense of self-control
(including control over distressing internal states) (Fairburn, Shafran, & Cooper, 1998).
Negative emotions may also be a causal factor for anorexia nervosa through their effect on body
dissatisfaction. Experimental studies that induce negative mood states have been found to produce
increases in body dissatisfaction, another identified risk factor for the development of an eating disorder
(Stice, 2002a). That is, individuals who are dissatisfied with their body shape/weight may attempt
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to improve their body image through engaging in severe dietary restriction and other maladaptive
weight-control behaviours.
Cognitive theorists have highlighted the role of dysfunctional thinking regarding eating, shape and
weight in the development and maintenance of anorexia nervosa. According to Fairburn and Harrison
(2003), the most important aspect is a dysfunctional system for evaluating self-worth. Specifically,
individuals with an eating disorder judge their worth as a person largely, or even exclusively, in terms
of their eating habits, body shape and weight: if they are not thin, it proves that they are weak, lazy,
unlovable and incompetent. Since self-worth is highly dependent on their success in controlling their
eating, shape and weight, these individuals become intensely focused on pursuing weight loss and
avoiding weight gain. Thus it is proposed that the over-importance of shape and weight for self-
evaluation is not just a symptom of anorexia nervosa (and bulimia nervosa), but plays a central role in
driving extreme weight-loss behaviours.
Perfectionism (among other personality traits) has also been found to be a factor that predisposes
an individual to developing anorexia nervosa. This construct has been defined in various ways, but
common to most definitions is the notion of striving to attain unrealistically high standards, even
in the face of negative consequences (Shafran, Cooper, & Fairburn, 2002). In the case of anorexia
nervosa, these unrealistically high standards are pursued in the domain of eating, shape and weight,
despite all of the negative psychological and physical consequences of extreme weight loss. Research
has found that perfectionism does in fact precede the development of anorexia nervosa and that it
is higher in individuals who go on to develop this disorder compared to those who develop other
psychiatric conditions (Fairburn, Cooper, Doll, & Welch, 1999).
Since experimental research provides the strongest support for causality, one study investigated the
possible causal role of perfectionism in triggering eating-disordered attitudes and behaviours using
an experimental design (Shafran, Lee, Payne, & Fairburn, 2006). In an attempt to induce high or low
levels of perfectionism, 41 young women without any history of an eating disorder were randomly
allocated to either the ‘high personal standards’ or the ‘low personal standards’ condition. The
participants in the high personal standards condition were required to agree to and sign a contract
stating that throughout the following day they would consistently strive to achieve the highest possible
standards. Ten items were developed in collaboration between the researcher and each participant that
gave examples of striving to achieve high standards. Items relating to the type or amount of food eaten
were deliberately left out. The procedure was the same for participants allocated to the low personal
standards condition except that they were required to consistently act according to low standards.
Example contracts for the high and low personal standards conditions are shown in Table 9.4.
TABLE 9.4 Example contracts signed by participants in the high and low personal standards condition in the experiment
by Shafran et al. (2006)
HIGH PERSONAL STANDARDS LOW PERSONAL STANDARDS
I confirm that for the next 24 hours, EVERYTHING that I do I confirm that for the next 24 hours, EVERYTHING that I do
will be done to the HIGHEST POSSIBLE STANDARD. This will will be done to the MINIMAL POSSIBLE STANDARD. This will
include everything that I think and say and do. In particular I include everything that I think and say and do. In particular I
agree to: agree to:
1. Be early or at least on time for everything 1. Leave work early
2. Drive perfectly (e.g., when parking keep doing it until I am 2. Surf the internet at work
completely parallel with the pavement) 3. Put off all non-urgent tasks . . .
3. Be the perfect hostess to my mother who is staying with [10 items were specified]
me tonight . . .
[10 items were specified]
Source: From Shafran, R., Lee, M., Payne, E., & Fairburn, C. G. (2006). The impact of manipulating personal standards on eating attitudes and behaviour. Behaviour
Research and Therapy, 44, 897–906, Elsevier.
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When each participant returned the next day, her eating during the past 24-hour period was assessed
in detail. Participants in the high personal standards condition were found to have eaten significantly
fewer high-calorie foods (e.g., pizza, chocolate and ice-cream), to have engaged in significantly more
attempts to restrict the amount of food that they ate, and to have experienced significantly higher
levels of regret after eating compared to those in the low personal standards condition. The results thus
support the contention that attempting to meet high personal standards (i.e., perfectionism) results in
increased levels of eating-disordered behaviours and attitudes.
SOCIAL FACTORS
Finally, a range of social and cultural factors are believed to contribute to the development of anorexia
nervosa. These include the influences of family members and peers, as well as values promoted by the
wider cultural context.
Research on family factors and anorexia nervosa has revealed a great deal of variation, with no one
particular pattern characterising the functioning of families in which a child has anorexia nervosa. A
primary difficulty in interpreting the results from these studies is differentiating between cause and
effect—that is, does family dysfunction contribute to the development of anorexia nervosa or do the
strains associated with such a severe disorder result in dysfunctional changes in family functioning?
One attempt to minimise this problem is to ask individuals with anorexia nervosa to describe their
family functioning before they developed the disorder. Unfortunately, such retrospective accounts may
be negatively biased as a result of any deterioration in family functioning that has occurred since the
development of the disorder. With this caveat in mind, individuals with anorexia nervosa report that
their families were characterised by higher levels of criticism and lower levels of care and affection
from their parents before they developed anorexia nervosa compared to the reports of healthy controls
(Fairburn et al., 1999). For those families in which parental approval and support are seen as lacking,
anorexia nervosa may be one way in which children attempt to communicate their distress and need
for support to their parents. For example, individuals with anorexia nervosa may state that ‘Anorexia
is my cry for help when things go wrong’ or ‘I use anorexia to communicate my distress/unhappiness
to others’ (Serpell, Teasdale, Troop, & Treasure, 2004, p. 424).
In addition to general family functioning, the family may contribute to the development of an eating
disorder through the behaviours and attitudes displayed by family members regarding eating, shape
and weight. For example, one study assessed the attitudes and behaviours regarding eating, shape and
weight of fourth- and fifth-grade schoolgirls and boys as well as their mothers and fathers (Smolak,
Levine, & Schermer, 1999). The study was particularly interested in whether parents influence their
children through (a) direct comments they make about their child’s eating and body and/or (b) weight
concerns and disturbed eating that they model for their children. In support of the former, the study
found that the more frequently parents mentioned their child’s weight to the child, the more likely
the child was to have made weight-loss attempts, to feel less satisfied with his/her body and to be
concerned about weight gain. In support of the latter, the more often parents complained about their
own weight and engaged in weight loss-attempts, the more likely daughters were to attempt to lose
weight, to feel less satisfied with their bodies and to be concerned about weight gain. Yet parental
modelling appeared to have minimal impact on the attitudes and behaviours of boys.
Adolescence, the typical age of onset for anorexia nervosa, is a period characterised by the growing
importance of peers. Not surprisingly, then, research supports the role of peer factors in the development
of anorexia nervosa. For instance, believing that peer approval (particularly from boys) can be attained
through thinness (e.g., being thinner means that ‘I would be more popular among my male friends’)
has been found to be associated with higher body dissatisfaction and dieting among adolescent girls
(Gerner & Wilson, 2005). In addition, adolescent girls occupying peer groups in which eating, shape
and weight concerns are high have been found to be at increased risk of reporting restrictive eating and
extreme weight-loss behaviours themselves (Paxton, Schutz, Wertheim, & Muir, 1999).
Certain cultural values are also believed to contribute to the development of anorexia nervosa.
According to this view, anorexia nervosa is more likely to occur during historical periods and in
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cultures that place a high value on the control of eating, shape and weight. For instance, in his book
Holy Anorexia, Rudolph Bell (1985) documents the lives of religious women dating back to the
thirteenth century who, in their pursuit of self-starvation, resemble contemporary cases of anorexia
nervosa. One such individual was Catherine of Siena, who lived in the fourteenth century. At times
Catherine limited her consumption to chewing on bitter herbs and then spitting out the juice. She
was known to have engaged in vigorous physical activity and self-induced vomiting, and died as a
result of her self-induced starvation at about the age of 32. According to Catherine’s religious beliefs,
the suffering of her starved body was a means of uniting with Christ. Thus her self-starvation was
consistent with cultural values regarding bodily deprivation.
In contemporary Western culture, religious language has been replaced by an emphasis on thinness
sociocultural as a key aspect of attractiveness, particularly for women. The sociocultural approach takes as one of its
approach key starting points the fact that the vast majority of individuals with an eating disorder are female, and
Theories it attributes this marked gender difference to the emphasis on thinness in females. It has been argued
that focus on that the increasing prevalence of both anorexia nervosa and bulimia nervosa during the twentieth
interpersonal
century was due to the frequent promotion in the media of unrealistic and unhealthy levels of thinness
relationships,
culture and as the ideal of female attractiveness that occurred during this period and continues to be the case. For
social institutions instance, it has been estimated that one quarter of the models appearing in some magazines meet the
to understand weight criterion for anorexia nervosa (Stice, 2002b).
the causes of If cultural values regarding the idealisation of thinness contribute to the development of
abnormality. eating disorders, then an increased incidence of eating disorder symptoms should occur following
incidence exposure to the thin ideal. One unique study was able to put this hypothesis to the test. Specifically,
Number of Becker, Burwell, Gilman, Herzog, and Hamburg (2002) assessed eating disorder symptoms
new cases of a in two groups of Fijian girls with a mean age of 17 years. The first group was assessed in 1995
specific disorder and the second group in 1998. Traditionally, Fijian culture endorsed larger physiques, promoted
that develop robust appetites and celebrated feeding as an expression of familial care. However, when
during a specific
television was introduced to the girls’ province in 1995, the investigators were able to determine
period of time.
the possible impact of Western media exposure (with its promotion of the thin ideal) on the girls’
eating disorder symptoms. Consistent with the negative impact of Western media exposure in
terms of eating disorders, a significantly higher percentage of girls in the second group (29.2%)
scored in the clinical range on an eating disorder
questionnaire compared to the percentage of girls

in the first group (12.7%). The qualitative data
obtained from interviewing the girls is consistent
with the notion that exposure to Western images
of female attractiveness did indeed influence their
body image and dieting behaviour. For example, one
of the girls stated that ‘the actresses and all those
girls, I just like them. I just admire them and I want
to be like them. I want their body, I want their size.
Because most of us Fijians, we are brought up with
those heavy foods, and our bodies, we are getting
fat. And now we feel that it is bad to have this huge
body. We have to have those thin, slim bodies’
(in Becker et al., 2002, p. 513).
A more recent and concerning medium for the
DAL
transmission of values regarding thinness has been

In 2015, France introduced legislation attempting to minimise exposure the emergence of pro-anorexia websites (Norris,
to harmful media content. As a result, fashion models in France are now Boydell, Pinhas, & Katzman, 2006). These websites
required to have medical certificates stating that they are healthy in promote anorexia nervosa and often present the
terms of their body mass index, and images that are digitally altered to condition as an idealised state rather than a disorder.
make a person appear thinner need to be labelled as such. They contain so-called ‘thinspirational content’
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that aims to encourage the pursuit of thinness (Norris et al., 2006, p. 445). This content typically
includes visual images of thin models/celebrities, extremely emaciated women and obese women, as
well as verbal messages intended to inspire striving for thinness (e.g., ‘Being thin and not eating are
signs of true power and success’ and ‘Being thin is more important than being healthy’) (Bardone-
Cone & Cass, 2006, p. 262). Pro-anorexia websites also typically have a ‘tips and tricks’ section in
which information is provided regarding weight-loss methods (often through dangerous means) and
strategies for concealing from others the extent of weight loss and caloric restriction (Norris et al.,
2006, p. 445). While the potential of these websites to adversely affect the health of young women
has yet to be thoroughly investigated, preliminary findings suggest that even a single viewing of such
material may have a negative influence on women’s mood, self-esteem and body image (Bardone-
Cone & Cass, 2006).
The treatment of anorexia nervosa

It may appear surprising that, although Sir William Gull coined the term ‘anorexia nervosa’ well
over 100 years ago, there is still little consensus on the most effective psychological treatment for
these patients, especially for adults (Hay, 2013; National Institute for Clinical Excellence [NICE],
2004). Unfortunately, there have been few controlled studies evaluating the effectiveness of treatments
for anorexia nervosa due to the fact that the disorder is relatively rare, generally requires long-term
treatment, and can be associated with high treatment dropout rates. Given the seriousness of the
disorder, developing and evaluating the most effective treatments for anorexia nervosa is a high priority
for future studies. The research to date suggests that motivational enhancement therapy, cognitive
behaviour therapy and family therapy are promising approaches, the latter particularly for adolescents.
Such treatments may be delivered in an inpatient, day-patient or outpatient setting.
TREATMENT SETTING
The treatment of patients with anorexia nervosa has moved away from long-term to short-term
inpatient treatment (where the patient is admitted to hospital) followed by day-patient treatment (in inpatient
which the patient attends the treatment centre for several days each week and returns home in the treatment
evening) or outpatient treatment (in which the patient sees a therapist, typically for one-hour sessions Treatment that
once or twice a week) (Beumont et al., 2004). Alternatively, day- or outpatient care may be sufficient entails the
patient being
for the entire treatment (Gowers et al., 2007).
hospitalised.
The decision regarding treatment setting is determined by the patient’s level of medical and
psychological functioning, the patient’s preference, the therapist’s recommendation, and what is day-patient
available. Many cities, for example, do not have specialised day programs, despite their important treatment
advantages (such as offering support around mealtimes while being less disruptive of the patient’s Type of
life compared to inpatient treatment). While inpatient treatment is the most disruptive of the treatment where
patient’s life, there are several indications of when it is likely to be necessary. These include for patients individuals with
who: (a) are severely underweight or losing weight rapidly; (b) have severe medical complications psychological
disorders attend
(e.g., cardiac problems); (c) are engaging in bingeing, vomiting or laxative abuse that poses serious
the treatment
medical risks; (d) have serious comorbid psychological problems (e.g., feeling suicidal); (e) are not setting during the
improving with outpatient or day treatment; or (f) have an unsupportive home environment. day but return
home at night.
MOTIVATIONAL ENHANCEMENT THERAPY (MET)
Contrary to many other psychological disorders, most individuals with anorexia nervosa value their outpatient
disorder highly since it is seen as fulfilling important needs for them (e.g., improving their self-esteem treatment
and body image, helping them to manage distressing emotions or providing a way of communicating Treatment
received at a
their distress to others). This strong attachment to the disorder is evident in the firsthand accounts hospital or clinic
of those who have experienced anorexia nervosa, with one recovered patient stating that ‘I would but where the
compare putting anorexia behind me to losing my best friend’ (in Shelley, 1997, p. 125) and another patient is not
claiming that ‘Anorexia nearly killed me; it also saved my life’ (in Shelley, 1997, p. 11). Just some of hospitalised.
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the needs that anorexia nervosa is seen as fulfilling (e.g., a way of seeking care from others, having
a sense of control over one’s life and a source of self-esteem) are evident in a newspaper article in
which Clare Wallmeyer (pictured with her twin sister Rachel and fellow sufferer of anorexia nervosa)
stated that, ‘All I’ve got is my anorexia, the only thing that can make people care about me. The
only thing I can control about my life is my weight. Some might say that’s a weakness but it’s also a
fortitude . . . people can see I’m a fantastic dieter’ (cited in van Tiggelen, 2006, p. 18).
Given the disorder’s immense value in the mind of the sufferer, the vast majority of individuals
with anorexia nervosa lack motivation to recover and resist attempts by others to help them change
(Rieger, 2015). In the absence of a genuine desire to change, it is unlikely that individuals will be
able to make substantial changes in their weight and other anorexic symptoms or to maintain these
changes over time and avoid relapse. Indeed, studies have found that greater motivation to change
at the commencement of treatment generally predicts lower eating disorder symptoms at the end of
treatment (Rieger, 2015).
motivational Motivational enhancement therapy (MET) aims to help patients increase their motivation to
enhancement change so that they are more able to engage in treatment and make a lasting recovery. For instance, in
therapy (MET) the four-session MET program developed by Dean, Touyz, Rieger, and Thornton (2007) for inpatients
Type of with anorexia nervosa, one exercise involves asking patients to explore the full range of perceived
psychological advantages of the disorder (e.g., providing a sense of achievement), as well as its disadvantages (e.g.,
treatment
the medical and psychological effects of starvation). An example of this decisional analysis exercise
that aims to
increase the is shown in Table 9.5. Through conducting a decisional analysis, it is hoped that patients will become
client’s intrinsic more aware of the negative consequences of their illness (rather than focusing almost exclusively on
motivation to its benefits) and thus will experience greater motivation to recover.
change. A study conducted to evaluate the effectiveness of this program was conducted by Dean and
colleagues (2007), in which 42 inpatients with an eating disorder (most of whom had anorexia nervosa)
were randomised to receive four sessions of either MET or a CBT skills group (e.g., learning relaxation
skills). Six weeks after these treatments ended it was found that a higher percentage of the MET patients
(84%) were in inpatient or day-patient programs compared to the CBT patients (44%), suggesting that
TABLE 9.5 A sample decisional analysis exercise that involves asking patients to explore the full range
of immediate and delayed positive and negative consequences of anorexia nervosa
DECISIONAL ANALYSIS SHEET
IMMEDIATE CONSEQUENCES DELAYED CONSEQUENCES
POSITIVE NEGATIVE POSITIVE NEGATIVE
If I stay at my Losing weight is the Thoughts of I will feel more My grades will fall
current weight one thing I do really food go round in control of my because I can’t
or continue to well—it helps me and round in my life—by focusing concentrate on
lose weight . . . to feel better about head—I can’t stop only on my eating my work.
myself. thinking about it. and weight I won’t
have to deal with
other problems.
Whenever I eat I I feel unwell most I will lose friends

feel really guilty of the time—tired, because I don’t
and anxious—I can headaches, really have the energy
avoid these feelings cold, hair falling or interest to
by not eating. out. socialise.
I feel guilty about I will probably do

how irritable I am long-term damage
with others. to my health.
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the MET patients were more engaged in the recovery process. In addition, the percentage of MET
patients classified as being actively working to recover increased over time from pre-treatment (13%)
to post-treatment (31.6%) to the six-week follow-up (41.2%), while the percentage of CBT patients
actively working to recover increased from pre-treatment (15.8%) to post-treatment (25%) but then
decreased at the six-week follow-up (9.1%). Thus, while the MET program helped patients to build on
their intrinsic motivation to change, any increases in motivation for the CBT patients were short-lived.
COGNITIVE BEHAVIOUR THERAPY (CBT)

Particularly for those patients who have some motivation to change, cognitive behaviour therapy cognitive
(CBT) is often seen as the treatment of choice. Treatment is usually conducted for a minimum of behaviour
40 sessions over one year since patients need to regain a substantial amount of weight and will likely therapy (CBT)
experience fluctuating levels of motivation to change (with periods of weight gain interspersed with Type of
periods of weight stability or even loss). psychological
treatment that
With the introduction of behaviour modification techniques in the 1960s and 1970s, strict operant
combines both
behavioural programs (involving the reward of weight gain and punishment of weight loss) were cognitive and
widely used in the inpatient treatment of anorexia nervosa. With hindsight, these programs were behavioural
unnecessarily punitive, as patients were confined to their beds and deprived of all possessions and concepts and
contact with their families until they had gained sufficient weight to be rewarded with family visits and techniques.
the like. These programs were challenged in the 1980s when more lenient approaches were found to
be as effective in achieving weight gain and were much less likely to exacerbate pre-existing problems
for patients such as a lack of control and low self-esteem (Touyz, Beumont, Glaun, Phillips, & Cowie,
1984). Pike, Carter, and Olmsted (2005) summarised this well when they wrote that ‘the primary
focus on weight gain may be effective in treating the “anorexia” but fails to adequately address the
psychological aspects of the disorder, the “nervosa”’(p. 10).
The first stage

Current CBT for anorexia nervosa is conducted over three stages. The first stage entails establishing
the basis of a supportive and collaborative relationship between the patient and therapist and
instituting a meal plan. By the nature of the disorder, this requires patience and empathy for
patients’ very real fear of losing control and realising their worst nightmare—that is, becoming fat.
The goals of therapy are established in a collaborative manner between the patient and therapist.
Garner, Vitousek, and Pike (1997) describe two main goals of treatment: (a) normalising eating,
weight and weight-control behaviours, and (b) dealing with psychological problems such as poor
self-esteem, perfectionism, coping with negative emotions and interpersonal functioning. Since
many of these psychological problems are a consequence of the starvation state (as found by
Keys et al. [1950] in the starvation study mentioned previously), food and weight themes should
be addressed first. Attempting to work on psychological issues before some degree of eating and
weight normalisation has occurred would be like trying to treat an individual dependent on alcohol
while s/he is intoxicated.
Establishing a meal plan is usually done with the assistance of a dietitian. The daily caloric
content is gradually increased and is necessarily cautious to avoid the medical dangers of the re-
feeding syndrome, which occurs when rapid re-feeding overwhelms the patient’s metabolic state and
can result in shortness of breath, physical collapse, seizures, delirium, coma, heart failure and death.
Early stages of recovery can thus at times be more dangerous for patients than when they were losing
weight. Ensuring compliance with the program is the main psychological challenge at this stage, as
patients are generally terrified of eating.
The second stage

With some degree of weight gain underway, the second stage of therapy begins. In this phase,
dysfunctional beliefs regarding food and weight are targeted. In addition, the focus of therapy
is broadened to address wider issues (such as self-esteem, perfectionism, mood and interpersonal
functioning). Both behavioural and cognitive strategies are utilised to assist the patient in modifying
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his/her cognitions. For example, the meal plan is a behavioural strategy that helps patients to challenge
the belief that they will rapidly gain large amounts of weight if they consume three meals a day.
Cognitive approaches to overcoming unrealistic beliefs entail assisting the patient to:
∙ identify his/her dysfunctional thoughts

∙ examine the evidence for and against these thoughts
∙ replace any thoughts found to lack supportive evidence with more realistic beliefs.
An example of a common dysfunctional thought is the ‘anorexic wish’ (Garner, Vitousek, &
Pike, 1997). This is when the individual believes that s/he can recover while continuing to diet and
have a low weight (e.g., ‘I can feel happy without giving up dieting or reaching a normal weight’).
Here, the therapist’s task is to help the patient see that symptoms such as depressed mood are a
direct consequence of starvation and that the individual cannot be both happy and underweight at
the same time.
The dysfunctional cognitions experienced by patients with anorexia nervosa typically include a
pattern of critical thinking that continually provokes and challenges the individual regarding his/her
supposed inadequacies. Some patients have given this ‘inner critic’ a special name such as ‘gremlin’,
‘minx’, ‘the anorexia’ or simply ‘ana’. The inner critic demands ultimate perfection and labels the
patient as being fat, lazy, weak and incapable. This ongoing battle has a devastating impact on the
psychological wellbeing of the patient, who experiences intense guilt and powerlessness against
this unforgiving and forceful enemy. Examples of just some of the rules of the inner critic that the
individual may need to follow in order to feel a sense of self-worth include ‘I must always have total
control’, ‘I must be the best at what I do’, ‘I must earn the respect of everyone’ and ‘I must do things
perfectly and never make mistakes’. It is essential, therefore, that therapy helps the patient to overcome
not only dysfunctional thoughts regarding eating, shape and weight, but also beliefs regarding the
broader theme of self-worth.
The third stage

The third stage entails preparing the patient for the end of treatment and developing strategies to prevent
relapse. The aspects of treatment that have been helpful in improving the patient’s functioning are
reviewed, future times of vulnerability for relapse are identified (e.g., during periods of interpersonal
conflict or low mood), the patient is encouraged to recognise the early-warning signs of relapse
(e.g., any weight loss or increased preoccupation with eating, shape and weight) and the strategies to
respond to these signs are identified (e.g., returning to therapy).
Effectiveness
While anorexia nervosa in adults has been described as one of the most difficult psychological
disorders to treat (Halmi et al., 2005), a recent study using CBT obtained some promising results. In
this study, 99 adults with anorexia nervosa were offered 40 sessions of CBT over 40 weeks (Fairburn
et al., 2013). Approximately two-thirds of the patients completed the treatment, which is superior
to the high dropout rate (due, for example, to patients’ low motivation to change) of many previous
studies. Importantly, there was a substantial increase in weight over the course of the treatment, with
patients who completed the treatment gaining a mean of 7.5 kg by the end of treatment so that they
were within the healthy weight range. These patients then maintained this weight gain during the
60 weeks following treatment (a period when relapse is common). Another noteworthy finding was
that almost 90 per cent of the patients reported minimal eating disorder attitudes (such as shape and
weight concerns) at the end of treatment. Similarly positive results have been reported using CBT for
adolescents with anorexia nervosa (Dalle Grave, Calugi, Doll, & Fairburn, 2013).
Few controlled studies have been conducted comparing the effectiveness of CBT with alternative
approaches. One study by Serfaty, Turkington, Heap, Ledsham, and Jolley (1999) randomly allocated
patients with anorexia nervosa to 20 sessions of individual CBT or nutritional counselling (which
involves educating patients regarding healthy nutrition). While two participants dropped out of the
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CBT intervention, all participants dropped out of the nutritional counselling intervention, indicating
that the latter is insufficient on its own to treat those with a disorder as serious as anorexia nervosa.
Another study unexpectedly found that supportive clinical management (which primarily consisted
of the provision of information regarding healthy weight and eating in the context of a supportive
therapeutic relationship) was comparable to CBT with regards to weight gain and improvement in
eating-disorder attitudes in patients with anorexia nervosa (McIntosh et al., 2005). However, as in so
many clinical trials of anorexia nervosa, there were methodological problems with the study, including
overlap in the content of the therapies. For example, both approaches emphasised the importance
of a supportive relationship between the therapist and patient and provided education about healthy
nutrition. As the study was short term (20 sessions only), many patients remained underweight in both
treatments, indicating that these approaches may be a useful first step in longer-term therapy.
Beyond the weight-gain phase, the efficacy of CBT has been demonstrated in terms of preventing
relapse. This is an important area of investigation since relapse after weight gain is common among
patients with anorexia nervosa. In a study by Pike, Walsh, Vitousek, Wilson, and Bauer (2003),
33 patients with anorexia nervosa were randomly allocated to one year of either CBT or nutritional
counselling after they had gained weight through inpatient treatment. The study found that CBT
resulted in a significantly lower proportion of patients relapsing or dropping out of treatment compared
to nutritional counselling (22% versus 73% respectively). In addition, a significantly higher percentage
of patients who received CBT (44%) were defined as having made a good recovery compared to those
who received nutritional counselling (7%).
FAMILY THERAPY
Family therapy is currently considered to be the treatment of choice for younger patients (children and
adolescents) with anorexia nervosa, which is a far cry from Gull’s (1874) early dictum that patients
and families should be separated. A variety of family approaches has been developed, of which the
Maudsley model family-based treatment has received the most recognition (Eisler et al., 1997; Lock,
Le Grange, Agras, & Dare, 2001).
The Maudsley model of family-based treatment begins with promoting re-feeding and weight gain
by encouraging parents to take responsibility for ensuring healthy eating in the home. Once normal
weight has been achieved, therapy focuses on establishing a new pattern of family relationships. An
important aspect of this stage is working towards personal autonomy for the adolescent and ensuring
that disordered eating is no longer the focus of family interactions.
In a study evaluating the effectiveness of the Maudsley model, 80 patients with anorexia nervosa
were randomly allocated to receive one year of either family therapy or individual treatment after
discharge from hospital. Patients with an early onset of the illness (before the age of 19 years) and a
short duration of illness (less than three years) did significantly better when treated with family therapy
in comparison to individual therapy both at the end of treatment (Russell, Szmukler, Dare, & Eisler,
1987) and five years later (Eisler et al., 1997). The study’s findings suggest that family-based treatment
is to be preferred over individual treatment for younger patients. Since this early research, additional
randomised controlled trials comparing family-based treatment with individual or other approaches
have provided further support for its effectiveness (Hay, 2013). However, more recent developments
in CBT have produced very promising results in adolescents with anorexia nervosa (Dalle Grave et al.,
2013), indicating the need to directly compare CBT and family-based therapy in this population.
PHARMACOLOGICAL APPROACHES
At present, there is little evidence to recommend a central role for medication in the treatment of
anorexia nervosa. Several placebo-controlled trials have not found evidence that antidepressants
improve weight gain, eating disorder symptoms or general psychopathology in patients with anorexia
nervosa (Claudino et al., 2006; Mitchell, Roerig, & Steffen, 2013). In regard to relapse prevention,
there have been only two trials conducted, and these reported inconsistent results. In light of the
research, antidepressants are indicated only for anorexia nervosa patients who have major depression.
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selective Selective serotonin reuptake inhibitors (SSRIs) are often used, whereas tricyclic antidepressants
serotonin (TCAs) are avoided because they may affect cardiac functioning in this medically vulnerable group.
reuptake There have been a number of trials of antipsychotic medication (neuroleptics) in patients
inhibitors (SSRIs) with anorexia nervosa (Mitchell et al., 2013). Trials of the older, ‘typical neuroleptics’ (such as
Class of chlorpromazine) had mixed results and adverse side effects were common. More recently, however,
antidepressant
the newer, ‘atypical neuroleptics’ (such as olanzapine and quetiapine) appear to offer some benefits
drugs (such
as fluoxetine)
in reducing compulsive activity and anxiety, as well as improving adherence to treatment during
that inhibit the the re-feeding phase. Yet their use can also have several disadvantages, including metabolic and
reuptake of cardiovascular side effects, the patient not learning to tolerate weight gain without the assistance of
serotonin. medication, and a patient preference not to be prescribed such medications. It is therefore generally
tricyclic recommended that neuroleptics, if used at all, be withdrawn when weight is in the normal range.
antidepressants
(TCAs) TREATMENT FOR SEVERE AND ENDURING ANOREXIA NERVOSA
Class of Severe and enduring anorexia nervosa has received increasing attention in the past decade, and has now
antidepressant been included in the Australia and New Zealand guidelines for the treatment of eating disorders (Hay
drugs such as et al., 2014). It is a chronic, highly debilitating form of anorexia nervosa. While there is no agreed-
imipramine and
amitriptyline.
upon definition of how longstanding the individual’s disorder needs to be in order to be classified
as ‘enduring’, most researchers agree that it is at least seven years. In addition to the psychological
neuroleptics and medical symptoms typically seen in people with anorexia nervosa, those with the severe and
Drugs used to enduring type of the disorder experience problems in broad domains of life such as in family, social
treat psychotic
symptoms.
and occupational settings stemming from the toll that such a serious condition takes on most or even
all areas of functioning.
Given the pervasive problems across broad domains of their lives that individuals with severe
and enduring anorexia nervosa tend to experience, some have argued that adaptations to standard
treatment need to be made for those with this form of the disorder (Touyz & Hay, 2015; Touyz, Le
Grange, Lacey, & Hay, 2016). A randomised controlled trial conducted by Touyz and colleagues
(2013) compared two psychological treatments that were specifically adapted for those with severe
and enduring anorexia nervosa: cognitive behaviour therapy (CBT-SE) and specialist supportive
clinical management (SSCM-SE). What both treatments had in common, and what was the hallmark
feature of this study, was that for the first time improvement in the core symptoms of anorexia
nervosa (such as weight gain) was not the primary treatment outcome of interest. While weight gain
was actively promoted, the driving force behind this study was helping patients to have an enhanced
quality of life, given the many problems they tend to experience in their lives. Both treatments were
found to be successful in promoting change in both quality of life and eating disorder symptoms, but
one year after treatment ended, those patients who had received CBT-SE had lower eating disorder
symptoms as well as higher motivation to recover than those who had received SSCM-SE. One
noteworthy aspect of this study was the extremely low percentage (13%) of patients who did not
complete the study, which is one of the lowest attrition rates ever reported in treatment trials on
anorexia nervosa.
CASE STUDY: ANOREXIA NERVOSA

Charlotte is a 34-year-old single women who has a degree in accountancy. She is the only child of professionally
successful parents. Her father was an ambitious and driven lawyer who was the chief executive officer of a well-known
Australian company while her mother ran a highly successful fashion house.
Charlotte has a 20-year history of severe and enduring anorexia nervosa. She was first diagnosed with anorexia
nervosa at the age of 14 following an episode of extreme and rapid weight loss, which she did her best to hide from her
parents. But when her mother walked into her bedroom one evening unannounced and saw her daughter naked (as she
had just showered and was about to put on her pyjamas), the extent of Charlotte’s weight loss became starkly evident.
Her parents took her to see a leading psychiatrist specialising in the field of eating disorders, even though Charlotte was
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of the opinion that both her parents were over-reacting to her weight loss and she threatened to run away if she was
coerced into treatment.
During the assessment, Charlotte insisted that she was ‘still too fat’ (despite having a BMI of only 12). After a
comprehensive psychological and medical assessment, she was found to have abnormal liver function tests and a very
slow heart beat (a pulse of only 30 beats per minute), so it was recommended that she be urgently admitted to a private
eating disorders unit followed by a day-patient program at the same hospital. Charlotte protested vehemently, stating
that she ‘would rather be dead’ than gain any weight and that she would not cooperate with her treatment team in the
hospital. She wanted to return to her private school where she was the top student in her year, won awards for being
the most outstanding debating student in her year and was captain of the netball team. Charlotte stated that she would
‘never, ever overcome the humiliation of being in a psychiatric hospital’ and that she ‘never wanted to see her friends
again’. Although her parents were both terrified and distressed by her comments, they were strongly of the view that they
could not manage her at home and, with a great deal of trepidation, insisted on her admission to hospital.
Charlotte remained true to her word. She went on a ‘hunger strike’, refusing to eat the hospital food that she was
prescribed—she regarded it as being too rich in calories and insisted on a diet low in carbohydrates and fat, which
she was denied. A nasogastric tube was inserted, but Charlotte repeatedly pulled it out while exercising strenuously
in her room, including 500 star jumps at a time. After a long admission period, during which she ran away on at least
two occasions and had to be brought back by the police, Charlotte was eventually moved to the day-hospital program
(even though she was still not fully eating her prescribed diet and remained underweight) because she was not as
undernourished as she was on admission, and her medical status, including her heart rate, was now normal. But within
a few days of starting the day program, she refused to go back and her parents were unable to get her to attend on a
voluntary basis. Since then, Charlotte has had 16 admissions to hospital, several of them involuntary.
Despite her severe illness, for a time in her life she was able to continue to achieve academically. She completed Year
12 with an ATAR of 99.6 and completed her accountancy degree and practical clerkships. She achieved distinctions/high
distinctions throughout her university studies. However, once she started full-time work, Charlotte found interpersonal
relationships particularly difficult and work-related social activities terrifying. She felt very anxious in social situations,
which was made even worse by the fact that she could not eat with her colleagues because of her highly restrictive diet.
While she wanted to use alcohol to try to dampen her social anxieties, she did not drink alcoholic beverages (because of
the calories). The stress of work intensified her dieting and weight loss. But as her weight fell, her psychological problems
intensified: she slept poorly, became increasingly fatigued, and found it very difficult to concentrate. For the first time in
her life she started to make silly mistakes at work, which were pointed out to her. This was in stark contrast to the very
high standards she had previously set herself and managed to achieve. She became increasingly depressed. Charlotte
started taking sick days from work (something that had previously been anathema to her) and eventually resigned as she
came to the conclusion that she could no longer offer the standard of work an employer deserved.
Without her work, she spent long days alone at home and became increasingly preoccupied with thoughts about
food, shape and weight. She would eat only the same rigid low-calorie diet each day, avoided any interpersonal contact
other than with her parents, with whom she lived, and would desperately try to exercise whenever she thought her
parents were not supervising her. This led to daily, explosive emotional outbursts at home, especially with her father,
which eventually culminated in her physically attacking him and threatening him with a knife. As a result of this very
distressing incident, Charlotte’s father decided that she could no longer live in the family home and she moved into a
one-bedroom apartment, in which she still lives. She began receiving a disability pension from the federal government.
Charlotte was not only experiencing an exceptionally poor quality of life, but faced a shortened life expectancy as
well. The only option before her was the prospect of returning to the very hospital wards that she had been coerced
into attending in the past and where treatment had failed. She had no interest in doing so. Then one day, when paging
through her local newspaper, she came across a treatment study investigating a new approach. In this new approach,
while weight gain was actively promoted, the driving force was an enhanced quality of life.
Charlotte decided to volunteer for the study. This was an entirely new experience for her, given that her quality of life
became the primary focus of her treatment, with strong encouragement to gain weight as well. She responded better
to this new approach. As she began to make slow but gradual improvements in her social activities (which had become
non-existent), she became even more motivated to improve her physical health so that she would be more able to
socialise. She managed to gain a few kilograms for the first time in years and, as a result, found that she did indeed have
more interest and energy for social activities. With a taste of the doors that recovery could open up for her, Charlotte
asked to be referred to a clinical psychologist with whom she could continue treatment.
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LO 9.3 Bulimia nervosa

Bulimia nervosa is the second type of eating disorder to be addressed. It is characterised by the regular
occurrence of binge eating episodes and inappropriate weight-control behaviours (such as self-induced
vomiting) as well as the excessive influence of shape/weight on self-worth.
The epidemiology of bulimia nervosa

Bulimia nervosa primarily affects females, but tends to have a later age of onset than anorexia nervosa.
Medical and psychological problems are commonly experienced by individuals with the disorder.
PREVALENCE
The number of individuals presenting with bulimia
nervosa in industrialised countries increased during
the decade that followed its recognition in the
late 1970s (Hall & Hay, 1991). Since that time it
is possible the incidence has remained stable or
even fallen (Currin, Schmidt, Treasure, & Hershel,
2005; Keel, Heatherton, Dorer, Joiner, & Zalter,
2006; van Son, van Hoeken, Bartelds, van Furth,
& Hoek, 2006). Like anorexia nervosa, bulimia
nervosa primarily affects females. It is estimated
that 1–3 per cent of women will experience bulimia
nervosa at some point in their lifetime compared
with 0.1–0.3 per cent of men (Hoek, 2006; Hudson
et al., 2007). However, some of this gender
DAL
difference may be due to the fact that eating

A core symptom of bulimia nervosa is regularly engaging in binge disorders are under-diagnosed in men.
eating episodes, which are often done in secret due to the shame that
While research on eating disorders in males is
people can experience regarding this loss of control over their eating.
limited, there are several general statements that
can be made about men with eating disorders.
First, men and women with eating disorders are generally similar in terms of their symptoms, family
histories of psychiatric disorder, family dynamics, course of the illness and response to treatment
(Strober, Freeman, Lampert, Diamond, & Kaye 2001; Woodside et al., 2001) and in the impact of
eating disorder features on their functioning (Mitchison, Mond, Slew-Younan, & Hay, 2013). For
example, men find disordered eating equally debilitating and are as likely to be distracted from work
or other activities by weight, shape or eating preoccupations as women with an eating disorder. In
addition to the much lower prevalence, some notable differences are that men have an older age of
onset of the eating disorder and tend to present later for treatment compared to women. Men may
also be more likely than women to use extreme exercise as a weight-control method, with purging
being less frequent. In addition, there is evidence that homosexuality acts as a risk factor for eating
disorders in men, with 20 per cent of males with an eating disorder being homosexual (Carlat,
Camargo, & Herzog, 1997). This figure compares to an estimated 1.6 per cent of Australian adult
males in the general population who identify themselves as homosexual and a further 0.9 per cent
who identify themselves as bisexual (Smith, Rissel, Richters, Grulich, & de Visser, 2003).

In general, bulimia nervosa has a later age of onset than anorexia nervosa, emerging in late adolescence
and young adulthood (Hay, 2003; Stice, Killen, Hayward, & Taylor, 1998). The symptoms can become
chronic for some individuals, with an estimated 50 per cent still having the disorder after 10 years
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(Keel, Mitchell, Miller, Davis, & Crow, 1999). Poorer outcomes are reported where there is a history
of childhood obesity, low self-esteem or a personality disorder.
ASSOCIATED MEDICAL AND PSYCHOLOGICAL PROBLEMS

There are fewer medical complications for those with bulimia nervosa compared to anorexia nervosa, but
problems related to purging behaviours are still of concern (see Table 9.2). Perhaps the most dangerous
of the disorder’s physical complications are depletions in the electrolytes of potassium, chloride and
sodium stemming from purging behaviours. Electrolytes are so named because they are capable of
carrying an electric charge. Electrolyte disturbances, which have been found in approximately 50 per cent
of individuals with bulimia nervosa, may result in weakness, tiredness, constipation, depression,
irregular heartbeats and sudden death. Additional physical problems include swollen salivary glands
and accompanying facial swelling from vomiting; severe abdominal pain and, in extreme cases,
stomach rupture and death from binge eating; serious tearing/ulceration of tissue in the mouth and
throat from exposure to gastric acid from vomiting; loss of normal bowel function through laxative
misuse, resulting in cramping, diarrhoea or constipation; dental deterioration resulting from exposure
of the teeth to gastric acid from vomiting; dehydration from purging followed by rebound oedema
(fluid retention) evident in swelling or puffiness in the fingers, ankles and face; and amenorrhoea and
menstrual irregularities. Depression, anxiety and substance use disorders are common psychological
comorbidities in individuals with bulimia nervosa (Hudson, Hiripi, Pope, & Kessler, 2007).
The aetiology of bulimia nervosa

There is a high degree of overlap in the biological, psychological and social factors that are believed to
be involved in the development of anorexia nervosa and bulimia nervosa. This overlap in causal factors
is not surprising given that both disorders have many features in common, including the tendency to
base self-worth almost entirely on shape and weight, the intense fear of gaining weight, and the desire
to attain unrealistic levels of thinness. Some theorists argue that the same model should be applied in
understanding the aetiology of all eating disorders (such as the transdiagnostic model developed by
Fairburn, Cooper, & Shafran [2003]), although this issue is debated and awaits further research. Since
key factors that encourage the pursuit of thinness were highlighted in the section on anorexia nervosa,
the current section on bulimia nervosa will examine factors involved in causing binge eating.
BIOLOGICAL FACTORS
As in anorexia nervosa, there is a moderate heritability for bulimia nervosa (Bulik, Sullivan, Wade, &
Kendler, 2000). In addition, a familial predisposition to obesity, and family histories of substance use
and mood disorders, are common in bulimia nervosa patients. Differences in familial predisposition
(e.g., a higher rate of obsessive-compulsive personality disorder in the family members of those with
anorexia nervosa, and of substance use in bulimia nervosa) support the distinction between anorexia
nervosa and bulimia nervosa (Grilo, 2006).
As regards neurotransmitter dysfunction, it has been proposed that the reduced serotonergic
(5-HT) function evident in those with bulimia nervosa may lead to overeating and thus play a role
in causing the condition. The possible role of low serotonin in triggering binge eating is based on
the fact that reduced serotonin activity has been found to be associated with increased appetite and
decreased impulse control (Jimerson, Lesem, Kaye, & Brewerton, 1992). Epigenetic factors (e.g.,
exposure to maternal stress or under-/over-nutrition in utero that affects gene expression) may also be
occurring, which would increase the risk of bulimia nervosa, obesity and other disorders characterised
by overeating (Campbell, Mill, Uher, & Schmidt, 2011).
PSYCHOLOGICAL FACTORS affect

According to the dual pathway model of bulimia nervosa, there are two main factors that trigger binge Experience
eating episodes: dieting and negative affect (Stice, Shaw, & Nemeroff, 1998). These two factors have of feeling or
been found to operate independently and in interaction with each other to cause binge eating (Stice, emotion.
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Akutagawa, Gaggar, & Agras, 2000). First, dietary restriction may precipitate binge eating, as the
intensifying states of hunger, starvation and craving eventually result in a loss of control over eating.
Second, negative affect may trigger a binge as the individual attempts to reduce distressing emotions
through the comfort and distraction provided from binge eating. Third, dieting and negative affect
may act together in that the self-control dieters need in order to maintain their restrictive eating can be
temporarily disrupted by negative emotions. As a result of such disruption, the dieter’s physiological
need for food, arising from semi-starvation, temporarily prevails and the dieter consequently eats a
large amount of food in the form of a binge.
Unfortunately, episodes of binge eating in turn trigger renewed attempts at strict dieting (and other
methods of weight control such as vomiting) due to anxiety about weight gain. A vicious cycle thus
develops, with dieting and binge eating exacerbating each other. Similarly, binge eating tends to result
in negative emotions such as shame, loneliness, anxiety and depression so that a vicious cycle is
once again established, with negative affect and binge eating tending to exacerbate one another. The
interactions between dieting, negative affect and binge eating are shown in Figure 9.1.
Dietary
Negative affect
restriction
Binge eating
episode
FIGURE 9.1 According to the dual pathway model, binge

eating episodes are triggered by dietary restriction, negative
affect or both (blue arrows). Binge eating episodes in turn result
in increased dieting and negative affect (grey arrows), thus
increasing the likelihood of further binge eating
SOCIAL FACTORS
Given the central role of dieting and negative affect in triggering binge eating, any social and cultural
factors that encourage dieting or result in negative affect will be of causal relevance for binge eating.
For instance, in terms of increasing the likelihood of dieting, individuals with bulimia nervosa report
that they received significantly higher levels of critical comments and teasing about their eating, shape
or weight from others in the period before they developed the disorder compared to healthy individuals
(Fairburn, Welch, Doll, Davies, & O’Connor, 1997). In terms of triggering negative affect, individuals
with bulimia nervosa also report having experienced significantly poorer family functioning (e.g.,
higher levels of arguments and criticism, and lower levels of care and affection, from their parents)
before they became ill compared to healthy individuals (Fairburn et al., 1997).
Do negative interpersonal events trigger negative mood and in turn binge eating episodes? One
study examined this hypothesis by asking women with bulimia nervosa to record the tone of their
social interactions (e.g., accepting/rejecting), mood and binge eating over a 28-day period (Steiger,
Guavin, Jabalpurwala, Séguin, & Stotland, 1999). Consistent with the hypothesis, the mood of the
women decreased as their interactions with others became more rejecting, critical and hostile. Also,
the women rated the tone of social interactions as significantly more rejecting, critical and hostile
before binge eating episodes compared to the tone of their social interactions on binge-free days.
Finally, both mood and social interactions were significantly worse after binge eating episodes
compared to binge-free days. This last finding suggests a vicious cycle in which binge eating increases
the likelihood of further negative social interactions and mood, thereby triggering more binge eating.
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The treatment of bulimia nervosa

Treatment effectiveness for bulimia nervosa has been more extensively and soundly researched
compared to the limited number of controlled treatment trials for anorexia nervosa. The relatively
broad research base of treatment for bulimia nervosa indicates that CBT is the treatment of choice.
However, as will be shown, even after CBT a substantial proportion of bulimia nervosa patients
continue to experience eating disorder symptoms, indicating the need for improved CBT and other
treatment approaches for bulimia nervosa.
MOTIVATIONAL ENHANCEMENT THERAPY (MET)
Similar to those with anorexia nervosa, individuals with bulimia nervosa may not be highly motivated
to recover. While sufferers of bulimia nervosa may be motivated to stop binge eating (because feeling
out of control in this way is usually very distressing), they may be unwilling to give up their pursuit
of unrealistic and unhealthy levels of thinness given the supreme importance they attach to thinness.
One of the largest studies to investigate MET in the context of bulimia nervosa was conducted by
Treasure and colleagues (1999). This treatment study compared the effectiveness of four weekly sessions
of MET and CBT for 125 patients with bulimia nervosa. It was found that higher levels of motivation to
recover at the beginning of treatment were associated with significantly greater reductions in binge eating
by the end of treatment. It was also found that the MET and CBT interventions were equally effective in
producing significant reductions in binge eating, vomiting and laxative abuse from pre- to post-treatment.
The fact that the MET results were equivalent to those for CBT is particularly impressive given that the
CBT group had a greater proportion of highly motivated patients compared to the MET group (18% of
the CBT patients versus 2% of the MET patients were highly motivated to change at the beginning of
treatment), and higher levels of motivation at pre-treatment predicted a better treatment response.
SELF-HELP APPROACHES
Self-help approaches may be ideal for those individuals who are motivated to receive treatment,
at least as a first phase of treatment that can then be followed up by more intensive interventions
(e.g., weekly sessions with a therapist) if needed. In self-help interventions, bulimia nervosa patients
are provided with manuals (presented as books or via a computer) usually based on CBT techniques.
A summary of the content of one self-help program is presented in Table 9.6. Patients work through
TABLE 9.6 The content of Fairburn’s (1995) self-help manual for bulimia nervosa based on CBT principles
MODULE CONTENT
1 Getting started Begin keeping a daily record of eating and weight-control behaviours and their triggers.
Begin weighing once a week, mainly to gain reassurance that weight gain does not generally
occur with treatment.
2 Regular eating Begin a pattern of regular eating consisting of three main meals and three snacks each day
to replace dieting alternating with binge eating.
Stop vomiting and using laxatives/diuretics since these behaviours encourage binge eating.
3 Alternatives to binge eating Develop a range of alternative activities to help resist the urge to binge (e.g., meeting a
friend, taking a bath or going for a walk).
4 Problem solving Learn how to solve problems effectively since stressful situations can trigger binge eating.
5 Stopping dieting Stop all forms of dieting (e.g., not eating for long periods, restricting the amount of food eaten,
and avoiding eating certain foods entirely) since dieting is a major trigger of binge eating.
6 Preventing relapse Have a plan in case binge eating recurs.
Do not resume dieting.
Deal with any ongoing problems (e.g., depression, anxiety, low self-esteem or relationship
difficulties).
Source: From Fairburn, C. G. (1995). Overcoming binge eating. New York: Guilford Press.
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these self-help manuals either alone (pure self-help) or with some support and guidance from a
therapist (guided self-help). The main advantages of self-help approaches are that they are available
for individuals in rural and regional areas where eating disorder treatment services are limited, can
provide immediate help for those on long waiting lists for treatment, and may reduce the amount of
time needed in more intensive forms of therapy and so reduce the cost of treatment.
Research has provided little support for the benefits of pure self-help approaches in bulimia nervosa
(Carter et al., 2003) but does suggest that guided self-help is a very effective form of treatment for
some patients with the disorder (Fairburn & Wilson, 2013). For example, one study compared bulimia
nervosa patients who received guided self-help with those on a treatment waiting list (Banasiak,
Paxton, & Hay, 2005). The guided self-help approach consisted of working through a CBT-based
manual while receiving direction and support in 10 sessions, each of 30 minutes’ duration, with a
general practitioner. The manual was Peter Cooper’s (1995) Bulimia Nervosa and Binge Eating:
A Guide to Recovery. At the end of treatment, 28 per cent of patients in the guided self-help condition
had stopped all binge eating and maladaptive weight-control behaviours compared to 11 per cent of
those in the control group. In another study, the outcome achieved from 18 short sessions of guided
self-help was at least as strong as that obtained from 18 1.5-hour sessions of group CBT (Bailer et
al., 2004). Given that a proportion of patients with bulimia nervosa respond well to guided self-help,
future research is needed to identify which patients are most likely to benefit from such an approach
versus those patients who will need more intensive forms of treatment. In addition, guided self-help
can be adapted to be delivered using electronic media and video-conferencing with some empirical
support for the efficacy of these modalities (Fairburn & Wilson, 2013).

CBT approaches have been applied very successfully in bulimia nervosa, with the most extensively
evaluated being that developed by the Oxford University research group (Fairburn, Marcus, & Wilson,
1993). This treatment entails 19 sessions over 20 weeks and comprises three stages.
The first stage
The first stage aims to educate the patient about bulimia nervosa and, most importantly, emphasises the
self-perpetuating cycle of dieting (and other weight-control behaviours) and binge eating as outlined
in the dual pathway model. Thus the goal is to eliminate dieting and other methods of weight control
and to follow instead a regular eating pattern of three meals and two or three snacks a day. To resist the
urge to binge and use extreme weight-control behaviours, patients are taught a range of strategies to
distract themselves until the urge subsides, with an emphasis on activities that are incompatible with
binge eating (e.g., seeking the company of others, since binge eating typically occurs in secret). As
with CBT for anorexia nervosa, self-monitoring of eating patterns and associated features is essential
to help patients become aware of the triggers and consequences of binge eating and weight-control
behaviours. An example of a monitoring form is shown in Table 9.7.
TABLE 9.7 An example of a daily eating monitoring form of a patient with bulimia nervosa
TIME WHAT WAS EATEN BINGE PURGE PLACE/THOUGHTS/FEELINGS

7.30 am Black coffee Home (kitchen)
10.15 am Diet coke and nuts (handful) Staffroom at work. Trying not to eat anything but the
nuts were sitting there.
3.30 pm 2 chocolate bars, 10 biscuits, √ √ Felt really hungry—ate it in the classroom. Felt guilty
large iced coffee and fat afterwards.
10.00 pm 6 pieces of toast with peanut √ √ Watching a movie. Angry at my eating during the day—
butter, bottle diet coke felt like I’d blown my diet badly. After eating felt really
disgusted. I will not eat anything tomorrow.
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The second stage

Once a regular pattern of eating has been achieved, stage two begins, which seeks to eliminate all dieting
and target dysfunctional cognitions regarding eating, shape and weight. To reduce dietary restraint,
a graded reintroduction of previously ‘forbidden’ foods is undertaken, commencing with those foods
that cause the least anxiety. Forbidden foods are those that are associated with extreme anxiety due to
their high energy content and the fact that they often trigger binge eating episodes. Patients learn to eat
such foods as part of a regular diet, in normal quantities, and without anxiety. In addition, strategies to
correct dysfunctional cognitions regarding eating, shape and weight are implemented. These include
challenging negative thoughts (e.g., ‘If I eat dessert I’ll gain 5 kilograms’) by evaluating the evidence
and replacing them with a more realistic view (e.g., ‘Lots of people occasionally eat dessert without
gaining any weight, let alone 5 kilograms’). The second stage also addresses effective strategies
for managing negative affect given that this can be a key trigger of both binge eating episodes and
inappropriate weight-control behaviours.
The third stage

In the third stage the focus is on relapse prevention. This stage is comparable to the final stage of CBT
for anorexia nervosa.
Predictors of outcome
Regarding the predictors of outcome following CBT, greater progress in the early course of treatment
predicts a better outcome (Agras et al., 2000a). One study found that higher weight suppression (the
difference between an individual’s highest weight ever and his/her current weight) was associated
with a higher treatment dropout rate and lower symptom improvement (Butryn, Lowe, Safer, &
Agras, 2006). Other important features predicting a poorer outcome with CBT include the presence
of comorbidities (specifically borderline personality disorder and substance use disorder), lack of
motivation to change, obesity and frequent bingeing and/or purging (NICE, 2004). In controlled trials,
CBT has been found to be more effective than other psychological and pharmacological treatments
(Hay, Bacaltchuk, & Stefano, 2004).
INTERPERSONAL PSYCHOTHERAPY (IPT)

The one possible exception to the superiority of CBT compared to other psychological treatments
for bulimia nervosa is interpersonal psychotherapy (IPT). The primary focus of IPT is to help
individuals identify and change any current interpersonal problems (e.g., conflict with others or a
lack of social support) that are assumed to be maintaining the eating disorder. These interpersonal
problems are hypothesised to result in poor self-esteem and/or negative affect, which in turn trigger
eating disorder symptoms.
To assess the relative strength of IPT and CBT in the treatment of bulimia nervosa, Agras,
Walsh, Fairburn, Wilson, and Kraemer (2000b) randomly allocated 220 patients to 19 sessions of
either IPT or CBT. Immediately after treatment, CBT was found to result in significantly higher rates
of recovery: 29 per cent of patients who completed CBT were no longer binge eating or purging
compared to 5 per cent of those who completed IPT. However, when the patients were re-assessed one
year later, there was no longer a statistically significant difference between the two treatments, with
26 per cent of those completing CBT having recovered compared with 17 per cent of those completing
IPT. On the basis of these findings, CBT must be considered to be the preferred approach since it
produces more rapid improvement than IPT, a result that has also been found in more recent research
on a sample of patients with different types of eating disorders (Fairburn et al., 2015). The challenge
for future research on IPT will be to identify strategies that produce a faster and higher treatment
response. For instance, Wilfley and Rieger (2003) have suggested that patients be given greater
assistance to identify the links between their interpersonal problems and eating disorder behaviours,
since these connections are not always obvious to patients.
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Antidepressants are the only type of medication currently indicated in the treatment of bulimia nervosa
(Mitchell, Roerig, & Steffen, 2013; NICE, 2004). The use of antidepressant medication was prompted by
the common occurrence of mood disorders in individuals with bulimia nervosa. Systematic reviews of
controlled trials have found that antidepressants are more effective than placebo drugs in reducing binge
eating and mood disturbance. Interestingly, comparisons of depressed and non-depressed patients with
bulimia nervosa reveal that both groups respond equally to antidepressant medication, suggesting that
these drugs do not necessarily achieve their beneficial effects on bulimic symptoms by improving mood.
Despite these promising results, there are limitations associated with the use of antidepressants in
the treatment of bulimia nervosa. First, psychological treatments (mostly CBT) have been found to be
superior to antidepressants for both the reduction and cessation of binge eating. Second, medication
is associated with a high treatment dropout rate due to side effects and patients’ attitudes towards
medication use. Finally, medication is associated with a high relapse rate in the months after treatment.
Overall, the research suggests that patients should be offered psychological treatment initially, with
medication reserved for those who fail to benefit sufficiently from psychotherapy or when the patient
has a depressive disorder that warrants treatment in its own right.
CASE STUDY: BULIMIA NERVOSA

Amy is a 25-year-old primary school teacher who lives with a flatmate. She is not currently in a relationship.
Amy describes having had a difficult childhood and adolescence. She has a younger sister whom she states has
‘always been Dad’s favourite’. While Amy feels very close to her mother, this relationship is also an unstable one stemming
from her mother’s struggles with depression and excessive drinking. Her parents often argued while she was growing up,
and eventually divorced when Amy was 15. At around the same age, she found herself the victim of bullying by a group
of girls at high school. She says, ‘I can remember as a teenager never feeling good enough. According to Dad, I wasn’t as
good as my sister. With Mum, I always felt powerless to help her feel better. And for reasons I’ve never understood, some
girls at school teased me relentlessly.’
While of a normal weight, Amy decided that losing weight might help her to feel better about herself and possibly
increase her popularity at school. So at the age of 16 she embarked on a strict diet, which was made easier by the fact
that her father no longer lived in the family home and her mother’s depression and drinking problems often meant that
she was not present to supervise Amy’s meals. Amy began to lose weight and for the first time that she could recall, she
began to feel better about herself: ‘I didn’t exactly like myself, but my constant self-critical thoughts seemed to lessen, at
least when I managed to stick to my diet.’
But after about six months of dieting, Amy found it increasingly difficult to stick to her diet. Each afternoon she would
begin experiencing cravings for foods she did not usually allow herself to eat. She recalls one particular day when these
cravings overwhelmed her. ‘It had been a really bad day at school. I found out that my boyfriend at the time had kissed
one of the girls who teased me. I felt so betrayed, so defeated. Why was I bothering to try to improve myself? Mum
was in bed when I got home. I went to the fridge and started picking on some cheesecake. I just focused on how good
it tasted and before I knew it, the whole cake was gone.’ While the experience had given her some time out from the
distress regarding her boyfriend, Amy felt appalled at herself for having ‘lost control’. She decided that she would not eat
anything the following day in an attempt to compensate for the calories she had consumed. But as her hunger became
more intense throughout the next day, she had a biscuit that one of her friends offered her. Believing that she had broken
her diet, Amy then went to the school tuck shop and bought a packet of chips, a chocolate bar and an ice cream, which
she ate alone in the locker room. Filled again with feelings of remorse as well as a desperate need to get rid of what she
had eaten, she made herself vomit and felt immediate relief.
This began a cycle of ever-increasing intensity in which Amy would resolve to restrict her eating, which eventually
broke down in the form of a binge eating episode, and which was followed by self-induced vomiting and further resolve
to restrict her eating. For most of the rest of high school and during university, she would highly restrict her eating during
the day, and then binge and purge alone at home in the evening. The shame that she felt regarding her binge eating and
vomiting added another layer to the longstanding feelings of worthlessness she had. So, too, did the fact that she was
falling behind in her university studies—her eating disorder meant that she often did not have the levels of concentration,
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energy and motivation to attend lectures and complete her assignments. Her feelings of worthlessness also made it
hard for her to reach out to others and form friendships. In her isolation, binge eating and vomiting became her one
way of managing her distress, at least in the short term as the binge eating provided her with a sense of comfort and
the vomiting helped her to feel more in control. But after yet another evening of binge eating and vomiting, she would
usually feel even worse.
After almost 10 years of suffering in silence with her daily battles and feeling increasingly overwhelmed by her
emotional distress, Amy found the courage to reach out for help. She located a GP whom she trusted, and shared
with the GP something about her struggles with eating, body image and self-worth. Fortunately the GP had a good
understanding of eating disorders and, after conducting a psychological and medical assessment, diagnosed
Amy with bulimia nervosa. Amy was referred to a clinical psychologist who specialised in the treatment of eating
disorders. She responded well to a cognitive behavioural treatment approach, although the process of recovery was
at times a challenging one. Given Amy’s history of difficult interpersonal relationships, the psychologist needed to
gradually gain Amy’s trust. With that growing trust, Amy was able to more honestly share all of her thoughts, feelings
and behaviours during therapy so that the psychologist could help her. Another challenge stemmed from the fact
that, in the absence of using binge eating to cope with her emotions, Amy began to experience various distressing
emotions. During the course of treatment, she learned a range of strategies for eating in a balanced way, managing
her distressing emotions, improving her self-worth and developing mutually rewarding relationships with others.
After about a year of treatment her binge eating had ceased and she no longer induced vomiting. Her mood had also
greatly improved. Even though she still struggled at times with feelings of worthlessness, she became more sociable
(e.g., joining her colleagues in the staffroom for lunch) and these fledgling friendships were helping her to discover
her many valuable qualities.
LO 9.4 Binge eating disorder

The third major eating disorder to be addressed is binge eating disorder. It is characterised by binge
eating episodes in the absence of inappropriate weight-control behaviours.
The epidemiology of binge eating disorder

Compared to anorexia nervosa and bulimia nervosa, binge eating disorder is more evenly distributed
across the genders and across different age groups. Individuals with binge eating disorder are at
heightened risk of developing obesity and its adverse health consequences.
PREVALENCE
Community surveys in North America (Hudson, Hiripi, Pope, & Kessler, 2007) and Europe (Fichter,
Quadflieg, Georgopoulou, Xepapadakos, & Fthenakis, 2005) suggest that binge eating disorder
affects approximately 3–5 per cent of young women. The gender difference is less stark in binge
eating disorder compared to anorexia nervosa and bulimia nervosa, with an estimated two-thirds of
those with the disorder being female (Hay, Mond, Buttner, & Darby, 2008).

The age of onset for binge eating disorder is unknown, but the best estimates are that it initially occurs
in late adolescence and young adulthood (Hay, 2003; Stice, Shaw, & Nemeroff, 1998). Most patients
with binge eating disorder are in the young or middle-age adult years. Subthreshold levels of the
disorder are also common and can progress to full spectrum binge eating disorder with or without
crossover into bulimia nervosa (Stice, Marti, Shaw, & Jaconis, 2009).
The course of binge eating disorder over time has been the subject of much debate. Some argue that it
is a short-term condition that tends to spontaneously resolve (even without treatment) (Fairburn, Cooper,
Doll, Norman, & O’Connor, 2000), whereas others contend that the disorder typically persists over
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years (Wilfley, Wilson, & Agras, 2003). The former position is largely based on a five-year prospective
study conducted by Fairburn and colleagues (2000) in which they compared the outcome of individuals
with binge eating disorder with that of individuals diagnosed with bulimia nervosa. The study found
that only 18 per cent of the individuals with binge eating disorder still had some type of eating disorder
at the five-year point compared to 51 per cent of the bulimia nervosa group. However, this finding must
be tempered by several considerations. First, there was no significant difference between the binge
eating disorder (10%) and bulimia nervosa (15%) groups in terms of the percentage of individuals who
still had their original diagnosis at the five-year time-point. Thus the worse outcome associated with
bulimia nervosa compared to binge eating disorder was largely due to the development of other eating
disorders rather than the persistence of bulimia nervosa. Second, there was no significant difference
between the binge eating disorder and bulimia nervosa groups in terms of the reduction in shape and
weight concerns or general psychiatric symptoms over the course of the five years. Third, in at least one
aspect, the outcome for individuals with binge eating disorder was worse than that for individuals with
bulimia nervosa in that a higher proportion had developed obesity at the five-year time-point. In contrast
to this study’s findings are the reports of patients receiving treatment for binge eating disorder who
generally claim that their disorder began approximately two decades earlier (Wilfley et al., 2003). Such
reports fail to support the contention that binge eating disorder is a condition of short duration. Perhaps
individuals do experience temporary remissions of their symptoms but the disorder then reoccurs in a
manner akin to other serious psychological disorders (e.g., major depressive disorder). Clearly, further
prospective research is required to clarify the course of binge eating disorder over time.
ASSOCIATED MEDICAL AND PSYCHOLOGICAL PROBLEMS

The most prominent physical problem for patients with binge eating disorder is overweight or obesity
(De Zwann, 2001; Hudson, Hiripi, Pope, & Kessler, 2007; Yanovski, 2003). The five-year study
conducted by Fairburn and colleagues (2000) found that the prevalence of obesity increased from
22 per cent to 39 per cent in young women with binge eating disorder over this period. The rate of
obesity among individuals with binge eating disorder has been found to be as high as 65 per cent
(Striegel-Moore et al., 2001) compared to 20 per cent in the general Australian population (Cameron
et al., 2003). As such, individuals with binge eating disorder are at heightened risk of developing
hypertension the adverse health consequences of obesity such as hypertension, type II diabetes and cardiovascular
Condition in disease, which are among the leading causes of death in Western countries (National Task Force on
which the blood the Prevention and Treatment of Obesity, 2000).
supply through
As with anorexia nervosa and bulimia nervosa, individuals with binge eating disorder often
the blood vessels
is excessive
experience a range of associated psychological problems. Specifically, mood disorders, anxiety
and is a major disorders, substance use disorders and personality disorders are common comorbidities among those
risk factor for with binge eating disorder (Grilo, 2006; Hudson et al., 2007).
heart disease
and stroke (also
known as high
The aetiology of binge eating disorder
blood pressure). Certain features are common to individuals with binge eating disorder and those with anorexia nervosa
and bulimia nervosa, such as the tendency to base self-worth largely on one’s shape and weight in
at least a subgroup of those with the disorder. Yet there are also important differences, including
the older age, greater number of affected males, higher rates of obesity and lower levels of dieting
in binge eating disorder compared to other eating disorders. This combination of overlapping and
distinct features points to both similarities and differences in the aetiological factors for binge eating
disorder and other eating disorders.
BIOLOGICAL FACTORS
Biological factors in binge eating disorder are much less studied than the two more established
disorders of anorexia nervosa and bulimia nervosa. However, there is preliminary support for a
moderate heritability for binge eating syndromes in the absence of extreme weight-control behaviours
from twin studies (Bulik et al., 2000; Reichborn-Kjennerud, Bulik, Tambs, & Harris, 2004).
rie66620_ch09_235-280.indd 264 07/29/17 01:42 PM

This genetic vulnerability may entail dysfunction in the serotonin neurotransmitter system, given
an association between binge eating disorder and abnormalities in the serotonin transporter gene
(Monteleone, Tortorella, Castaldo, & Maj, 2006). Hormonal disturbances have also been investigated
as having a possible causal role in binge eating disorder. For instance, ghrelin is a peptide found
largely in the stomach and duodenum and is believed to stimulate appetite and food intake. Thus
it may be one of the factors that trigger excessive eating in individuals with binge eating disorder.
However, ghrelin levels have actually been found to be significantly lower in women with binge
eating disorder compared with healthy women (Monteleone et al., 2005). These low ghrelin levels are
probably a consequence of overeating, and are a signal to the central nervous system to reduce hunger.
Clearly, further research is needed to determine whether individuals with binge eating disorder have
abnormalities in the neurotransmitter and hormonal systems involved in the regulation of appetite
and fullness that may contribute to the disorder. In addition, individuals with binge eating disorder
and other bulimic-type eating disorders may have similar problems of dysregulation of brain reward
circuitry to those people with addiction disorders (Gearhardt et al., 2011).
As discussed in the section on bulimia nervosa, the dual pathway model proposes that dieting and/
or negative mood trigger binge eating. Yet dieting is of less causal importance for binge eating in
binge eating disorder compared to bulimia nervosa. For instance, while 90 per cent of those with
bulimia nervosa report that a period of dieting preceded the onset of their binge eating, fewer than
50 per cent of those with binge eating disorder report the same (and fewer than 10% report having
been on a strict diet) (Wilfley, Wilson, & Agras, 2003). In addition, the eating patterns of individuals
with bulimia nervosa are characterised by extreme dietary restriction between binge eating episodes,
whereas individuals with binge eating disorder engage in moderate dieting at most, and may even
overeat, between binges.
In contrast to dieting, there is stronger support for the role of negative affect in binge eating
disorder. Individuals with binge eating disorder are more likely to eat in response to negative mood
states compared to those without an eating disorder who are matched for weight (Eldredge & Agras,
1996). This finding indicates that emotional eating is associated with binge eating disorder rather
than obesity. For some individuals with binge eating disorder, the mood disturbance may be severe
enough to warrant a diagnosis of major depression. An estimated 20 per cent of individuals report
that they experienced major depression in the period before they developed binge eating disorder
compared to a 6 per cent rate of depression among individuals without an eating disorder (Fairburn
et al., 1998).
SOCIAL FACTORS
Certain social factors may trigger the negative emotions that predispose individuals with binge eating
disorder to binge eat. Similar to the research findings for anorexia nervosa and bulimia nervosa, those
with binge eating disorder report poorer family functioning in the period before they developed the
disorder, including elevated levels of criticism (both in general and in terms of their shape and weight)
and reduced levels of affection from their parents (Fairburn et al., 1998).
Binge eating and subsequent weight gain potentially result in another trigger for negative affect—
that is, obesity stigma, which entails negative attitudes and behaviours from others towards obese
individuals. There is evidence of obesity stigma occurring in wide-ranging social contexts (e.g.,
in work, educational and healthcare settings) and already being evident in children as young as
3–5 years of age (Puhl & Brownell, 2003). Demonstrating the strength of obesity as a basis for social
rejection, one study found that fifth- and sixth-grade schoolchildren ranked an obese child as the least
desirable friend, after children in a wheelchair, with an amputated hand, using crutches or with a
facial disfigurement (Latner & Stunkard, 2003). The images used for the girls in the study are shown
in Figure 9.2. For overweight or obese children, the negative emotions resulting from social rejection
may trigger further overeating and so lead to further weight gain.
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Healthy Crutches Wheelchair Hand Face Obese
FIGURE 9.2 The drawings used in a study assessing obesity stigma in children, which included a child with
no visible disabilities, one holding crutches, one sitting in a wheelchair, one with no left hand, one with a
facial disfigurement, and one who was obese
Source: Adapted from Latner, J. D., & Stunkard, A. J. (2003). Getting worse: The stigmatisation of obese children. Obesity Research, 11,
452–456.
The treatment of binge eating disorder

Research conducted to date suggests that a number of approaches are highly beneficial in reducing
binge eating or eliminating it altogether in individuals with binge eating disorder. The results have
been less promising in terms of assisting obese individuals with the disorder to lose weight.
SELF-HELP APPROACHES
Just like those with bulimia nervosa, patients with binge eating disorder may be offered a self-help
approach as a first step, followed by more intensive treatment if needed. Also similar to bulimia nervosa
is the finding that guided self-help appears to be more effective than pure self-help in the treatment
of binge eating disorder. However, unlike bulimia nervosa, even pure self-help is of benefit for binge
eating disorder patients (Fairburn & Wilson, 2013). For instance, one study used a self-help manual
based on cognitive-behavioural principles with binge eating disorder patients (Loeb, Wilson, Gilbert,
& Labouvie, 2000). Patients worked through the manual either alone (the pure self-help condition)
or with the support of a therapist in six 30-minute sessions (the guided self-help condition). After
10 weeks of treatment, both groups experienced a significant reduction in the frequency of binge eating
episodes, although this reduction was significantly greater in the guided self-help group compared to
the pure self-help group. A substantial proportion of patients in both groups stopped binge eating
entirely: 30 per cent of patients in the pure self-help group and 50 per cent of patients in the guided
self-help group. However, neither condition resulted in significant weight loss for this generally obese
group of patients. Also, as there was no follow-up assessment it is not known whether improvements
in binge eating were maintained over time. As with bulimia nervosa, the use of electronic media to
deliver therapy is likely to play a larger role in the future (Fairburn & Wilson, 2013).

CBT has been the most extensively evaluated treatment for binge eating disorder and generally entails
the same cognitive and behavioural strategies utilised in the treatment of bulimia nervosa. Nevertheless,
there are some differences in the implementation of CBT for patients with binge eating disorder based
on the fact that they engage in less dieting and more overeating (even when not binge eating), do not
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engage in extreme weight-control behaviours, and are more often overweight compared to those with
bulimia nervosa. Thus the targets of treatment are a moderate eating plan (to avoid any tendency
to be under-restrictive or overly restrictive in eating), increasing the use of healthy weight-control
behaviours (e.g., regular, moderate physical activity), and achieving greater acceptance of a larger than
average body weight (given that it is unrealistic for most obese individuals to aim for a thin physique).
INTERPERSONAL PSYCHOTHERAPY (IPT)

IPT has been evaluated as a treatment for binge eating disorder given the existence of interpersonal
problems among this group of patients that, through the negative effect of such problems on mood,
are believed to contribute to binge eating. Wilfley and colleagues (2002) found that 20 sessions of IPT
were as effective as 20 sessions of CBT in the treatment of 162 binge eating disorder patients, both
at the end of treatment and at a follow-up assessment conducted one year after treatment ended. For
example, at the follow-up assessment, 70 per cent of patients who completed IPT and 72 per cent of
patients who completed CBT were no longer binge eating.
There are two main differences between these results and those obtained for bulimia nervosa
patients. First, IPT was as rapid as CBT in reducing binge eating in binge eating disorder patients
(whereas CBT produced a faster reduction than IPT in bulimia nervosa patients). Second, the
proportion of patients who were no longer binge eating after treatment is higher for binge eating
disorder patients than for bulimia nervosa patients. A comparison of the findings obtained for CBT
and IPT in the treatment of bulimia nervosa versus binge eating disorder is shown in Figure 9.3.
In sum, IPT is highly effective in reducing binge eating in binge eating disorder patients and is as
effective as CBT in doing so. However, an important limitation of IPT for binge eating disorder is that,
like CBT, it produces little if any weight loss among these overweight patients.
100
80
CBT for BED
IPT for BED

60 CBT for BN
IPT for BN
40
20
0
Post-treatment One year
FIGURE 9.3 The percentage of patients with bulimia nervosa (BN) (Agras et al., 2000b) and binge eating
disorder (BED) (Wilfley et al., 2002) who had recovered after receiving cognitive behaviour therapy (CBT) or
interpersonal psychotherapy (IPT) both immediately after treatment and one year later
BEHAVIOURAL WEIGHT LOSS (BWL)

CBT and IPT for binge eating disorder focus primarily on reducing binge eating, with secondary
importance placed on weight loss. In behavioural weight-loss treatment (BWL) this emphasis is
reversed: the focus is mainly on weight loss, with a secondary focus on binge eating. BWL approaches
are so named because patients are encouraged to alter the behaviours that result in weight loss—that
is, to restrict their caloric intake and to increase their physical activity. Mental health professionals do
not necessarily implement BWL since it is not a specialised psychological treatment like CBT or IPT.
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The research on BWL treatment for overweight patients with binge eating disorder suggests that
it is a promising approach. In one study comparing 24 sessions of BWL and CBT for 80 overweight
patients with binge eating disorder, both treatments resulted in significant reductions in binge eating
from the beginning to the end of treatment (Munsch et al., 2007). These improvements were maintained
one year later. For example, one year after treatment ended, 50 per cent of patients in the BWL group
were no longer binge eating compared to 52 per cent of those who received CBT. Although BWL
resulted in a significantly greater reduction in weight than CBT at the end of treatment, there was
no longer a significant difference between the two treatments at the one-year follow-up. This result
highlights a major challenge in treatments for overweight and obese individuals—that is, helping them
to maintain their weight loss over time rather than regaining weight.
An interesting finding on BWL treatment for binge eating disorder is that having patients engage
in dietary restriction does not result in an increase in their binge eating (and, in fact, reduces binge
eating). This finding would at first appear to challenge the dual pathway model, which states that
dieting is one of the key pathways into binge eating. However, on closer examination, the dieting of
individuals with bulimia nervosa that triggers binge eating and the dieting of individuals with binge
eating disorder in BWL treatment that reduces binge eating are different phenomena. That is, severe
dieting in bulimia nervosa is usually by healthy-weight individuals who are pursuing unrealistic levels
of thinness, while the moderate dieting advocated in BWL programs is aimed at helping individuals
return to what is a healthy weight for them.
Antidepressant medications have been supported in the treatment of binge eating disorder. Specifically,
research has found that selective serotonin reuptake inhibitors (SSRIs) are generally superior to
placebo drugs in achieving binge eating abstinence and in reducing depressive symptoms in patients
with binge eating disorder (NICE, 2004).
However, CBT has been found to be superior to SSRIs in the treatment of binge eating disorder.
For instance, in one study, Grilo, Masheb, and Wilson (2005) randomly allocated 108 patients with
binge eating disorder to receive 16 weeks of the SSRI fluoxetine, placebo pill, CBT plus fluoxetine or
CBT plus placebo. At the end of treatment, a significantly higher proportion of those in the two CBT
conditions were no longer binge eating compared to those who received fluoxetine alone. Also, the
addition of fluoxetine to CBT did not improve the treatment outcome compared with CBT alone. It is
unclear what the role of antidepressants might become with the conduct of further trials, but at present
their role is mostly limited to patients who have significant depressive symptoms.
Anticonvulsants, notably topiramate, have emerged as promising for the reduction of binge
eating and improved weight management in the treatment of binge eating disorder (Mitchell, Roerig,
&Steffen, 2013). However, adverse effects (such as unusual peripheral sensory experiences) can be
problematic with these medications.
The most recent systematic review and meta-analysis of randomised controlled trials for
binge eating disorder in adults included nine psychological trials and 25 trials that evaluated
pharmacological or combined psychological/pharmacological treatment (Brownley et al., 2016).
One important aspect of this review is that it was the first to include the drug lisdexamphetamine, a
central nervous system stimulant that is also used for the treatment of attention deficit hyperactivity
disorder. This is an important inclusion as it is the first (and only) drug that has been approved by the
Food and Drug Administration in the United States for the treatment of binge eating disorder. It was
likewise approved in Canada in 2016 and is likely to become available in Australia on prescription
in 2017–2018. In their review, Brownley and colleagues concluded that lisdexamphetamine is both
effective in the treatment of binge eating disorder and tolerated by patients. It has been found to
result in a reduction in binge eating frequency, obsessive thoughts, compulsions and weight. It has
also been found to reduce triglyceride levels (a type of fat in the blood that may increase the risk of
heart disease).
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There is as yet insufficient evidence as to how best to integrate psychological and pharmacological
treatments for binge eating disorder. In an editorial entitled ‘Binge Eating Disorder Comes of Age’,
Devlin (2016) provides a helpful summary of the research to date and the various factors influencing
the choice of treatment for individuals with this disorder: ‘Given the array of psychological,
behavioural, and pharmacologic treatment approaches currently available, how should we proceed
after identifying the problem? Although Brownley and colleagues recommend cognitive and other
forms of behavioural therapy, second generation antidepressants, topiramate and lisdexamfetamine
as the most supported treatments for binge eating in binge eating disorder, they also point out that
comparative effectiveness and long-term studies are lacking. Thus the practitioner is faced with a
decision based on treatment availability, often limited for specialised psychotherapies; costs; adverse
effects; patient preference; individual goals; and patient-specific factors, such as comorbid depression
or eating-related obsessions and compulsions’ (pp. 445–446).
CASE STUDY: BINGE EATING DISORDER

Daniel is a 37-year-old man who was assessed by a psychologist as part of the preparation for undergoing bariatric
(weight loss) surgery. During the assessment, he reported that he had been overweight since primary school, which
shifted to obesity in his first years at high school. At the age of 13, his family moved to a much smaller town and he
did not adjust well to changing schools. He was teased about his weight (called ‘fat boy’), poor physical fitness and
‘city’ ways. He began ‘comfort’ eating and by the time he left school his BMI was 35. Since leaving school he has tried
many restrictive diets and exercise programs, always with some initial success, but after which he regained the weight,
plus more. Over time his BMI reached its present level of 50. As a consequence of his obesity he developed type II
diabetes mellitus.
As part of his assessment at the bariatric surgery clinic, Daniel completed a questionnaire, in which he reported
regular episodes of out-of-control overeating. When asked about these by the psychologist, he tearfully explained that
he has daily ‘binges’, usually on several packets of 10–20 chocolate biscuits that he buys cheaply (on ‘specials’) at the
supermarket. He said that he desperately wanted to stop as he felt nauseated and disgusted after binge eating. He had
tried to be ‘bulimic’ (i.e., to self-induce vomiting after overeating) but could not bring himself to do this. He had never
thought of using laxatives or skipping his diabetic medication or any other dangerous or ineffective methods of weight
control after binge eating. Instead, he would vow to himself not to eat for 12 hours after binge eating but his hunger levels
would become too intense and overwhelm his intention not to eat.
During the assessment, Daniel reported no other psychological symptoms, including no history of a current or past
depressive disorder. He reported he had never been underweight but has a sister with anorexia nervosa. Although he is
the only family member with morbid obesity, his parents are mildly obese, as was his sister before developing anorexia
nervosa. Daniel also reported that after leaving high school he drifted between unskilled short-term jobs on building
sites. He has experienced reluctance on the part of employers to hire an obese person. This, together with his poor
physical fitness, has made it difficult for him to find and keep jobs. He has one close friend from high school but has
never dated and described himself as very shy and insecure, mainly due to his weight. He is hopeful that the surgery and
weight loss will turn his life around.
Daniel was referred for CBT to help normalise his eating patterns prior to surgery. The treatment was successful in
helping him to reduce his binge eating and resulted in some improvement in his diabetes. He was accepted for surgery
after a month of abstinence from binge eating. Two years later his BMI had reduced to 35, his confidence had improved,
he had been able to find regular employment and he had started a building apprenticeship, although he was still socially
isolated. He also admitted to some continued problems with out-of-control eating, although this was now on smaller
quantities of food (e.g., five biscuits). He had also found he could now easily vomit after losing control of his eating. As
a result of these continuing interpersonal issues and eating disorder symptoms, Daniel agreed to further psychological
therapy, which involved interpersonal psychotherapy given his lack of supportive relationships in addition to reiterating
the CBT strategies he had previously learnt.
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LO 9.5 General topics in eating disorders

Current challenges and controversies
There are many challenges currently facing the field of eating disorders that have at times generated
much controversy as researchers grapple with the most effective strategies for advancing the field.
Chief among these challenges are confronting limitations in the currently available treatments,
identifying how best to assist those individuals who refuse treatment, gaining greater understanding of
the manifestation of eating disorder symptoms in males and discovering the most effective means for
preventing the development of eating disorders.
LIMITATIONS OF CURRENT TREATMENT APPROACHES

There are several important limitations of current treatments for eating disorders. First, the lack of
research on treatment for anorexia nervosa leaves many therapists with little guidance and contributes
to a diversity of approaches of unknown effectiveness.
A second limitation is that while CBT has been found to be the most effective treatment for bulimia
nervosa, there is still much room for improvement, with approximately half of the participants in
randomised controlled trials still binge eating at the end of the trials (Hay & Bacaltchuk, 2006). This
has prompted the development of an enhanced version of CBT for bulimia nervosa (and other eating
disorders) that extends the focus of therapy to include perfectionism, dysfunctional interpersonal
relationships and low self-esteem (Fairburn, 2008; Fairburn, Cooper, & Shafran, 2003). This enhanced
version of CBT has been found to be helpful for those patients who have a range of psychological
problems (e.g., interpersonal disturbance) in addition to their eating disorder (although after treatment
only 60% of these patients had levels of eating disorder symptoms comparable to those of a community
sample) (Fairburn et al., 2009). Thus future research will benefit from continuing to identify strategies
for improving outcomes as well as examining which are the most effective forms of treatment for
which groups of patients.
A third limitation of current treatments is the separation between eating disorders and obesity.
The prevalence of obesity is high in the bulimic eating disorders, especially binge eating disorder.
However, since patients more frequently seek help for their weight problem than their eating problem,
health professionals may not identify the eating disorder and may lack training in its treatment. The
challenge for future researchers is to develop treatments that effectively integrate approaches for eating
disorders and obesity.
Finally, there is the challenge that most sufferers are not accessing available treatments and
that a wide gap persists between the presence of an eating disorder and its diagnosis and treatment
(Hart, Granillo, Jorm, & Paxton, 2011). The development of treatments that are more accessible,
such as guided self-help, is important in redressing this, but more work is needed to overcome
misperceptions about treatment in the general public and among health professionals that may
act as barriers to treatment. For example, a community sample of women from the Australian
Capital Territory indicated that they mistakenly viewed bulimia nervosa as very difficult to treat,
antidepressants as harmful, and the weight-reducing strategies of people with eating disorders as
desirable (Mond, Hay, Rodgers, Owen, & Beumont, 2004a; 2004b). It has also been found that many
health professionals (up to a third or more) mistakenly believe that weight gain is likely with treatment
for bulimia nervosa and also consider treatment to be very difficult (Hay, Darby, & Mond, 2007).
Another feature that limits access to appropriate treatment is the fact that mental health professionals
may lack sufficient expertise in delivering the interventions known to be most effective for eating
disorders. One innovative approach that is currently being investigated is the use of internet-based
training programs so that health professionals are better able to access the necessary training in order
to implement effective psychological therapies for individuals with an eating disorder (Fairburn &
Wilson, 2013).
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INVOLUNTARY TREATMENT
Most therapists treating patients with eating disorders, and anorexia nervosa in particular, will not be
able to avoid being confronted by a gravely ill patient who is determined to relentlessly pursue thinness
irrespective of what the consequences might be and who steadfastly refuses treatment. More so than in
almost any other branch of clinical psychology, such patients raise difficult clinical, ethical and legal
challenges (Carney et al., 2006). Therapists who accept decisions to refuse treatment by patients who
are inflicting harm on themselves (e.g., by consuming too much alcohol) may strongly challenge or
even impose involuntary treatment (e.g., a legally imposed period of inpatient treatment or the use of
tube feeding to ensure weight gain) on patients with anorexia nervosa who are placing their wellbeing
in jeopardy. Among the reasons for this discrepancy are the youth of eating disorder patients and the
fact that death may be imminent unless treatment is immediately imposed. In addition, it is often
argued that while patients with an alcohol problem, for example, are making their decision with a
clear understanding of the consequences of their behaviours, the judgment of the patient with anorexia
nervosa is clouded by his/her mental state, to which severe under-nutrition no doubt contributes.
Some argue, however, that the pursuit of extreme weight loss is not the product of mental illness but
the expression of deeply held values similar, for example, to the behaviour of protesters who engage
in a life-threatening hunger strike. Moreover, it has been suggested that compulsory treatment may
undermine the chances of recovery since it could threaten the relationship between the therapist and
patient, and intensify the patient’s need to seek control over his/her eating and weight (with patients
typically reporting feeling fearful, angry and powerless when treatment is imposed). As one patient,
Mary, describes it: ‘while coercion may save lives, it may also kill spirits’ (in Carney et al., 2006, p. 133).
Yet despite the potentially destructive nature of involuntary treatment, recovery is possible only if the
immediate risk of death is avoided (Tan, Stewart, Fitzpatrick, & Hope, 2010). Schmidt Holm, Brixen,
Andries, Horder, & Klinkby Stoving (2012) maintain that ‘misplaced respect for patient autonomy may
lead to a fatal outcome in anorexia nervosa’ (p. 99) and they describe five fatal cases of patients with
anorexia nervosa, four of whom could have been saved if compulsory treatment had been implemented
(based on the fact that, for example, they had previously responded well to compulsory treatment).
Thus it is generally acknowledged that, even with the best efforts to build a collaborative approach
between the therapist and patient, some patients with anorexia nervosa will need to be treated without
their consent. In such cases, great care must be taken to ensure that involuntary treatment is implemented
in a respectful and humane manner. Patients often comment that the manner in which coercive
treatment is imposed is more destructive than its involuntary nature (Tan et al., 2010). The contrasting
experiences of Mary and Denise during the meetings in which the decision for involuntary treatment
was made illustrate this point. For Mary, this experience was ‘extremely intimidating. They were also
rather degrading, focusing so strongly on all the negatives [that] they reinforced my sense that I was a
failure. I also felt that I was seen first and foremost as an “anorexic” rather than a person’ (in Carney et
al., 2006, p. 126). In contrast, Denise described the experience as ‘really pleasant . . . They were just all
really caring and understanding and listening and encouraging’ (in Carney et al., 2006, p. 128).
In retrospect, most patients treated involuntarily tend to acknowledge that, despite its difficulty,
such an approach was needed. For example, in discussing her involuntary treatment, Olivia stated: ‘I
knew that eventually they’d put the weight on me. So I just thought “No, I’d rather die than let them do
this”. And ooooh, I hated them. But now I can look back and I don’t think that was wrong. I think that
was what needed to be done’ (in Carney et al., 2006, p. 28).
MUSCLE DYSMORPHIA AS AN EATING DISORDER

It has been noted earlier in the chapter that eating disorders predominantly affect females. Yet this
may be partly an artefact of our current diagnostic systems, which fail to include within the eating
disorders category the types of eating, shape and exercise concerns that are more characteristic of
males, namely, concerns regarding one’s degree of muscularity. The DSM-5 includes the disorder
‘muscle dysmorphia’, which occurs almost exclusively in males and is characterised by excessive
concern that one’s body is too small or insufficiently muscular. While the DSM-5 classifies muscle
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dysmorphia as a type of body dysmorphic disorder,

Murray et al. (2012) have suggested that it should
instead be classified as an eating disorder. They
argue that muscle dysmorphia and anorexia nervosa
comprise ‘two sides of the same coin’, with muscle
dysmorphia entailing the relentless pursuit of
increased muscularity (consistent with sociocultural
messages regarding male body ideals) while anorexia
nervosa involves the relentless pursuit of thinness
(consistent with sociocultural messages regarding
female body ideals). In support of this reclassification
of muscle dysmorphia as an eating disorder, Murray et
al. (2012) found that males with muscle dysmorphia
and anorexia nervosa had comparable levels of body
image disturbance, disordered eating and compulsive
exercise. As well as their similarity in symptoms,
muscle dysmorphia and anorexia nervosa may have
similarities in the factors that drive these symptoms.
For instance, just as research has demonstrated a link
between eating disorder symptoms and constructs
such as perfectionism, negative mood and low self-
esteem, Murray, Rieger, Karlov, and Touyz (2013)
DAL
found that these same factors predicted the severity of

The central feature of muscle dysmorphia muscle dysmorphia symptoms.
is excessive concern that one’s body is not
muscular enough, even though the individual
PREVENTION OF EATING DISORDERS
is of average or even above-average
The extensive suffering experienced by those with an
musculature.
eating disorder, their often poor response to treatment,
and the fact that the number of affected individuals far
exceeds the availability of specialised treatment all provide a strong rationale for developing programs
that can prevent eating disorders from occurring in the first place. Unfortunately, most of these
prevention approaches (32 out of 38 interventions in one review paper) have failed to produce lasting
reductions in eating disorder symptoms (Stice & Shaw, 2004). Some studies even suggest that these
programs can actually increase eating disorder symptoms such as dieting, perhaps because their focus
on eating and body image encourages individuals to become preoccupied with such concerns (Carter,
Stewart, Dunn, & Fairburn, 1997).
While it would be ideal to be able to prevent the occurrence of eating disorders, what (if any) are
the most beneficial ways of doing so? Conflicting responses have been offered to this question. One
suggestion has been to focus on general risk factors for psychological disorders (e.g., low self-esteem)
rather than specific risk factors for eating disorders (e.g., dieting) so as to avoid a discussion of eating
disorder topics, which may implant unhealthy ideas in some individuals. For instance, a school-based
program entitled ‘Everyone’s Different’ was developed to improve the self-esteem of adolescent
girls and boys (O’Dea & Abraham, 2000). The program was delivered in the classroom over nine
lessons and included components such as identifying one’s unique qualities, discovering what factors
can threaten self-image and using role-plays to explore different ways of responding to threatening
situations. When used with 11–14-year-olds, this intervention was found to have beneficial effects
in comparison to students who took part in their regular health classes: those who participated in the
program had significantly greater improvements in body satisfaction and greater reductions in
the importance of physical appearance as a basis for feeling good about oneself.
In contrast to those who advocate avoiding eating disorder topics in prevention programs, other
researchers support such approaches. Their suggestion for improving prevention efforts is to focus
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only on individuals who are at heightened risk of developing an eating disorder (e.g., those who are
dissatisfied with their bodies). Such individuals are more likely to be motivated to participate in the
program since the material is highly relevant to them. One such approach is ‘Student Bodies’, an eight-
week internet-based intervention designed for young women with high body dissatisfaction (Taylor
et al., 2006). The program includes several components, including:
∙ weekly readings providing education about body image, unhealthy weight-control behaviours
and nutrition
∙ weekly exercises (e.g., observing real women in public and contrasting them with images of
women in magazines)
∙ keeping an online body image journal to identify triggers for body dissatisfaction and challenging
these
∙ participating in online discussion groups regarding the readings and exercises.
Despite concerns that interventions focusing on eating disorder features may end up promoting the
very concerns they are trying to reduce, this has not been found to be the case. Several studies support
the use of these programs with high-risk adolescents (Stice, Shaw, Burton, & Wade, 2006) and young
adults (Jacobi et al., 2007; Taylor et al., 2006) in terms of significant reductions in body-image concerns
and dieting compared to students not receiving the intervention. These results have been found to be
maintained up to two years after the program (Taylor et al., 2006). Importantly, these interventions
not only reduce eating disorder symptoms but also reduce the onset of full-blown eating disorders and
obesity (Stice, Marti, Spoor, Presnell, & Shaw, 2008; Stice et al., 2006; Taylor et al., 2006).
So it appears that a focus on eating disorder symptoms may be appropriate for individuals at risk of
developing an eating disorder: since these individuals are already beginning to display eating disorder
symptoms, the program does not run the risk of creating such concerns in the first place. As well
as targeting high-risk individuals, eating disorder prevention programs have also been found to be
more effective if they target factors known to predict the development of eating disorders (e.g., body
dissatisfaction and thin-ideal internalisation) (Stice, Shaw, & Marti, 2007). So future research on
COURTESY STANFORD UNIVERSITY
An example webpage from the internet-based eating disorders prevention program ‘Student Bodies’.
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prevention programs would benefit from investigating the value of targeting additional risk factors for
eating disorders such as negative affect (Stice, Black Becker, & Yokum, 2013).
Eating disorder organisations

A number of eating disorder organisations throughout Australia and New Zealand have been
established to improve the services available to individuals with an eating disorder, family members,
healthcare professionals and the general community. These include:
∙ national-based organisations such as the Butterfly Foundation (www.thebutterflyfoundation.org.
au) and state-based organisations such as the Eating Disorders Foundation of Victoria (www.
eatingdisorders.org.au), which are non-profit organisations that provide a wide range of services
including telephone and online counselling, support groups, information on eating disorders and
educational seminars for professionals and the general community
∙ the Australia and New Zealand Academy for Eating Disorders (ANZAED), which is an association
of professionals with an interest in eating disorders that aims to foster research and professional
training in the treatment of eating disorders (www.anzaed.org.au).
SUMMARY
The eating disorders recognised in the DSM-5—anorexia nervosa, bulimia nervosa and binge eating disorder—have been the focus
of this chapter. Eating disorders predominantly affect females, although this gender difference is less pronounced for binge eating
disorder compared to anorexia nervosa and bulimia nervosa. They are associated with a range of comorbid psychological disorders
and medical problems, some of which may be life-threatening. The serious problems associated with eating disorders are particularly
concerning given that these disorders (especially anorexia nervosa) are often longstanding in nature and may be lifelong.
The aetiology of eating disorders is not completely understood but research suggests that a range of biological, psychological and
social factors are involved. Biologically, there is evidence supporting a genetic vulnerability for each of the eating disorders. In terms
of understanding the nature of the mechanism that is inherited, much focus has been on neurotransmitter systems (e.g., serotonin)
and hormones (e.g., leptin) known to be associated with the regulation of appetite and fullness. A variety of psychological factors
are believed to trigger dieting and binge eating, including low self-esteem, body dissatisfaction, self-worth that is heavily based on
shape and weight, mood disturbance and personality traits such as perfectionism. The social factors that are likely to contribute to the
development of eating disorders are disturbances in family functioning, negative comments from family and peers regarding one’s
shape or weight, and cultural attitudes that endorse unrealistic levels of thinness and denigrate those with obesity.
In terms of treatment for eating disorders, most research has been conducted on bulimia nervosa, for which there is strong
evidence supporting the effectiveness of cognitive behaviour therapy (CBT) over other psychological and pharmacological
approaches. Few randomised controlled trials have been conducted to evaluate the effectiveness of treatments for anorexia
nervosa, although preliminary evidence suggests that motivational enhancement therapy, CBT, family-based treatment and even
supportive clinical management are of benefit. Research has identified a range of effective treatments for binge eating disorder
including self-help approaches, CBT, interpersonal psychotherapy and behavioural weight-loss programs, although assisting those
with obesity to lose weight and maintain weight losses remains a challenge. Medication does not appear to have a central role in
the treatment of eating disorders but may be useful in treating accompanying psychological problems (such as depression) or if the
patient does not respond sufficiently to psychological treatment.
While the past 30 years have witnessed a dramatic increase in research on eating disorders, much remains to be clarified in
understanding these complex conditions. Even the most promising results (e.g., CBT for bulimia nervosa and binge eating disorder)
indicate the need for improved treatment modalities for patients with eating disorders. Identifying the most effective approaches for
enhancing the motivation of individuals who deeply value and hence are strongly attached to their symptoms remains a challenge,
most obviously when involuntary treatment is undertaken. Greater understanding is also needed regarding the manifestation of
eating, shape, weight and exercise concerns in males. Finally, given the serious and often longstanding nature of these disorders,
the fact that individuals are affected at a young age, and the limitations in current treatments, identifying the optimal strategies for
preventing eating disorders is a high priority.
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KEY TERMS
affect. . . . . . . . . . . . . . . . . . . . . . . . . . . . 257 day-patient treatment . . . . . . . . . . . . . 249 neuroimaging. . . . . . . . . . . . . . . . . . . . 244
amphetamines . . . . . . . . . . . . . . . . . . . 242 dizygotic twins . . . . . . . . . . . . . . . . . . . 244 neuroleptics . . . . . . . . . . . . . . . . . . . . . 254
anorexia nervosa. . . . . . . . . . . . . . . . . 237 heritability . . . . . . . . . . . . . . . . . . . . . . . 243 outpatient treatment . . . . . . . . . . . . . . 249
barium swallow. . . . . . . . . . . . . . . . . . . 240 hypertension. . . . . . . . . . . . . . . . . . . . . 264 selective serotonin reuptake
binge eating disorder . . . . . . . . . . . . . 239 incidence. . . . . . . . . . . . . . . . . . . . . . . . 248 inhibitors (SSRIs). . . . . . . . . . . . . . . . . . 254
binge eating episode. . . . . . . . . . . . . . 238 inpatient treatment. . . . . . . . . . . . . . . . 249 sociocultural approach. . . . . . . . . . . . 248
bulimia nervosa . . . . . . . . . . . . . . . . . . 237 monozygotic twins. . . . . . . . . . . . . . . . 244 tricyclic antidepressants (TCAs). . . . . 254
cognitive behaviour therapy (CBT). . . 251 motivational enhancement tube feeding. . . . . . . . . . . . . . . . . . . . . 239
concordance rate. . . . . . . . . . . . . . . . . 244 therapy (MET). . . . . . . . . . . . . . . . . . . . 250
REVIEW QUESTIONS
LO 9.1
9.1 Binge eating is a core feature of bulimia nervosa and binge eating disorder and can occur in cases of anorexia
nervosa. What are the essential characteristics of a binge eating episode?
9.2 What are the main differences between bulimia nervosa and binge eating disorder?
LO 9.2
9.3 List some of the key biological, psychological and social factors thought to be involved in the aetiology of
anorexia nervosa.
9.4 Why is normalising eating and weight an essential first stage in the treatment of anorexia nervosa before other
psychological problems (e.g., negative mood) can be addressed?
LO 9.3
9.5 According to the dual pathway model of bulimia nervosa, what are the two main triggers of binge eating
episodes?
9.6 What are some of the main cognitive-behavioural strategies used to eliminate dieting in individuals with bulimia
nervosa?
LO 9.4
9.7 What are some key differences in the epidemiology of binge eating disorder versus anorexia nervosa and
bulimia nervosa?
9.8 Which treatment approaches have been found to be effective for individuals with binge eating disorder?
LO 9.5
9.9 What are some of the main limitations with current treatments for eating disorders?
9.10 While several programs have been found to be effective in preventing the development of eating disorders,
what is one way in which these programs could be improved even further?
REFERENCES
Agras, W. S., Crow, S. J., Halmi, K. A., Mitchell, J. E., Wilson, G. T., & Agras, W. S., Walsh, T., Fairburn, C. G., Wilson, G. T., & Kraemer,
Kraemer, H. C. (2000a). Outcome predictors for the cognitive- H. C. (2000b). A multicentre comparison of cognitive-behavioural
behavioral treatment of bulimia nervosa: Data from a multisite therapy and interpersonal psychotherapy for bulimia nervosa.
study. American Journal of Psychiatry, 157, 1302–1308. Archives of General Psychiatry, 57, 459–466.
rie66620_ch09_235-280.indd 275 07/29/17 01:42 PM

American Psychiatric Association (1980). Diagnostic and statistical problems in adolescent girls: Questionnaire findings. British
manual of mental disorders (DSM-III) (3rd ed.). Washington, DC: Journal of Clinical Psychology, 35, 193–203.
Author. Cameron, A. J., Welborn, T. A., Zimmet, P. Z., Dunstan, D. W.,
American Psychiatric Association (1987). Diagnostic and statistical Owen, N., Salmon, J., . . . Shaw, J. E. (2003). Overweight and
manual of mental disorders (DSM-III-R) (3rd ed., revised). obesity in Australia. Medical Journal of Australia, 178, 427–432.
Washington, DC: Author. Campbell, I. C., Mill, J., Uher, R., & Schmidt, U. (2011). Eating
American Psychiatric Association (1994). Diagnostic and statistical disorders, gene–environment interactions and epigenetics.
manual of mental disorders (DSM-IV) (4th ed.). Washington, DC: Neuroscience and Biobehavioral Reviews, 35, 784–793.
Author. Carlat, D., Camargo, C. A., & Herzog, D. (1997). Eating disorders in
American Psychiatric Association (2000). Diagnostic and statistical males: A report on 135 patients. American Journal of Psychiatry,
manual of mental disorders (4th ed., text revision). Washington, 154, 1127–1132.
DC: Author. Carney, T., Tait, D., Touyz, S., Ingvarson, M., Saunders, D., &
American Psychiatric Association (2013). Diagnostic and statistical Wakefield, A. (2006). Managing anorexia nervosa: Clinical, legal
manual of mental disorders (5th ed.). Arlington: Author. and social perspectives on involuntary treatment. New York: Nova
Arcelus, J., Mitchell, A. J., Wales, J., & Nielsen, S. (2011). Mortality Science Publishers.
rates in patients with anorexia nervosa and other eating disorders: Carter, J. C., Olmsted, M. P., Kaplan, A., McCabe, R. E., Mills, J. S., &
A meta-analysis of 36 studies. Archives of General Psychiatry, 68, Aimé, A. (2003). Self-help for bulimia nervosa: A randomised
724–730. controlled trial. American Journal of Psychiatry, 160, 973–978.
Bailer, U., de Zwaan, M., Leisch, F., Strnad, A., Lennkh-Wolfsberg, Carter, J. C., Stewart, A., Dunn, V. J., & Fairburn, C. G. (1997).
C., El-Giamal, N., . . . Kasper, S. (2004). Guided self-help versus Primary prevention of eating disorders: Might it do more harm than
cognitive-behavioural group therapy in the treatment of bulimia good? International Journal of Eating Disorders, 22, 167–172.
nervosa. International Journal of Eating Disorders, 35, 522–537. Ciseaux, A. (1980). Anorexia nervosa: A view for the mirror.
Banasiak, S. J., Paxton, S. J., & Hay, P. (2005). Guided self-help for American Journal of Nursing, 80, 1468–1470.
bulimia nervosa in primary care: A randomised controlled trial. Claudino, A., Hay, P., Lima, M. S., Bacaltchuk, J., Schmidt, U., &
Psychological Medicine, 35, 1283–1294. Treasure, J. T. (2006). Antidepressants for anorexia nervosa. The
Bardone-Cone, A., & Cass, K. (2006). Investigating the impact of Cochrane Database System Review. Chichester: John Wiley &
pro-anorexia websites: A pilot study. European Eating Disorders Sons.
Review, 14, 256–262. Cooper, P. J. (1995). Bulimia nervosa and binge eating: A guide to
Becker, A., Burwell, R., Gilman, S., Herzog, D., & Hamburg, P. recovery. London: Robinson Publishing.
(2002). Eating behaviours and attitudes following prolonged Currin, L., Schmidt, U., Treasure, J., & Hershel, J. (2005). Time
exposure to television among ethnic Fijian adolescent girls. British trends in eating disorder incidence. British Journal of Psychiatry,
Journal of Psychiatry, 180, 509–514. 186, 132–135.
Bell, R. M. (1985). Holy anorexia. Chicago: The University of Dalle Grave, R., Calugi, S., Doll, H. A., & Fairburn, C. G. (2013).
Chicago Press. Enhanced cognitive behaviour therapy for adolescents with
Beumont, P., Hay, P., Touyz, S., Ben-Tovim, D., Birmingham, L., anorexia nervosa: An alternative to family therapy? Behaviour
Derham, H.,  . 
. 
. Weigall, S. (2004). Australian and New Research and Therapy, 51, R9–R12.
Zealand clinical practice guidelines for the treatment of anorexia Dean, H. Y., Touyz, S. W., Rieger, E., & Thornton, C. E. (2007).
nervosa. Australian and New Zealand Journal of Psychiatry, 38, Can motivational enhancement therapy improve a cognitive-
659–670. behaviourally based inpatient program for eating disorders?
Boskind-Lodahl, M., & White, W. C. (1978). The definition and In D. Einstein (Ed.), Innovations and advances in cognitive
treatment of bulimarexia in college women: A pilot study. Journal behaviour therapy (pp. 171–183). Bowen Hills: Australian
of the American Health Association, 27, 84–97. Academic Press.
Brownley, K. A., Berkman, N. D., Peat, C. M., Lohr, K. N., Devlin, M. J. (2016). Binge-eating disorder comes of age. Annals of
Cullen, K. E., Bann, C. M., & Bulik, C. M. (2016). Binge-eating Internal Medicine, 165, 445–446.
disorder in adults: A systematic review and meta-analysis. Annals De Zwann, M. (2001). Binge eating disorder and obesity. International
of Internal Medicine, 165, 409–420. Journal of Obesity, 25 (Supp.), S51–S55.
Bruch, H. (1973). Eating disorders: Obesity, anorexia nervosa, and Eckert, E. D., Pomeroy, C., & Raymond, N. (1998). Leptin in anorexia
the person within. London: Routledge & Kegan Paul. nervosa. Journal of Endocrinology and Metabolism, 83, 791–794.
Bulik, C. M., Sullivan, P. F., Wade, T. D., & Kendler, K. S. (2000). Eisler, I., Dare, C., Russell, G. F., Szmukler, G., Le Grange, D., &
Twin studies of eating disorders: A review. International Journal Dodge, E. (1997). Family and individual therapy in anorexia
of Eating Disorders, 27, 1–20. nervosa: A 5-year follow-up. Archives of General Psychiatry, 54,
Butryn, M. L., Lowe, M. R., Safer, D. L., & Agras, W. S. (2006). 1025–1030.
Weight suppression is a robust predictor of outcome in the Eldredge, K. L., & Agras, W. S. (1996). Weight and shape overconcern
cognitive-behavioural treatment of bulimia nervosa. Journal of and emotional eating in binge eating disorder. International
Abnormal Psychology, 115, 62–67. Journal of Eating Disorders, 19, 73–82.
Button, E. J., Sonuga-Barke, E., Davies, J., & Thompson, M. (1996). Fairburn, C. G. (1995). Overcoming binge eating. New York:
A prospective study of self esteem in the prediction of eating Guilford Press.
rie66620_ch09_235-280.indd 276 07/29/17 01:42 PM

Fairburn, C. G. (2008). Cognitive behaviour therapy and eating P. E. Garfinkel (Eds.), Handbook of treatment for eating disorders
disorders. New York: Guilford Press. (2nd ed.) (pp. 94–144). New York: Guilford Press.
Fairburn, C. G., Bailey-Straebler, S., Baden, S., Doll, H. A., Gearhardt, A. N., Yokum, S., Orr, P. T., Stice, E., Corbin, W. R., &
Jones, R., Murphy, R., . . . Cooper, Z. (2015). A transdiagnostic Brownell, K. D. (2011). Neural correlates of food addiction.
comparison of enhanced cognitive behaviour therapy (CBT-E) and Archives of General Psychiatry, 68, 808–816.
interpersonal psychotherapy in the treatment of eating disorders. Gerner, B., & Wilson, P. H. (2005). The relationship between
Behaviour Research and Therapy, 70, 64–71. friendship factors and adolescent girls’ body image concern, body
Fairburn, C. G., Cooper, Z., Doll, H. A., Norman, P., & O’Connor, M. dissatisfaction, and restrained eating. International Journal of
(2000). The natural course of bulimia nervosa and BED in young Eating Disorders, 37, 313–320.
women. Archives of General Psychiatry, 57, 659–665. Gorwood, P., Bouvard, M., Mouren-Simeoni, M. C., Kipman, A., &
Fairburn, C. G., Cooper, Z., Doll, H. A., O’Connor, M., Bohn, K., Ades, J. (1998). Genetics and anorexia nervosa: A review of
Hawker, D. H.,  . 
. 
. Palmer, R. L. (2009). Transdiagnostic candidate genes. Psychiatric Genetics, 8, 1–12.
cognitive-behavioral therapy for patients with eating disorders. Gowers, S. G., Clark, A., Roberts, C., Griffiths, A., Edwards, V.,
American Journal of Psychiatry, 166, 311–319. Bryan, C.,  . 
. 
. Barrett, B. (2007). Clinical effectiveness of
Fairburn, C. G., Cooper, Z., Doll, H. A., O’Connor, M. E., treatments for anorexia nervosa in adolescents: Randomised
Palmer, R. L., & Dalle Grave, R. (2013). Enhanced cognitive controlled trial. British Journal of Psychiatry, 191, 427–435.
behaviour therapy for adults with anorexia nervosa: A UK–Italy Grilo, C. M. (2006). Eating and weight disorders. New York:
study. Behaviour Research and Therapy, 51, R2–R8. Psychology Press.
Fairburn, C. G., Cooper, Z., Doll, H. A., & Welch, S. L. (1999). Grilo, C. M., Masheb, R. M., & Wilson, G. T. (2005). Efficacy of
Risk factors for anorexia nervosa: Three integrated case-control cognitive behavioural therapy and fluoxetine for the treatment
comparisons. Archives of General Psychiatry, 56, 468–476. of binge eating disorder: A randomised double-blind placebo-
controlled comparison. Biological Psychiatry, 57, 301–309.
Fairburn, C. G., Cooper, Z., & Shafran, R. (2003). Cognitive
behaviour therapy for eating disorders: A ‘transdiagnostic’ theory Gull, W. W. (1874). Anorexia nervosa. Transactions of the Clinical
and treatment. Behaviour Research and Therapy, 41, 509–528. Society of London, 7, 22–28.
Hall, A., & Hay, P. J. (1991). Eating disorder patient referrals from a
Fairburn, C. G., Doll, H. A., Welch, S. L., Hay, P. J., Davies, B. A., &
population region 1977–1986. Psychological Medicine, 21, 697–701.
O’Connor, M. E. (1998). Risk factors for binge eating disorder:
Halmi, K. A., Agras, W. S., Crow, S., Mitchell, J., Wilson, G. T.,
A community-based, case-control study. Archives of General
Bryson, S. W., & Kraemer, H. C. (2005). Predictors of treatment
Psychiatry, 55, 425–432.
acceptance and completion in anorexia nervosa: Implications for
Fairburn, C. G., & Harrison, P. J. (2003). Eating disorders. The
future study designs. Archives of General Psychiatry, 62, 776–781.
Lancet, 361, 407–416.
Hart, L. M., Granillo, M. T., Jorm, A. F., & Paxton, S. J. (2011).
Fairburn, C. G., Marcus, M. D., & Wilson, G. T. (1993). Cognitive- Unmet need for treatment in the eating disorders: A systematic
behavioral therapy for binge eating and bulimia nervosa: A review of eating disorder specific treatment seeking among
comprehensive treatment manual. In C. G. Fairburn & G. T. community cases. Clinical Psychology Review, 31, 727–735.
Wilson (Eds.), Binge eating: Nature, assessment, and treatment Hay, P. J. (2003). Quality of life and bulimic eating disorder
(pp. 361–404). New York: Guilford Press. behaviours: Findings from a community-based sample.
Fairburn, C. G., Shafran, R., & Cooper, Z. (1998). A cognitive International Journal of Eating Disorders, 33, 434–442.
behavioural theory of anorexia nervosa. Behaviour Research and Hay, P. (2013). A systematic review of evidence for psychological
Therapy, 37, 1–13. treatments in eating disorders: 2005–2012. International Journal
Fairburn, C. G., Welch, S. L., Doll, H. A., Davies, B. A., & of Eating Disorders, 46, 462–469.
O’Connor, M. E. (1997). Risk factors for bulimia nervosa: Hay, P., & Bacaltchuk, J. (2006). Bulimia nervosa. Clinical Evidence,
A community-based case-control study. Archives of General 15, 1315–1331.
Psychiatry, 54, 509–517. Hay, P. J., Bacaltchuk, J., & Stefano, S. (2004). Psychotherapy for
Fairburn, C., & Wilson, T. (2013). The dissemination and bulimia nervosa and binge eating. Cochrane Database Systematic
implementation of psychological treatments: Problems and Reviews, 3, CD000562.
solutions. International Journal of Eating Disorders, 46, 516–521. Hay, P., Chinn, D., Forbes, D., Madden, S., Newton, R., Sugenor,
Fichter, M. M., Quadflieg, N., Georgopoulou, E., Xepapadakos, F., & L., . . . Ward, W. (2014). Royal Australian and New Zealand
Fthenakis, E. W. (2005). Time trends in eating disturbances in College of Psychiatrists clinical practice guidelines for the
young Greek migrants. International Journal of Eating Disorders, treatment of eating disorders. Australian and New Zealand Journal
38, 310–322. of Psychiatry, 48, 977–1008.
Frank, G. K., Bailer, U. F., Henry, S., Wagner, A., & Kaye, W. H. Hay, P. J., Darby, A., & Mond, J. (2007). Knowledge and beliefs
(2004). Neuroimaging studies in eating disorders. CNS Spectrums, 9, about bulimia nervosa and its treatment: A comparative study
539–548. of three disciplines. Journal of Clinical Psychology in Medical
Garner, D. M. (2004). EDI-3: Eating Disorder Inventory-3 Settings, 14, 59–68.
professional manual. Lutz: Psychological Assessment Resources. Hay, P. J., Mond, J., Buttner, P., & Darby, A. (2008). Eating
Garner, D. M., Vitousek, K. M., & Pike, K. M. (1997). Cognitive- disorder behaviours are increasing: Findings from two sequential
behavioral therapy for anorexia nervosa. In D. M. Garner & community surveys in South Australia. PLoS ONE 3(2): e1541.
rie66620_ch09_235-280.indd 277 07/29/17 01:42 PM

Hay, P. J., & Sachdev, P. (2011). Brain dysfunction in anorexia with eating disorder features: A general population study.
nervosa: Cause or consequence of under-nutrition? Current International Journal of Eating Disorders, 46, 375–380.
Opinion in Psychiatry, 24, 251–256. Mond, J. M., Hay, P. J., Rodgers, B., Owen, C., & Beumont, P. J. V.
Hoek, H. W. (2006). Incidence, prevalence and mortality of anorexia (2004a). Beliefs of women concerning the severity and
nervosa and other eating disorders. Current Opinion in Psychiatry, prevalence of bulimia nervosa. Social Psychiatry and Psychiatric
19, 389–394. Epidemiology, 39, 299–304.
Hudson, J. I., Hiripi, E., Pope, H. G., & Kessler, R. C. (2007). The Mond, J. M., Hay, P. J., Rodgers, B., Owen, C., & Beumont, P. J.
prevalence and correlates of eating disorders in the National V. (2004b). Beliefs of women concerning causes and risk factors
Comorbidity Survey Replication. Biological Psychiatry, 61, for bulimia nervosa. Australian and New Zealand Journal of
348–358. Psychiatry, 38, 463–469.
Jacobi, C., Hayward, C., de Zwaan, M., Kraemer, H. C., & Agras, W. S. Monteleone, P., Fabrazzo, M., Tortorella, A., Martiadis, V.,
(2004). Coming to terms with risk factors for eating disorders: Serritell, C., & Maj, M. (2005). Circulating ghrelin is decreased in
Application of risk terminology and suggestions for a general non-obese and obese women with binge eating disorder as well as
taxonomy. Psychological Bulletin, 130, 19–65. in obese non-binge eating women, but not in patients with bulimia
Jacobi, C., Morris, L., Beckers, C., Bronisch-Holtze, J., Winter, J., nervosa. Psychoneuroendocrinology, 30, 243–250.
Winzelberg, A. J., & Taylor, C. B. (2007). Maintenance of internet- Monteleone, P., Tortorella, A., Castaldo, E., & Maj, M. (2006).
based prevention: A randomised controlled trial. International Association of a functional serotonin transporter gene
Journal of Eating Disorders, 40, 114–119. polymorphism with binge eating disorder. American Journal of
Jimerson, D. C., Lesem, M. D., Kaye, W. H., & Breweton, T. D. Medical Genetics, 141, 7–9.
(1992). Low serotonin and dopamine metabolite concentrations in Munsch, S., Biedert, E., Meyer, A., Michael, T., Schlup, B., Tuch,
the cerebrospinal fluid from bulimic patients with frequent binge A., & Margraf, J. (2007). A randomised comparison of cognitive
episodes. Archives of General Psychiatry, 49, 529–534. behavioural therapy and behavioural weight loss treatment for
Kaye, W. H., Frank, G. K., Bailer, U. F., & Henry, S. E. (2005). overweight individuals with binge eating disorder. International
Neurobiology of anorexia nervosa: Clinical implications of Journal of Eating Disorders, 40, 102–113.
alterations of the function of serotonin and other neuronal systems. Murray, S., Rieger, E., Hildebrandt, T., Karlov, L., Russell, J.,
International Journal of Eating Disorders, 37 (Supp.), 15–19. Boon. E., . . . Touyz, S. (2012). A comparison of eating, exercise,
Keel, P. K., Heatherton, T. F., Dorer, D. J., Joiner, T. E., & Zalter, A. K. shape, and weight related symptomatology in males with muscle
(2006). Point prevalence of bulimia nervosa in 1982, 1992, and dysmorphia and anorexia nervosa. Body Image, 9, 193–200.
2002. Psychological Medicine, 36, 119–127. Murray, S., Rieger, E., Karlov, L., & Touyz, S. (2013). An
Keel, P. K., Mitchell, J. E., Miller, K. B., Davis, T. L., & Crow, S. J. investigation of the transdiagnostic model of eating disorders in
(1999). Long-term outcome of bulimia nervosa. Archives of the context of muscle dysmorphia. European Eating Disorders
General Psychiatry, 56, 63–69. Review, 21, 160–164.
Keys, A., Brozek, J., Henschel, A., Mickelsen, O., & Taylor, H. L. National Institute for Clinical Excellence (NICE) (2004). Eating
(1950). The biology of human starvation (2 vols.). Minneapolis: disorders—Core interventions in the treatment and management of
University of Minnesota Press. anorexia nervosa, bulimia nervosa and related eating disorders.
Lasègue, C. (1873/1997). On hysterical anorexia. Obesity Research, NICE clinical guideline No. 9. London: Author.
5, 492–497. National Task Force on the Prevention and Treatment of Obesity
Latner, J. D., & Stunkard, A. J. (2003). Getting worse: The (2000). Overweight, obesity, and health risk. Archives of Internal
stigmatisation of obese children. Obesity Research, 11, 452–456. Medicine, 160, 898–904.
Lock, J., Le Grange, D., Agras, W. S., & Dare, C. (2001). Treatment Norris, M., Boydell, K., Pinhas, L., & Katzman, D. (2006). Ana
manual for anorexia nervosa. New York: Guilford Press. and the internet: A review of pro-anorexia websites. International
Loeb, K. L., Wilson, G. T., Gilbert, J. S., & Labouvie, E. (2000). Journal of Eating Disorders, 39, 443–447.
Guided and unguided self-help for binge eating. Behaviour Oakley Browne, M. A., Wells, J. E., & Scott, K. M. (Eds.) (2006).
Research and Therapy, 38, 259–272. Te Rau Hinengaro: The New Zealand Mental Health Survey.
Maguire, S., Touyz, S. W., Surgenor, L., Lacey, H., & Le Grange, D. Wellington: New Zealand Ministry of Health.
(2011). Why DSM needs to consider a staging model for anorexia O’Dea, J. A., & Abraham, S. (2000). Improving the body image,
nervosa. In Y. Latzer, J. Merrick, & D. Stein (Eds.), Understanding eating attitudes, and behaviours of young male and female
eating disorders: Integrating culture, psychology and biology adolescents: A new educational approach that focuses on self-
(pp. 15–26). New York: Nova Publications. esteem. International Journal of Eating Disorders, 28, 43–57.
McIntosh, V. V. W., Jordan, J., Carter, F., Luty, S. E., McKenzie, J. M., Osler, W. (1892). Principles and practice of medicine. Philadelphia:
Bulik, C. M., . . . Joyce, P. R. (2005). Three psychotherapies for Williams & Wilkins.
anorexia nervosa: A randomised controlled trial. American Journal Pawluck, D. E., & Gorey, K. M. (1998). Secular trends in the incidence
of Psychiatry, 162, 741–747. of anorexia nervosa: Integrative review of population-based studies.
Mitchell, J. E., Roerig, J., & Steffen, K. (2013). Biological therapies International Journal of Eating Disorders, 23, 347–352.
for eating disorders. International Journal of Eating Disorders, 46, Paxton, S. J., Schutz, H. K., Wertheim, E. H., & Muir, S. L. (1999).
470–477. Friendship clique and peer influences on body image concerns,
Mitchison, D., Mond, J., Slew-Younan, S., & Hay, P. (2013). Sex dietary restraint, extreme weight-loss behaviours, and binge eating
differences in health related quality of life impairment associated in adolescent girls. Journal of Abnormal Psychology, 108, 255–266.
rie66620_ch09_235-280.indd 278 07/29/17 01:42 PM

Pike, K. M., Carter, J., & Olmsted, M. (2005). Cognitive behavioral attraction and sexual experience among a representative sample of
therapy manual for anorexia nervosa. (Available upon request: adults. Australian and New Zealand Journal of Public Health, 27,
Kmp2@columbia.edu) 138–145.
Pike, K. M., Walsh, B. T., Vitousek, K., Wilson, G. T., & Bauer, J. Smolak, L., Levine, M., & Schermer, F. (1999). Parental input and
(2003). Cognitive behavior therapy in the posthospitalisation weight concerns among elementary school children. International
treatment of anorexia nervosa. American Journal of Psychiatry, Journal of Eating Disorders, 25, 263–271.
160, 2046–2049. Spitzer, R. L., Devlin, M., Walsh, B. T., Hasin, D., Wing, R., Marcus,
Polivy, J., & Herman, C. P. (2002). Causes of eating disorders. M., . . . Nonas, C. (1992). Binge eating disorder: A multisite field
Annual Review of Psychology, 53, 187–213. trial of the diagnostic criteria. International Journal of Eating
Puhl, R. M., & Brownell, K. D. (2003). Psychosocial origins of Disorders, 11, 191–203.
obesity stigma: Toward changing a powerful and pervasive bias. Steiger, H., Guavin, L., Jabalpurwala, S., Séguin, J. R., & Stotland,
Obesity Reviews, 4, 213–227. S. (1999). Hypersensitivity to social interactions in bulimic
Reichborn-Kjennerud, T., Bulik, C., Tambs, K., & Harris, J. R. syndromes: Relationship to binge eating. Journal of Consulting
(2004). Genetic and environmental influences on binge eating and Clinical Psychology, 67, 765–775.
in the absence of compensatory behaviours: A population- Steinhausen, H. C. (2002). The outcome of anorexia nervosa in the
based twin study. International Journal of Eating Disorders, 36, 20th century. American Journal of Psychiatry, 159, 1284–1293.
307–314. Stice, E. (2002a). Risk and maintenance factors for eating pathology.
Rieger, E., (2015). Motivational approaches. In T. Wade (Ed.), Psychological Bulletin, 128, 825–848.
Encyclopedia of feeding and eating disorders. Singapore: Springer. Stice, E. (2002b). Sociocultural influences on body image and eating
doi:10.1007/978-981-287-087-2 disturbance. In C. G. Fairburn & K. D. Brownell (Eds.), Eating
Russell, G. F. M. (1970). Anorexia nervosa: Its identity as an illness and disorders and obesity (2nd ed.) (pp. 103–107). New York: Guilford
its treatment. In J. H. Price (Ed.), Modern trends in psychological Press.
medicine (vol. 2) (pp. 131–164). London: Butterworth. Stice, E., Akutagawa, D., Gaggar, A., & Agras, W. S. (2000).
Russell, G. F. M. (1979). Bulimia nervosa: An ominous variant of Negative affect moderates the relation between dieting and
anorexia nervosa. Psychological Medicine, 9, 429–448. binge eating. International Journal of Eating Disorders, 27,
Russell, G. F. M. (1983). Anorexia nervosa and bulimia nervosa. 218–229.
In G. F. M. Russell & L. Hersov (Eds.), Handbook of psychiatry: Stice, E., Black Becker, C., & Yokum, S. (2013). Eating disorder
The neuroses and personality disorders (vol. 4) (pp. 285–298). prevention: Current evidence-base and future directions.
Cambridge: Cambridge University Press. International Journal of Eating Disorders, 46, 478–485.
Russell, G., Szmukler, G., Dare, C., & Eisler, I. (1987). An evaluation Stice, E., Killen, J. D., Hayward, C., & Taylor, C. B. (1998). Age
of family therapy in anorexia nervosa and bulimia nervosa. Archives of onset for binge eating and purging during late adolescence: A
of General Psychiatry, 44, 1047–1056. 4-year survival analysis. Journal of Abnormal Psychology, 107,
Schmidt Holm, J., Brixen, K., Andries, A., Horder, K., & Klinkby 671–675.
Stoving, R. (2012). Reflections on involuntary treatment in the Stice, E., Marti, C. N., Shaw, H., & Jaconis, M. (2009). An 8-year
prevention of fatal anorexia nervosa: A review of five cases. longitudinal study of the natural history of threshold, subthreshold,
International Journal of Eating Disorders, 45, 93–100. and partial eating disorders from a community sample of
Serfaty, M., Turkington, D., Heap, M., Ledsham, L., & Jolley, E. adolescents. Journal of Abnormal Psychology, 118, 587–597.
(1999). Cognitive therapy versus dietary counselling in the Stice, E., Marti, C. N., Spoor, S., Presnell, K., & Shaw, H. (2008).
outpatient treatment of anorexia nervosa. European Eating Dissonance and healthy weight eating disorder prevention
Disorders Review, 7, 334–350. programs: Long-term effects from a randomized efficacy trial.
Serpell, L., Teasdale, J. D., Troop, N. A., & Treasure, J. (2004). The Journal of Consulting and Clinical Psychology, 76, 329–340.
development of the P-CAN, a measure to operationalise the pros Stice, E., & Shaw, H. (2004). Eating disorder prevention programs: A
and cons of anorexia nervosa. International Journal of Eating meta-analytic review. Psychological Bulletin, 130, 206–227.
Disorders, 36, 416–433. Stice, E., Shaw, H., Burton, E., & Wade, E. (2006). Dissonance and
Shafran, R., Cooper, Z., & Fairburn, C. (2002). Clinical perfectionism: healthy weight eating disorder prevention programs: A randomised
A cognitive-behavioural analysis. Behaviour Research and efficacy trial. Journal of Consulting and Clinical Psychology, 74,
Therapy, 40, 773–791. 263–275.
Shafran, R., Lee, M., Payne, E., & Fairburn, C. G. (2006). The Stice, E., Shaw, H., & Marti, C. N. (2007). A meta-analytic review
impact of manipulating personal standards on eating attitudes and of eating disorder prevention programs: Encouraging findings.
behaviour. Behaviour Research and Therapy, 44, 897–906. Annual Review of Clinical Psychology, 3, 207–231.
Sheehan, H. L., & Summers, V. K. (1948). The syndrome of Stice, E., Shaw, H., & Nemeroff, C. (1998). Dual pathway model
hypopituitarism. Quarterly Journal of Medicine, 18, 319–378. of bulimia nervosa: Longitudinal support for dietary restraint
Shelley, R. (1997). Anorexics on anorexia. London: Jessica Kingsley and affect-regulation mechanisms. Journal of Social and Clinical
Publishers. Psychology, 17, 129–149.
Simmonds, M. (1914). Ueber embolische prozesse in der hypophysis. Striegel-Moore, R., Cachelin, F., Dohm, F., Pike, K., Wilfley, D.,
Archives of Pathology and Anatomy, 217, 226–239. & Fairburn, C. (2001). Comparison of binge eating disorder and
Smith, M. A., Rissel, C. E., Richters, J., Grulich, A. E., & de bulimia nervosa in a community sample. International Journal of
Visser, R. O. (2003). Sex in Australia: Sexual identity, sexual Eating Disorders, 29, 157–165.
rie66620_ch09_235-280.indd 279 07/29/17 01:42 PM

Strober, M., Freeman, R., Lampert, C., Diamond, J., & Kaye, W. bulimia nervosa: First phase of a sequential design comparing
(2001). Males with anorexia nervosa: A controlled study of eating motivation enhancement therapy and cognitive behavioural
disorders in first degree relatives. International Journal of Eating therapy. Behaviour Research and Therapy, 37, 405–418.
Disorders, 29, 263–269. van Son, G. E., van Hoeken, D., Bartelds, A. I. M., van Furth, E.
Stunkard, A. J. (1993). A history of binge eating. In C. G. Fairburn & F., & Hoek, H. W. (2006). Time trends in the incidence of eating
G. T. Wilson (Eds.), Binge eating: Nature, assessment and disorders: A primary care study in the Netherlands. International
treatment (pp. 15–34). New York: Guilford Press. Journal of Eating Disorders, 39, 565–569.
Tan, J. O. A., Stewart, A., Fitzpatrick, R., & Hope, T. (2010). van Tiggelen, J. (2006, November 4). Two of us. Good Weekend, 18.
Attitudes of patients with anorexia nervosa to compulsory treatment Wade, T. D., Bulik, C. M., Heath, A. C., Martin, N. G., &
and coercion. International Journal of Law and Psychiatry, 33, Eaves, L. J. (2001). The influence of genetic and environmental
13–19. factors in estimations of current body size, desired body size, and
Taylor, C. B., Bryson, S., Luce, K. H., Cunning, D., Doyle, A. C., body dissatisfaction. Twin Research, 4, 260–265.
Abascal, L. B., Rockwell, R., . . . Wilfley, D. E. (2006). Prevention Wilfley, D. E., & Rieger, E. (2003). Further perspectives on
of eating disorders in at-risk college-age women. Archives of psychological interventions for eating disorders. In M. Maj,
General Psychiatry, 63, 881–888. K. Halmi, J. J. Lopez-Ibor, & N. Sartorius (Eds.), Eating disorders
Touyz, S. W., Beumont, P. J. V., Glaun, D., Phillips, T., & Cowie, I. (pp. 353–357). Sussex: Wiley.
(1984). A comparison of lenient and strict operant conditioning Wilfley, D. E., Welch, R. R., Stein, R. I., Spurrell, E. B., Cohen, L. R.,
programmes in refeeding patients with anorexia nervosa. British Saelens, B. E., . . . Matt, G. E. (2002). A randomised comparison
Journal of Psychiatry, 144, 517–520. of group cognitive-behavioural therapy and group interpersonal
Touyz, S., & Hay, P. (2015). Severe and enduring anorexia nervosa psychotherapy for the treatment of overweight individuals with
(SE-AN): In search of a new paradigm. Journal of Eating binge eating disorder. Archives of General Psychiatry, 59, 713–721.
Disorders, 3, 26. Wilfley, D. E., Wilson, G. T., & Agras, W. S. (2003). The clinical
Touyz, S., Le Grange, D., Lacey, H., & Hay, P. (2016). Managing significance of binge eating disorder. International Journal of
severe and enduring anorexia nervosa: A clinician’s guide. New Eating Disorders, 34 (Supp.), S96–S106.
York: Routledge. Woodside, D. B., Garfinkel, P. E., Lin, E., Goering, P., Kaplan, A. S.,
Touyz, S., Le Grange, D., Lacey, H., Hay, P., Smith, R., Maguire, Goldbloom, D. S., & Kennedy, S. H. (2001). Comparisons of men
S., . . . . Crosby, R. D. (2013). Treating severe and enduring with full or partial eating disorders, men without eating disorders,
anorexia nervosa: A randomized controlled trial. Psychological and women with eating disorders. American Journal of Psychiatry,
Medicine, 43, 2501–2511. 158, 570–574.
Treasure, J. L., Katzman, M., Schmidt, U., Troop, N., Todd, G., & Yanovski, S. (2003). Binge eating disorder and obesity in 2003.
de Silva, P. (1999). Engagement and outcome in the treatment of International Journal of Eating Disorders, 34 (Supp.), S117–S120.
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CHAPTER 10
Addictive disorders
Alex Blaszczynski
Robert Tait
CHAPTER OUTLINE
● Substance use disorders
● Gambling disorder
● Summary

10.1 Describe the diagnostic criteria, epidemiology, aetiology and treatment of substance use disorders.
10.2 Describe the diagnostic criteria, epidemiology, aetiology and treatment of gambling disorder.
ADDICTIVE BEHAVIOURS: AN AUSTRALASIAN FOCUS

A decline in the availability of heroin in Australia at the turn of the twenty-first century marked the start of a transition
towards the increased use of synthetic drugs, especially methamphetamine. Australia is adjacent to the world’s largest
manufacturing hubs, East and South-East Asia, with the quantity of methamphetamine seized quadrupling between 2008
and 2013 (United Nations Office on Drugs and Crime, 2015).
Over recent years there has been a dramatic increase in the number of people in Australia who use methamphetamine
regularly and who are dependent on it (Degenhardt et al., 2016). This has been driven in particular by the availability of
a more potent form of the drug (crystal methamphetamine), which can be smoked. In this form, users can experience a
much stronger effect, without the stigma of engaging in injecting drug use.
In response to growing public concerns about the health, social and economic impacts of methamphetamine, the
Australian government established a national task force to investigate and report on the issue (Commonwealth of
Australia Department of the Prime Minister and Cabinet, 2015). The task force’s recommendations included that an extra
$240 million be allocated to treatment. Currently, access to effective and affordable treatment is difficult, and is even
more challenging for those living in rural areas. As such, the rapid spread of the drug into rural and remote areas of
Australia is of particular concern (Roche & McEntee, in press).
Unfortunately, the shortage of treatment and the long waiting lists have resulted in desperate families turning to
private clinics to help their loved ones access help. These private clinics are typically expensive and may involve
unproven treatments with little prospect of successful outcomes. This problem was highlighted in a program on ABC’s
Four Corners entitled ‘Rehab Inc: The high price parents pay to get their kids off ice’ (Knight, Hichens, & Worthington,
2016). The program highlighted that, ‘Across Australia, there are parents risking everything to rescue their children
from ice addiction . . . Parents are risking bankruptcy to get their child a place. They’re encouraged to access their
superannuation or to re-mortgage their homes in order to pay out tens of thousands of dollars to ensure their child gets
in quickly. And the price is driven by demand, rather than the service provided.’ The program also highlighted a lack of
regulation over private clinics such that, as one addiction specialist noted, ‘I could start a rehab up tomorrow and hire
staff who aren’t suitably qualified and call it a rehab, and charge top dollar. With no questions asked.’
continued
Rieger, E. (2017). Abnormal psychology : Leading researcher perspectives. McGraw-Hill Education (Australia) Pty Limited.
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In addition to the difficulties experienced by those with a

methamphetamine use disorder and their family members,
media and public health campaigns have focused on the issue
KAESLER MEDIA / SHUTTERSTOCK.COM

of methamphetamine psychosis and the danger of attacks
on front-line health and police workers as they attempt to
assist highly agitated individuals. Without minimising the
significant harm to others stemming from methamphetamine
use, it is important to put these incidents into perspective
relative to the problems stemming from alcohol use. For
example, about one-third of hospital Emergency Department
presentations are alcohol-related and more than 90 per
cent of Emergency Department doctors and nurses have
reported violence or threats related to alcohol (Australian
Medical Association, 2016). In Australia, the number of people who use
This chapter on addictive disorders is divided into two methamphetamine regularly has increased
sections: the first is on psychoactive substance use and significantly.
associated disorders and the second section is on gambling
disorder. In each of these there is a description of the
criteria for diagnosing the disorders, plus information regarding the prevalence, age of onset, course and problems
associated with these conditions. There is also a discussion of the current understanding and approaches to aetiology
and treatment, within a biopsychosocial framework.
LO 10.1 Substance use disorders

The diagnosis of substance use disorders
The current version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American
Psychiatric Association [APA], 2013) includes a chapter entitled ‘Substance-related and Addictive
Disorders’, addressing problems stemming from the use of substances and engaging in gambling. The
substance-related disorders comprise two groups: substance use disorders (which are the main focus of
this section) and substance-induced disorders (which include specific mental health problems induced
as a result of substance use, such as stimulant-induced psychosis and alcohol-induced depression).
Substance use disorders are classified on a continuum from mild to severe. A ‘mild’ disorder requires
the endorsement of two or three of the eleven criteria for a substance use disorder; four or five criteria
indicate a ‘moderate’ disorder and six or more a ‘severe’ disorder. The listed substances or classes of
substance are alcohol, cannabis, hallucinogens, inhalants, opioids, sedatives (hypnotics or anxiolytics),
stimulants, tobacco and other (or unknown) substances. Caffeine use can result in intoxication and
subsequent withdrawal symptoms but is not classified as a substance use disorder.
From a historical perspective, addiction to alcohol and opium has been recognised for centuries,
but it was not until the 1970s that the formal characteristics of alcohol dependence were specified.
At this time, Edwards and Gross (1976) provided a description of an alcohol dependence syndrome
consisting of behaviours such as priority given to drinking over other activities, a subjective awareness
of a compulsion to drink, increased tolerance of the effects of the alcohol, repeated alcohol withdrawal
symptoms, consuming alcohol to avoid withdrawal symptoms and a rapid reinstatement of dependence
even after a period of abstinence. Subsequently, the same ‘dependence syndrome’ has been applied
to all substances capable of inducing physiological dependence (defined as tolerance and withdrawal)
and/or psychological dependence. While the earlier descriptions of alcohol dependence referred to
‘alcoholism’, this term is no longer used in the classification systems (APA, 2013; World Health
Organization, 1993).
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Chapter 10 Addictive disorders 283
The approach of Edwards and Gross (1976) influenced the subsequent editions of the DSM,
including the current diagnostic criteria for substance use disorder (APA, 2013). These criteria
represent a complex cluster of cognitive/psychological, behavioural and physiological symptoms. An
individual must have at least two of the following symptoms within a 12-month period, which have
resulted in clinically significant distress or impairment, to be diagnosed with a substance use disorder:
1. Larger amounts of the substance are consumed than the individual intended.
2. There is a persistent desire, or unsuccessful attempts, to reduce substance use.
3. A large amount of time is spent obtaining, using or recovering from the effects of the substance.
4. Strong desires or craving to use the substance are present.
5. The individual experiences a failure to fulfil major role expectations (e.g., at home, work or
school) due to recurrent substance use.
6. There is continued substance use even though it results in social or interpersonal difficulties.
7. Substance use interferes with the individual’s ability to engage in social or occupational activities,
so that these activities are reduced or cease entirely.
8. Substance use occurs in situations where it is physically hazardous (e.g., while driving a car).
9. There is continued use of the substance even though the individual is aware of problems caused
by the substance.
10. Tolerance is present, as evident by either:
(i) a need for increased amounts of the substance in order to achieve the same effect
(ii) a markedly diminished effect for the same amount of the substance.
11. Withdrawal is present, as evident by either:
(i) a range of characteristic physical and psychological symptoms that emerge after a cessation
or reduction in substance use
(ii) taking the substance (or a closely related substance) in order to alleviate these symptoms.
CASE STUDY: SEVERE ALCOHOL USE DISORDER

The criteria for severe substance (alcohol) use disorder are evident in the case of Steve, a 65-year-old man who has
been using alcohol heavily since he retired three years ago. His parents (especially his father) drank heavily and alcohol
was a part of family interactions as he grew up. He had always been a regular moderate drinker who enjoyed a couple
of beers every night, drinking more heavily at weekends and occasionally he could not remember events from the night
before. He had also been convicted of ‘drink driving’ twice. Since retiring, his drinking had increased. He had become
noticeably more argumentative with his wife, and it was she who persuaded him to get help for his drinking. During an
assessment with a clinical psychologist, Steve reported:
All my life I’ve enjoyed a drink, especially to help me unwind at the end of the day and to have a good time with
mates. After the second drink driving case when I was 55, I did manage to cut back, but since I’ve retired, there
doesn’t seem much point in cutting back—I mainly drink at home so there’s less risk of losing my licence. There’s
nothing to do at home so I end up drinking from lunchtime onwards, although sometimes I need a few drinks just
to get me through the morning, which I never used to do. Most days I just sit in front of the TV drinking until I fall
asleep—a few months ago I even set fire to the sofa when I fell asleep after drinking and my cigarette fell out of the
ashtray. Without the actions of my wife it would have been a disaster. My doctor told me that I have to stop drinking
because of my diabetes. I tried to stop but can’t seem to stay away from drinking for more than a few days. I just
feel terrible when I try, like I’ve got the flu or something.
The interview revealed that Steve had the hallmarks of a long-term condition that for many sufferers will be lifelong,
especially in the absence of treatment. His alcohol use was characterised by a range of substance use symptoms
such as withdrawal, compulsion to drink, preoccupation with alcohol, large amounts of time involved with alcohol,
continued drinking despite its negative consequences and a desire to stop drinking alcohol but with great difficulty in
maintaining abstinence. Although Steve fulfils the criteria for an alcohol use disorder, he was far from the stereotyped
continued
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‘drunk-on-the-park-bench’, being a well-presented and accomplished man. Steve’s case reveals that, although
substance use disorders are conditions of the young (typically starting in the late teens and early 20s), individuals
rarely present for treatment until the effects of long-term heavy drinking are apparent.
The International Statistical Classification of Diseases and Related Health Problems (World
Health Organization, 1992), currently in its tenth edition (ICD-10), also lists disorders caused by
psychoactive substances. The ICD-10 distinguishes between two conditions: harmful use and, more
severely, substance dependence. ‘Harmful use’ refers to a pattern of psychoactive substance use that is
resulting in clear physical or psychological harm, and which may lead to disability or adverse outcomes
for relationships. ‘Substance dependence’ is defined as three or more of the following together over
the previous month or repeatedly over the previous twelve months:
1. a strong desire or compulsion to use the substance
2. impaired control over use of the substance
3. physiological withdrawal symptoms
4. evidence of tolerance
5. preoccupation with substance use
6. persistent use despite clear evidence of harm.
WITHDRAWAL
One of the criteria for substance use disorders is withdrawal, which refers to the development of a set
of symptoms that occur upon cessation of using the substance, especially after heavy or prolonged
use of the substance. Most substances (e.g., alcohol, opioids or sedatives) have a characteristic set of
withdrawal symptoms, but for others, such as cannabis and tobacco, withdrawal may be less clear-cut,
and withdrawal is generally not found with the hallucinogens (APA, 2013).
When alcohol withdrawal occurs, which is the only substance withdrawal state that can be life-
threatening, there is usually evidence of two or more of the following within 12–24 hours of ceasing
drinking: autonomic hyperactivity (e.g., heart racing and sweating); nausea or vomiting; shakiness,
especially increased hand tremor; insomnia; psychomotor agitation (e.g., restlessness in the form of
pacing); increased levels of anxiety; hallucinations (often visual, but can also be auditory or tactile);
and grand mal seizures. The risk of death from alcohol withdrawal is significant for severe withdrawal
states. While relatively rare, and while most withdrawal from alcohol is mild in severity, severe
withdrawal should be considered in individuals with a history of very heavy continuous drinking
followed by an abrupt cessation in use. Given the prevalence of alcohol dependence in hospital trauma
cases (e.g., patients who have been involved in a vehicle accident), it has been recommended that all
such patients should be assessed for alcohol use and potential withdrawal symptoms (Awissi, Lebrun,
Coursin, Riker, & Skrobik, 2013).
For the opioids such as heroin, methadone or morphine there is a characteristic withdrawal
syndrome commencing soon after cessation of the opioid, typified by nausea and vomiting, diarrhoea,
running nose and eyes, yawning and insomnia, muscle aches, piloerection (‘gooseflesh’) and negative
mood (Frei et al., 2012). Acute symptoms can last 5–10 days, although drugs with a longer half-
life than heroin, such as methadone, will have a slower onset and longer persistence of withdrawal
symptoms. Avoidance of the withdrawal syndrome is an important reason for continued use of opioids,
although opioid withdrawal is not life-threatening.
In the case of stimulant dependence (e.g., cocaine and amphetamine-type stimulants), withdrawal
syndrome can include the development of fatigue (‘the crash’), vivid and unpleasant dreams, sleep
disturbances, increased appetite and psychomotor agitation or retardation. While cannabis use was
initially thought not to have significant withdrawal symptoms, more recent research shows withdrawal
syndrome consisting of craving for cannabis, depressed mood, irritability, restlessness, sleep difficulty,
increased anger and aggression, decreased appetite, nervousness/anxiety and headache (Budney &
Hughes, 2006; Frei et al., 2012).
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CASE STUDY: CANNABIS WITHDRAWAL

The experience of cannabis withdrawal symptoms is clear in
the case of Anna, a 22-year-old Māori woman who started
using cannabis at the age of 12. Initially Anna’s cannabis use
was mainly on the weekend with friends. Although Anna was
never a high achiever academically, she began to fail subjects,
which had not happened before. Her truancy became so
common that her school expelled her at the end of Year 11. By
SHUTTERSTOCK.COM
the time she turned 18 she was smoking cannabis throughout
the day. Eventually her mother threw her out and Anna moved
in with her boyfriend and worked in various unskilled jobs. She
did not really enjoy the jobs she had after leaving school but
was unable to find more interesting work since she had not
completed any education after being expelled from school.
After the birth of her son, the Ministry of Social Development Cannabis can be cultivated indoors with artificial
became involved and organised a referral to a local Māori lighting and controlled conditions in order to
mental health service to assess both her cannabis use and increase productivity.
mental health: Anna was worried that she might lose her son if
she did not attend. At her assessment interview with a clinical
psychologist she described her use of cannabis in the following way:
I just can’t handle not being stoned. I don’t feel right when I’m not stoned. The times I’ve tried to stop, I’ve felt like
crap. I’d get really sick in the guts and would get the chills—it felt like I had the flu. I also had the shakes and couldn’t
keep still; I was really restless, agitated and uncomfortable all the time, and felt pretty panicky. The worst of it was
that I couldn’t sleep, which was horrible, because all I could do was lie awake and think about how much I wanted a
smoke. I’d snap at my boyfriend even more than usual: everything he’d do would irritate me. After a couple of days
I couldn’t handle it anymore—I had to smoke. For the last four years I’ve probably been smoking between 15 and
20 cones a day. During the times I’ve been out of work I’d probably smoke even more. I find it really hard to believe
that I used to get stoned after only one or two cones shared with a friend. It’s really hard to get myself motivated to
look for a job because I know that I would have to be straight to go for the interview. I really want to give up the stuff,
or at least cut down, so that I can feel like I have a life: at the moment my life is ruled by pot and I hate it. Giving it up
now for the baby is the first time I’ve felt I really have a chance of doing it. My Mum’s really worried that smoking when
I was pregnant would harm the baby; also she thinks that I’ll get schizophrenia because of the stuff she hears about
cannabis making you crazy. My uncle has schizophrenia and she’s always saying that I’ll end up like that.
Anna’s story shows how distressing the cannabis withdrawal syndrome can be. In addition to withdrawal, Anna reported
other symptoms of cannabis use disorder: she has experienced tolerance; she has found it hard to cut down or stop even
though she wants to; she spends most of her time using cannabis or finding ways to obtain cannabis; her educational
and occupational performance has suffered; and her relationships are breaking down. Without effective intervention,
Anna would most likely continue to find it difficult to stop using cannabis and suffer further problems with work and
relationships. Additionally, she runs the risk of suffering from respiratory problems and cognitive dysfunction. The fact
that she has a family member with schizophrenia indicates that Anna may be predisposed to suffer from a psychotic
disorder. As there is now evidence to suggest that cannabis may trigger a psychotic disorder in those who are vulnerable,
this could be a major negative outcome if Anna continues her use of cannabis (Semple, 2005).
The epidemiology of substance use disorders

PREVALENCE
The prevalence of substance use disorders among Australian adults was reported in the second National
Survey of Mental Health and Wellbeing, which assessed the number of people affected by a range
of mental disorders in a 12-month period, including substance use and substance-related problems
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(Slade et al., 2009). These data are presented in Table 10.1. The study utilised the International
Classification of Diseases (ICD-10) categories of ‘harmful use’ and ‘substance dependence’ (World
Health Organization, 1993).
TABLE 10.1 The twelve-month prevalence (%) of substance use a and the diagnoses of ICD-10 ‘harmful
use’ and ‘dependence’ for different substances in Australia and prevalence of use in New Zealand
AUSTRALIA: NON- AUSTRALIA: NEW ZEALAND: NEW ZEALAND:

INDIGENOUS (%) INDIGENOUS (%) NON-MĀORI (%) MĀORI (%)
Alcohol usea 78.0 72.1 79.5d 82.3

Harmful use 2.9
Dependence 1.4 2.4 4.9
Cannabis use 10.0 19.0 15.1 26.4

Harmful use 0.6
Dependence 0.4
Stimulants use 2.0b 3.1c 2.3 3.2

Harmful use 0.4
Dependence 0.3
Cocaine use 2.2 1.9c 0.6 1.0

b e f
Sedatives use 1.5 NR 1.6 1.9f
Harmful use 0.04
Dependence 0.1
Opioids use 0.1b NR 1.1 1.8

Harmful use 0.1
Dependence 0.1
Any illicit use 0.1b 24.1 17.0 28.0

Harmful use 0.1

Dependence 0.1 1.4 3.0
Any substance 5.1 NR 3.0 6.0

use disorder
a
‘Use’ = at least a full serve of alcohol and any use for all other drugs over the previous twelve-month period for people aged 14 years
or older; bOpioid use limited to heroin use; stimulant use limited to meth/amphetamine; sedative use limited to tranquilliser and sleeping
pills not for medical purposes; cEstimate has a relative standard error of 25–50% and should be used with caution; dIncludes all ethnicities;
e
‘NR’ = not reported; fIncludes kava (a narcotic sedative drink made in Polynesia)
Source Australian use: Adapted from Australian Institute of Health and Welfare (2014).
Source for disorders: Slade et al. (2009) – reported for the whole population.
Source New Zealand use: Ministry of Health (2015); Ministry of Health (2010).
Source for New Zealand disorders: Wells, Baxter, & Schaaf (2007) – reported as any disorder (harmful or dependence).
As can be seen from Table 10.1, alcohol is the most commonly used drug in both Australia and
New Zealand, with the ICD-10 categories of ‘harmful use’ and ‘dependence’ occurring in almost 1 in
20 people, mainly men. The diagnoses of opioid, cannabis and stimulant disorders are less prevalent.
While stimulant and opioid dependence are less prevalent than cannabis dependence, the serious
harms associated with the dependent use of these two classes of drugs (especially amphetamine-
related paranoid psychotic states and opioid-related deaths) make them important from a public health
perspective. Overall, the prevalence of any substance use disorder appears higher in Australia than in
New Zealand, although care should be taken in this interpretation due to different survey methods and
population demographics.
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Obviously, not everyone who uses a substance even regularly will develop a substance use disorder.
However, a substantial proportion of those who use heroin will develop a severe disorder, and alcohol and
cannabis use disorders are frequent in the Australian population. Amphetamine (stimulant) use disorder
is increasing in incidence as it becomes more widely used, more potent and is increasingly injected.
The use of alcohol and other drugs is a significant concern across Australian Indigenous
communities. Although the data in Table 10.1 suggest that alcohol use is more common in non-
Indigenous than Indigenous Australians, this is because more Indigenous Australians abstain from
alcohol use due to having had previous problems with alcohol. It is estimated that the prevalence of
harmful alcohol use among Indigenous Australians is twice that of non-Indigenous Australians, with
a similar pattern found for other drugs, including tobacco, cannabis, methamphetamine and inhalants
(Wilson, Stearne, Gray, & Saggers, 2010).
OCEANIA AND EAST AND SOUTH-EAST ASIA

Since the mid-2000s there has been a marked increase in the manufacture and use of synthetic Synthetic drugs
drugs or drugs that can be manufactured without plant-based materials, such as amphetamine-type Also known as
stimulants and novel psychoactive substances (United Nations Office on Drugs and Crime, 2015). new psychoactive
Novel psychoactive substances are typically designed to mimic existing controlled substances and substances,
use manmade
are thought to pose a public health threat, with side effects including psychosis, stroke and death
chemicals to
(Tait, Caldicott, Mountain, Hill, & Lenton, 2016). The Oceania and East and South-East Asia regions mimic the effects
now account for more than one-third of global seizures in amphetamine-type stimulants, with about of traditional
9.5 million users in these areas. Crystal methamphetamine was ranked by experts as the leading drug drugs such as
of concern in Brunei Darussalam, Cambodia, Indonesia, Japan, Malaysia, the Philippines and the cannabis or
Republic of Korea, and the second drug of concern in China, Singapore and Vietnam (United Nations cocaine.
Office of Drugs and Crime, 2015). In many countries, methamphetamine users constitute the large
majority of those in treatment (e.g., Laos 98%, Republic of Korea 96%, and Cambodia 94%) (United
Nations Office of Drugs and Crime, 2015). Nevertheless, it is still important to remember the extent
of disease caused by tobacco. While tobacco control measures have greatly reduced the prevalence of
smoking in some countries such as Australia, in Asia the tobacco epidemic is still in its early stages,
with the number of deaths expected to rise for many years. Currently, across Asia, 15.8 per cent of
deaths in men and 3.3 per cent in women are tobacco-related (Zheng et al., 2014).
CASE STUDY ACUTE INTOXICATION: SYNTHETIC CANNABINOIDS

Amelia, a 15-year-old girl, was brought into a hospital emergency department by friends. On arrival, she was agitated,
vomiting and distressed. Her heart rate (132 beats per minute) and blood pressure (160/100) were elevated. She reported
extreme anxiety and agitation, with chest pain and some visual disturbance. After a period of observation and symptom
management (including the use of a benzodiazepine to reduce her anxiety) she was stable enough to talk to the hospital
drug and alcohol worker.
Amelia reported that she had a good relationship with her parents and her older brother, and that she generally
enjoyed school and achieved good grades. Neither she nor her immediate family had any history of mental health
conditions. She drank alcohol occasionally (about once per month) and reported that she had not used any illicit drugs.
Amelia said that her boyfriend had bought a ‘legal’ herbal blend on the internet called ‘black diamond’, which they had
smoked together at a party earlier that evening. Within an hour she felt nauseous and vomited several times. When she
came back from the bathroom she was unable to find him and became increasingly anxious. She had difficulty breathing,
and felt as though someone was sitting on her chest. She went outside to get some air and became increasingly
disoriented and panicky. When her friends found her, she was walking up and down the road crying and shouting for her
boyfriend.
The following morning she was discharged from hospital, without any persisting symptoms. Due to the changing
composition and concentration of the chemicals in novel psychoactive substances, such as synthetic cannabinoids, it is
difficult to predict the effects they will have. Even when a patient provides a sample of the drug, treatment is generally
limited to observation and management of acute symptoms as they arise (Tait, Caldicott, Mountain, Hill, & Lenton, 2016).
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AGE OF ONSET AND COURSE

Substance use and its disorders predominantly occur in the young, with a decrease in the prevalence
of these with age. One of the reasons that substance use and substance use disorders predominate
in the young relates to birth cohort effects, in that younger generations have been exposed to the
easier availability of alcohol and drugs compared to older generations. This change has important
implications, with earlier first use associated with increased probability of substance use disorder in
later life, although this relationship may be due to early conduct disorder rather than the substance use
per se (Rossow & Kuntsche, 2013). However, data suggest that this trend may be beginning to reverse,
with the age at which people first start using a substance increasing, at least for some drugs. As shown
in Figure 10.1, in Australia the age of first use has significantly increased since 2010 for tobacco,
alcohol, cannabis and amphetamine-type stimulants (ATS). Yet in the same period, the age of first use
of heroin has decreased.
20.0
Tobacco
18.0
Alcohol
Age (years)
Cannabis
16.0
ATS
Heroin
14.0
Injected
12.0
1998 2001 2004 2007 2010 2013
Year
FIGURE 10.1 Average age of first use of selected drugs among those aged 14–24 years
Note: Significant changes occur between 2010 and 2013 for tobacco, alcohol, cannabis, ATS and heroin
Source: Adapted from Australian Institute of Health and Welfare (2014). 2013 National Drug Strategy Household Survey. Drug Statistics
Series no. 25 (cat. No. PHE 183), Canberra.
CASE STUDY: STIMULANT-INDUCED PSYCHOTIC DISORDER

Phil is a 28-year-old gay man who has been using methamphetamine for a decade. He first tried methamphetamine in
the form of methamphetamine powder (‘speed’) when he was 18 years old. He snorted lines of speed before going out to
clubs with his university friends. Once at the club, they would usually take ‘ecstasy’ (3,4-Methylenedioxymethamphetamine
or MDMA) or ‘poppers’ (alkyl nitrites). This quickly became something they did on a weekly basis. Occasionally, Phil
would stay out all weekend without sleep. He would quite often become depressed after a big weekend, but this would
usually pass. He frequently used benzodiazepines to ‘come down’ (i.e., to calm down and relax following a period of
using stimulants). Overall, during his university degree, he was able to maintain his marks and functioned reasonably
well despite his weekly methamphetamine, ecstasy and benzodiazepine use. After he finished his degree, he obtained
a position in a large insurance company. At the age of 24, he and his friends tried crystal methamphetamine (‘crystal’,
‘tina’ or ‘ice’) for the first time. Crystal is a potent form of methamphetamine that is usually smoked or injected. Smoking
crystal and partying became a regular activity for Phil. Once he had started to use he found it difficult to stop until all the
crystal had gone. He also required treatment for sexually transmitted infections on three occasions after having unsafe
sex while partying. When he was not intoxicated with methamphetamine his depression was impairing his functioning.
His work performance began to deteriorate considerably: his binges on crystal would necessitate days of recovery,
during which he would be unable to go to work. This resulted in him stopping work at the age of 26. The next two years
were spent using crystal methamphetamine for days at a time, followed by short periods of abstinence. He began to
notice that while he was intoxicated with methamphetamine he would become suspicious of others’ intentions and
started to think that people were conspiring against him. During his most recent binge, Phil became convinced that his
flatmate was spying on him and giving information to the police about his drug use. He became extremely agitated and
fled the flat. The police were called when he became aggressive with passers-by and was screaming at cars. He was
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hospitalised and referred for drug treatment. This is an excerpt from one of the interviews with the drug and alcohol
counsellor at the hospital:
I was so paranoid that everyone was out to get me and I would keep catching a glimpse of something out of the corner
of my eye but it was gone as soon as I turned to look at it. I was sure that my flatmate was spying on me and that he
was trying to get me arrested, he even had secret methods of communicating with the local police station. Every time he
talked on the phone I would think he was on the phone to the cops. I got so panicked that I decided to run for it. Once
I was out on the street, my paranoia spread to everything around me. Everyone I saw I thought was an undercover
cop and that all the cars were following me. I was out of control—nothing could convince me that I had it wrong. The
police eventually had to restrain me to get me into the ambulance. I was locked up in a special room in emergency and
sedated.
Crystal has taken over my life. I can’t think about anything else. I guess I don’t have much else in my life now—
no job and my family is sick of me asking for money and not turning up to events. I don’t keep in touch with my uni
friends anymore—they all see me as a junkie since they found out I had injected crystal. I don’t feel close to the
people I hang around with now though—they’re just drug-taking friends and they are all messed up like me anyway. I
would love to get my life back but the thought of never being able to have crystal again fills me with anxiety. Coming
down from the binges is so hard—I just feel so tired and swing between feeling angry and agitated to being really
depressed. I also see visions and things that aren’t there when I’m trying to sleep, which really freaks me out. I don’t
even really enjoy the effects of crystal anymore—the amazing rush I used to experience when I first started smoking
crystal just doesn’t happen these days. I just have to use it now to take away the bad feelings. I don’t even go out
partying anymore—I just sit around my house with my flatmate mostly.
Phil’s story shows clearly the adverse mental health effects that can occur with heavy methamphetamine use. Psychosis
is 11 times more common among regular methamphetamine users than in the general population in Australia (McKetin,
McLaren, Lubman, & Hides, 2006). Hospital data show that there has been an increase in methamphetamine-induced
psychosis admissions since 2000 that has been linked to the rise in the use of crystal methamphetamine over the same
period (Degenhardt, Roxburgh, & McKetin, 2007). These episodes of psychosis usually subside once methamphetamine
use is ceased. Phil also seems to suffer from depression, which is common among regular methamphetamine users,
with an Australian study finding that 40 per cent of treatment seekers had major depression, with a further 44 per cent
having substance-induced depression (McKetin, Lubman, Lee, Ross, & Slade, 2011).
His description of wanting to stop, but not being able to, is one of the criteria of substance use disorder. There
is also evidence for tolerance (when he states that he no longer gets the euphoric rush immediately following
methamphetamine that he used to) and withdrawal. His occupational performance has obviously suffered, although it
is difficult to determine what the major factor for leaving his job was—his depression, methamphetamine use or, most
likely, a combination of these. It is unlikely that Phil would go back to using the less potent forms of methamphetamine,
with the various forms of methamphetamine described in Table 10.2.
TABLE 10.2 The various forms of methamphetamine
IMAGE DESCRIPTION
Methamphetamine powder—‘speed’
This is the lowest-purity form of methamphetamine available
since it is the easiest form to cut (or mix) with adulterants.
Speed has been found to have a median purity of 10% and
is usually white or off-white, but can be yellow or brown.
SHUTTERSTOCK.COM
continued
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TABLE 10.2 (continued)
IMAGE DESCRIPTION
Damp/oily methamphetamine—‘base’
The form of methamphetamine known as base is a more
AAP IMAGE/POLICE HANDOUT
potent form of methamphetamine than speed. The major

difference between base and speed seems to be that
base has not been cut with as many adulterants as powder
methamphetamine. Base has been found to have a median
purity of 21% and is usually brown or yellow.
Crystal methamphetamine—‘crystal’
Crystal methamphetamine, known as ‘crystal’, ‘crystal meth’,
‘tina’ or ‘ice’, has the appearance of clear crystals and is
the purest form of methamphetamine. The median purity
SHUTTERSTOCK.COM
of crystal with a translucent or white appearance has been

found to be around 80%. However, there is also a lower-
purity methamphetamine on the market that has a crystalline
appearance and has a median forensic purity of 19% since it
has been cut with adulterants.
Source: Adapted from McKetin, R., Quinn, C., Groves, G., McLaren, J., & Kelly, E. (2005). Methamphetamine: Physical forms, purity and terminology. In R. McKetin, J.
McLaren, & E. Kelly (Eds.), The Sydney methamphetamine market: Patterns of supply, use, personal harms and social consequences. NDLERF Monograph Series
No. 13 (pp. 16–24). Marsden: National Drug Law Enforcement Research Fund.
ASSOCIATED PSYCHOLOGICAL PROBLEMS

Comorbidity of substance use disorders and other mental disorders is one of the major challenges of
treating substance use disorders. In Australia, approximately 35 per cent of those with a substance
use disorder in the previous 12 months also had another mental disorder (Mills, Teesson, Ross, &
Peters, 2009). Those with comorbid conditions typically have worse outcomes than those with single
disorders on a range of measures including physical health, social and occupational functioning, self-
harm or suicide, violence, homelessness and relationship problems (Mills et al., 2009). They are also
likely to have more severe mental health problems and more extensive substance use than those with
single conditions (Mills et al., 2009).
In terms of self-harm and suicide, people who use alcohol or other drugs or who have a substance
use disorder have increased risk of engaging in self-harm behaviours, such as cutting or burning
themselves or committing suicide. For example, opioid users are six times more likely to self-
harm and those with an opioid use disorder are 14 times more likely to commit suicide (Martin,
Swannell, Hazell, Harrison, & Taylor, 2010; Wilcox, Conner, & Caine, 2004). Substance use can be
a precipitating factor in suicide attempts, with 30–40 per cent of suicide attempts involving the acute
use of alcohol, perhaps as a result of the disinhibiting effects of alcohol (Hawton & Harriss, 2007).
There are a number of explanations for the fact that substance use disorders have a high frequency
of comorbidity with other psychological disorders. It may be that individuals become dependent
on a substance because they are attempting to escape negative feelings associated with their mental
health problem (i.e., they are using substances as a form of self-medication). Alternatively, the use of
substances may play a causal role in other mental health problems (e.g., depression may develop as
a result of relationship problems or occupational losses stemming from the substance use disorder).
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Finally, there may be a third factor (such as childhood abuse) that causes both the substance use
disorder and other psychological problems (Stone, Becker, Huber, & Catalano, 2012).
ASSOCIATED MEDICAL PROBLEMS

In addition to comorbid psychological problems, substance use disorders are associated with elevated
rates of physical problems and mortality. Older individuals face particular risks associated with their
substance use. Australia, like most developed economies, has an ageing population and this older cohort
differs markedly from previous generations in terms of their disposable income and their greater use
of alcohol and illicit drugs. This has potentially important implications given the risks associated with
alcohol use in older adults. Specifically, age-related changes in body composition mean that the body
typically contains a lower percentage of water, resulting in higher blood alcohol concentrations for a
given amount of alcohol. In addition, older adults typically use more prescription and over-the-counter
medications, which increases the potential for adverse interactions with alcohol. Overall, the age-related
changes in body composition and greater use of medications mean that with increasing age, people are
more susceptible to the intoxicating effects of alcohol and hence increased mortality from falls, motor
vehicle accidents and suicide (Sorock, Chen, Gonzalgo, & Baker, 2006). The misuse of prescription
medications (e.g. benzodiazepines, opioid pain medication) and, hence, the development of associated
substance use disorders are also likely to increase in elderly people. Given that drugs are metabolised
more slowly in elderly people, these individuals will be more vulnerable to their intoxicating effects,
which will exacerbate age-related declines in reaction time and physical functioning, in turn increasing
the likelihood of falls and accidents (Colliver, Compton, Gfroerer, & Condon, 2006).
One reason that the prevalence of substance use disorders declines with age is due to the fact that
mortality from excessive use of substances reduces the number of people with these disorders who
reach older age. Data from the United Kingdom show that those with a substance use disorder have a
life expectancy of about 14 years less than the general population (Chang et al., 2011). For example,
heavy alcohol use in the early 20s has been associated with death from accidents, violence and suicide.
Later life may bring premature death to heavy drinkers from the medical complications of excessive
alcohol consumption, such as liver cirrhosis and certain cancers. Lower life expectancy is also evident
in the context of other drug use disorders, especially where there is injecting drug use (particularly
opioids). Heroin-related deaths in Australia have declined from a peak of 1116 in 1999 to 374 in 2005
(Roxburgh, Ritter, Grech, Slade, & Burns, 2011), but remain a leading cause of death in young people.
Death from trauma, suicide and overdose, and infectious diseases such as HIV and hepatitis-related
complications, are too-frequent consequences of illicit drug use (Darke, Degenhardt, & Mattick, 2007).
Substance use also results in long-term effects that can be quantified as ‘disability adjusted life
years’ (DALYs), defined as the amount of time lost due to both fatal and non-fatal events, that is,
years of life lost due to premature death coupled with years of healthy life lost due to disability (Begg
et al., 2007). In Australia, alcohol accounts for 3.2 per cent of the total DALYs (61 091 DALYs),
illicit drugs 2.0 per cent (51 463 DALYs) and tobacco use 7.8 per cent (204 788 DALYs) (Begg
et al., 2007). Australian data show that in 2003 an estimated 15 000 Australians died from smoking.
The consumption of alcohol accounted for an estimated 1100 deaths. Illicit drug use (i.e., the use of
illegal drugs as well as the misuse of legal substances such as prescription medications) contributed a
further 1700 deaths (AIHW, 2011).
The adverse medical outcomes of substance misuse extend beyond the individual, with a 2010
report detailing that almost three-quarters of Australian adults had been affected in some way by the
drinking of others during the previous year (Laslett et al., 2010). Sixteen per cent had been adversely
affected by the drinking of a family member or partner, more than 10 per cent by the drinking of a
friend and 5 per cent by the drinking of a colleague. More than two-thirds of Australians reported
that the drinking of strangers had an impact on them, with 43 per cent reporting serious forms of
harm such as being threatened, physically assaulted or having their property damaged. Overall, it was
estimated that 367 people died and approximately 14 000 people were hospitalised as a result of the
drinking of others, for example, as victims of alcohol-related interpersonal violence or others driving
while under the influence of alcohol.
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The aetiology of substance use disorders

There are a variety of different theories that attempt to explain the causes of substance use disorders,
ranging from general theories to quite specific models of addiction to a particular substance. These
theories explain the development of substance use disorders in terms of biological, psychological or
social factors, or a combination of these.
IMPAIRED CONTROL VERSUS CHOICE THEORIES

Before considering specific biological, psychological and social theories, it is important to note the
existence of a longstanding debate regarding the degree to which substance use disorders entail a loss
of control versus choice. A loss of control is one of the central characteristics underpinning substance
use disorders. It is posited that individuals with a substance use disorder cannot cut down or stop
their drug use, despite the fact that it is causing them (or others they care about) harm. Inability to
control one’s substance use is reflected in a number of the DSM-5 criteria for substance use disorder.
Consistent with the notion of loss of control is one of the oldest theories of addiction, namely the
disease model of disease model of addiction. This model describes addiction as a medical disorder characterised by
addiction some form of brain impairment (Leshner, 1997). Those with a substance use disorder will experience
View that cravings for the drug that are so strong they cannot be ignored and the individual will do anything to
alcoholism obtain the substance. Thus loss of control is central to this theory (West, 2013).
(or another
In contrast to theories based on a loss of control, other theorists believe that the maladaptive use of
behavioural
addiction) is substances reflects a rational choice made by the individual at the time. That is, the individual weighs
an incurable up the costs and benefits of using the substance and decides that substance use is the favourable
physical disease, option. For example, Skog’s (2000) choice theory explains the apparent loss of control seen in those
like epilepsy or with a substance use disorder as a consequence of individuals changing their minds: at one time they
diabetes, such may be motivated to choose to abstain from drug use, but at another time the motivation to use drugs
that only total dominates. Skog (2000) argues that changing one’s mind does not suggest that one has lost control.
abstinence can
control it. BIOLOGICAL FACTORS
Substance use disorders tend to cluster in families. For example, it has been found that the first-
degree relatives of individuals with a substance use disorder are more likely to suffer from such a
disorder themselves, compared to the relatives of those without a substance use disorder. This could
be explained by the fact that family members share similar environments (such as exposure to drug
and alcohol use) or that they share genes, or a combination of both.
In addition to family studies, adoption studies suggest a considerable role for genetic factors. These
studies generally entail investigating whether adoptees are more similar to their biological relatives
(supporting a genetic influence) or their adoptive relatives (supporting an environmental influence).
However, adoption studies do not control for in utero environmental exposure, with both alcohol use
and tobacco use during pregnancy increasing the risk of substance use in young adulthood (Stone,
Becker, Huber, & Catalano, 2012). Another limitation of adoption studies is the potential that the
distress of adoption increases the risk of substance use disorders (Agrawal & Lynskey, 2008).
In twin studies, the concordance rates of substance use disorders among twins are compared: if
there is a genetic component, then the concordance (co-occurrence) rates of these disorders among
monozygotic (identical) twins should be greater than the concordance rates among dizygotic (fraternal)
twins, since the former share 100 per cent of their genes and the latter share approximately 50 per cent
of their genes. As with family and adoption studies, twin studies also support the belief that substance
use disorders have a strong genetic component. Specifically, these studies have found that monozygotic
twins have higher concordance rates for substance use disorders on a range of substances.
The heritability estimates for various substances are 0.39 for hallucinogens, 0.72 for cocaine,
0.50–0.70 for alcohol dependence and 0.30–0.75 for tobacco (Agrawal & Lynskey, 2008). Genetic
influences are likely to have a role in the initiation of substance use, continued use and the
development of dependence (Li & Burmeister, 2009). There is also likely to be an overlap in the
genetic predisposition to develop dependence to different drug classes (Li & Burmeister, 2009).
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The psychoactive effects of drugs occur as a result of their effects on the brain, so an
understanding of brain processes associated with drug use provides an essential component of
investigating the cause of substance use disorders. Substances that can lead to dependence act on
the brain’s reward systems. The major reward systems are the dopaminergic reward system and
the endogenous opioid system (Robinson & Berridge, 2003). Although many neurotransmitters are endogenous
involved in the neurochemistry of substances of dependence, dopamine is thought to be the most opioid system
important (Lingford-Hughes et al., 2003). Dopamine levels increase substantially following the The systems
administration of most drugs of dependence, including alcohol, nicotine, cannabis, heroin, cocaine within the body
that produce/
and amphetamines, with the speed of the increase a critical factor in the reinforcing properties of
respond to
these drugs (Volkow, Fowler, Wang, Baler, & Telang, 2009). The particular area of the brain in both internally
which dopamine increases is known as the nucleus accumbens and related structures, which receive produced opioids
information from the ventral tegmental area (VTA) in the midbrain. The pathway between these (e.g., endorphins)
areas is known as the mesolimbic dopamine pathway (Wise, 2002). From the nucleus accumbens, and ingested
messages are sent to the prefrontal cortex, where they are coded as experiences. This reward pathway opioids (e.g.,
is the same system implicated in a range of pleasurable activities (e.g., eating and sex), although morphine) or
opiates (e.g.,
substances with addictive potential often produce a much greater effect. The dopaminergic reward
opium).
pathway is shown in Figure 10.2.
Prefrontal
cortex
Nucleus
accumbens
VTA
FIGURE 10.2 The dopaminergic reward pathway in the brain,

through which messages from the dopamine-rich ventral
tegmental area (VTA) are sent to the nucleus accumbens and
on to the prefrontal cortex
The endogenous opioid system involves endogenous opioids (such as endorphins and enkephalins),
which bind to opioid receptors and form the body’s natural response to pain. Opioids such as heroin
and morphine mimic the action of endogenous opioids by also binding to these receptors. In addition
to the opioid class of drugs, there is evidence that the rewarding or withdrawal effects of other
substances also involve the endogenous opioid system, including alcohol, nicotine, cannabis and
psychostimulants (Trigo, Martin-García, Berrendero, Robledo, & Maldonado, 2010).
Lubman, Yucel, and Pantelis (2004) proposed the inhibition dysregulation theory, which drew
upon neuroimaging and neuropsychological research to explain addiction as being underpinned by
impairment of the neural system that is responsible for inhibiting rewarding behaviour. Parts of the
frontal region of the brain, such as the orbitofrontal cortex and anterior cingulate cortex, are thought
to comprise the ‘inhibitory system’. Impairment of the inhibitory system is theorised to result in
compulsive drug-taking as well as other compulsive behaviours (such as those occurring in obsessive-
compulsive disorder).
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PSYCHOLOGICAL FACTORS: BEHAVIOURAL THEORIES

Biological factors that help to explain the aetiology of substance use disorders are incorporated
into some primarily psychological theories in this field. Psychological explanations of the cause of
substance misuse are numerous. West (2001) lists over 100 published psychological theories or models
of addiction, although many of these are poorly formulated, making them problematic to evaluate.
This section will describe influential past theories and major current theories.
Traditional behavioural theories focus on learning and conditioning as the basis of acquiring
substance use disorders. This learning occurs unconsciously and automatically. Behavioural models
have been developed based on the directly observable behaviour of animals (Winger, Woods, Galuska,
classical & Wade-Galuska, 2005). The elements involved in classical conditioning can help to explain some
conditioning of the elements of substance use disorders, including tolerance, withdrawal and craving. In Pavlov’s
Form of learning classic experiment, the ringing of the bell (the conditioned stimulus) came to elicit salivation in dogs
in which a neutral (the conditioned response) even when food (the unconditioned stimulus) was not present because of
stimulus, through
repeated pairing of the bell ringing and food. Similarly, unrelated stimuli (e.g., the sight of a syringe—
its repeated
association with the conditioned stimulus) that become associated with drug use (e.g., heroin use—the unconditioned
a stimulus that stimulus) can come to elicit a response that prepares the body for the administration of the drug.
naturally elicits a This conditioned response has been proposed as the reason why tolerance develops: the body already
certain response, begins to compensate for the effects of the drug before it is administered and thus reduces the effect
acquires the of the drug. This compensation may be experienced as craving for the drug. This explains why, even
ability to produce after a long period of abstinence, craving can be experienced if a conditioned stimulus or a ‘cue’ (such
the same
as the sight of a syringe) is present, with this cue-elicited craving in turn increasing the risk of relapse.
response.
The instrumental (or operant) learning model of dependence is based on animal experiments which
instrumental have shown that rats will press a lever to gain access to a drug. The administration of the drug is the
(or operant) instrumental behaviour, which is positively reinforced by the consequences of the administration of the
learning model drug, which affects the brain’s reward pathways. The subjective sense of pleasure or ‘high’ associated
A model which with drug use is thus the positive reinforcer. Negative reinforcement occurs when the instrumental
posits that
behaviour of using a substance alleviates an unpleasant state (e.g., smoking a cigarette to reduce the
substance
use problems symptoms of nicotine withdrawal). This unpleasant state comes about due to neuroadaptation: the
develop as brain has adapted to the presence of the drug, and so is ‘unbalanced’ when the drug is not present,
a result of leading to the unpleasant symptoms of withdrawal (West & Brown, 2013). The elements of drug use
conditioning relevant to instrumental and classical conditioning can occur in those who have not yet developed a
based on substance use disorder. However, the more often the reinforcement or conditioning occurs, the more
instrumental likely it is that a disorder will develop (West & Brown, 2013).
learning
Learning theories on the causes of substance use disorders now acknowledge that the development
principles.
of these disorders is likely to involve additional processes. For example, the incentive–sensitisation
theory of addiction proposes that drugs of addiction change the areas of the brain that are responsible
for the incentive to use drugs (Robinson & Berridge, 2003). The brain then becomes hypersensitive
(sensitised) to the rewarding effects of the drugs and to the stimuli associated with drugs (via classical
conditioning). Once this neural sensitisation has occurred, the individual will want the drug to such a
great degree that it is termed ‘pathological wanting’ because the incentive (i.e., the drug’s rewarding
effects) has been increased. This pathological wanting to take the drug can be experienced consciously
or unconsciously: the conscious element of the theory sets it apart from traditional behavioural
theories of drug addiction. An important aspect of the theory is that the neural sensitisation does
not increase liking of the drug, which is mediated by separate neural systems. It is proposed that the
pleasure associated with drugs becomes less important as physical dependence develops: dependent
individuals ‘want’ rather than ‘like’ the drug more over time.
PSYCHOLOGICAL FACTORS: PERSONALITY THEORIES

There is a popular belief among the general community that some people acquire substance use
disorders because they have an ‘addictive personality’. Yet there is minimal evidence to support the
existence of an exact personality type that predisposes one to become dependent on a substance.
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One approach that has some support is Cloninger’s (1987) tri-dimensional personality theory. This
is a general personality theory which in part suggests that the interaction between three dimensions
of personality influences one’s vulnerability to developing a substance use disorder. These three traits
include novelty-seeking (characterised by risk taking and impulsivity), harm avoidance (characterised impulsivity
by caution and inhibition) and reward dependence (characterised by sensitivity to social cues and Difficulty in
emotional dependence). These traits are underpinned by neuroanatomical differences that result controlling
behaviours;
in variations in how people interact with their environments. Cloninger described two subtypes of
acting without
individuals who are dependent on alcohol: type I and type II. Compared to those with type I alcohol thinking first.
use disorder, individuals with type II alcohol use disorder have an earlier onset of their drinking
problem, are more likely to be male and suffer from more problems. Individuals with type II alcohol
use disorder have been found to have high levels of novelty-seeking, low harm avoidance and low
reward dependence (Gilligan, Reich, & Cloninger, 1987).
PSYCHOLOGICAL FACTORS: COGNITIVE THEORIES

Cognitive theories of addiction propose that cognitive processes contribute to the development of
substance use disorders. One cognitive approach is outcome expectancy theory, according to which
an individual’s expectations of positive consequences from substance use increase his/her propensity
to use the substance. This theory was originally developed to explain heavy alcohol use, with research
finding support for the notion that positive expectations regarding the effects of alcohol (e.g., increased
confidence and reduced tension) predict drinking to excess (Reich, Goldman, & Noll, 2004). One
study found that the expectation that alcohol would reduce tension was the strongest predictor of
the amount of alcohol consumed by individuals with panic disorder (Kushner, Abrams, Thuras, &
Hanson, 2000). The use of substances to alleviate unpleasant psychological states (e.g., depression,
stress and anxiety) may be one reason accounting for the high rate of comorbidity of substance use
disorders and other psychological disorders.
Relapse prevention theory is a well-known cognitive-behavioural theory of substance use and
disorders (Marlatt & Donovan, 2005; Marlatt & Gordon, 1985). This theory argues that individuals
who are in high-risk situations (e.g., in the presence of the substance or related cues) will use the
substance if they do not have the appropriate coping strategies, have positive expectations relating
to the effects of substance use and have a low degree of self-efficacy (i.e., the individual’s level of
confidence that s/he can maintain abstinence). Thus, a single lapse will become a full-blown relapse
into excessive substance use if the ‘abstinence violation effect’ occurs, which comprises guilty
feelings about the lapse and a sense of powerlessness against substance use. Therefore, in treatment
settings, both cognitive and behavioural skills should be developed—first, to prevent an initial lapse
and, second, to manage a lapse if it occurs (Marlatt & Donovan, 2005).
PSYCHOLOGICAL FACTORS: MOTIVATION

PRIME theory attempts to build a comprehensive theory of motivation relating to substance use
disorders. Plans, responses, impulses, motives and evaluations comprise the five levels of motivation
and form the first theme of PRIME theory (West, 2013; West & Brown, 2013). According to this
approach, a ‘plan’ is a mental map of what the individual intends to do in the future, such as planning
to quit smoking. So when there is an ‘impulse’ or desire to smoke, the ‘response’ may be to follow
the plan and not smoke. However, the ‘motives’ (i.e., the degree of attraction or repulsion to achieve
the plan) will affect the response. ‘Evaluations’ are a set of beliefs about a situation that may contain
contradictory elements, such as the belief that giving up smoking is positive as it will benefit the
individual’s health but negative as it will entail withdrawal symptoms.
The second theme of PRIME theory is a ‘focus on the moment’: that is, although a person may have
the intention to change behaviour, his or her actions will depend on moment-to-moment processes and
events. For instance, a plan to not smoke may fail when a cigarette is offered.
The third theme is one of neural plasticity, whereby exposure to substances, be it short- or long-term,
will affect the motivation system. For example, repeated exposure to a drug may result in sensitisation
(i.e., where the brain becomes hyper-responsive to drugs or drug-related stimuli such as injecting
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equipment, thereby making subsequent doses more attractive) or habituation (i.e., where there are
increasing levels of tolerance to a drug so that greater doses are required to get the same effect).
The fourth theme addresses the issues of identity and self-awareness, with the beliefs a person has
about him or herself being a major source of motivation. These mental representations of identity have
an impact on self-control, which is the cornerstone of changing behaviour. For example, believing that
one is a smoker may have a negative impact on the individual’s willingness or confidence to control
his or her smoking. Self-control is an effortful activity that has to be maintained from moment to
moment to overcome impulses.
The final theme is the ‘unstable mind’: that is, motivation is inherently unstable, with even a
seemingly trivial event (e.g., a change in mood or exposure to environmental cues such as the smell of
coffee that had often been paired with smoking) having the potential to trigger behaviours. The focus
on the dynamic and fluid aspects of substance misuse place this approach at odds with some other
models which propose that there are relatively stable processes operating in addictions (such as the
individual having a disease).
SOCIAL AND CULTURAL FACTORS

Stone and colleagues reviewed an extensive range of potential risk and protective factors for the
development of substance use problems in emerging adulthood (Stone, Becker, Huber, & Catalano,
2012). Familial characteristics were among the key factors identified, including maternal, paternal and
sibling substance use. Low levels of parental monitoring and either permissive or harsh disciplinary
approaches were also associated with increased substance use. The role of other family-related
variables is less well-established, with the research conflicting. For example, low levels of parental
education are associated with subsequent smoking, while higher parental education is associated with
subsequent binge drinking, cocaine and cannabis use (Humensky, 2010; Stone, Becker, Huber, &
Catalano, 2012). While some studies report that higher parental income is associated with higher
rates of binge drinking and cannabis use (Humensky, 2010), others find that lower income and
socioeconomic status are risk factors (Stone, Becker, Huber, & Catalano, 2012).
Turning to peer influences, a strong relationship has also consistently been found between an
individual’s substance use and that of his/her friends (Stone, Becker, Huber, & Catalano, 2012). In
an Australian cohort, the strongest predictor at Year 5 of having started drinking by Year 6 was the
use of drugs by friends (Scholes-Balog, Hemphill, Reid, Patton, & Toumbourou, 2013). Yet, it is
unclear whether this relationship reflects peer socialisation and/or peer selection. In the process of
peer socialisation, substance use is the result of influence from those in the individual’s social network
in the form of modelling, encouragement and/or pressure (i.e., ‘peer pressure’). In the process of peer
selection, the substance use behaviour exists prior to the friendship, with the individual choosing to
associate with others who have substance use behaviours similar to his/her own.
With respect to Indigenous peoples, such as Indigenous Australians and Māori, substance use
disorders need to be considered within the historical framework of colonisation and dispossession as
well as continuing social and economic marginalisation. High rates of substance use disorders are a
major contributory factor to reduced life expectancy in these populations compared to non-Indigenous
populations, but interventions need to consider the underlying sociocultural causes rather than simply
adopting an individualistic approach in which treatment is provided to the individual. Similar patterns
of substance use and poor health outcomes are also apparent in other Indigenous groups throughout
the world (Gracey & King, 2009).
Additional cultural influences in the development of substance use disorders include the availability,
cost and social acceptability of the substance, each of which might affect whether the substance is used
in the first place. In terms of social acceptability, public education campaigns on the harms associated
with smoking tobacco have been effective in reducing the prevalence of smoking, as shown in
Figure 10.3. Combining these campaigns with smoking restrictions also reduces the modelling of
smoking behaviour, increases the costs of the behaviour (e.g., having to go outside to smoke) and
reduces any normalisation of smoking by isolating smokers from non-smokers.
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26
Tobacco
advertising
prohibition act
24
National
tobacco
Excise campaign
22
rise
Health Point of sale
Advertising warnings on advertising bans
ban in print packs
20 media
Tackling
% Prevalence
Indigenous
Smoke-free Smoking
18
dining Initiative
16
Graphic health
warnings on
packs
14
12
10
1991 1993 1995 1998 2001 2004 2007 2010
Year
FIGURE 10.3 Smoking prevalence rates for smokers 14 years or older and key tobacco control measures in Australia from
1990–2010
Source: Post-implementation review: Tobacco plain packaging 2016, Australian Government Department of Health. http://ris.pmc.gov.au/sites/default/files/
posts/2016/02/Tobacco-Plain-Packaging-PIR.pdf ©Commonwealth of Australia
The treatment of substance use disorders

APPROPRIATE THERAPEUTIC GOALS
The goals of therapy may be complete abstinence from any substance use, reduced or controlled
use of the substance, or minimising the harms stemming from continued substance misuse (e.g.,
providing clean injecting equipment to minimise the spread of diseases such as HIV). Adopting
anything less than an abstinence goal has generated considerable controversy, particularly in the
alcohol literature. Proponents of controlled drinking argue that individuals with problem drinking
can learn to limit their alcohol intake to moderate levels (Sobell & Sobell, 1993), whereas those who
argue for abstinence as a goal (e.g., Alcoholics Anonymous) state that controlled drinking cannot be
maintained over time.
However, there is now general acceptance of the appropriateness of controlled drinking as a treatment
goal, at least for some patients, such as those with mild alcohol use disorder. Controlled drinking is
also usually an appropriate goal in the context of screening and brief interventions (described below)
that target those with ‘at-risk’ patterns of alcohol use (Heather, 2006). These drinkers do not fulfil
the clinical diagnosis for an alcohol use disorder but are consuming in a manner that puts their health
at risk or has already caused harm. Reduction in the quantity of alcohol consumed or changes in the
patterns of alcohol use (e.g., to eliminate binge drinking or ‘drinking and driving’) can have important
health benefits without complete abstinence.
For those dependent on alcohol, controlled drinking remains controversial, especially in the United
States. An analysis of over a thousand people seeking help for alcohol problems assessed treatment
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outcomes in terms of the individual’s drinking goal at the start of treatment. Those opting for complete
abstinence had the better outcomes in terms of the number of days of heavy drinking, the percentage
of days abstinent and global outcomes, while those selecting controlled drinking had fewer drinks
per drinking day (Bujarski, O’Malley, Lunny, & Ray, 2013). Thus both types of goals can result in
positive outcomes. Whether to aim for a goal of abstinence or controlled drinking is therefore made
on an individual basis.
DETOXIFICATION AND INPATIENT TREATMENT

The treatment setting for severe alcohol and other drug use disorders traditionally entailed the individual
being admitted as a patient to the treatment facility (such as a hospital), and such inpatient treatment
still has an important role in detoxification. For example, alcohol withdrawal can be life-threatening
and requires close monitoring, especially where previous attempts have resulted in complications such
as seizures (Awissi, Lebrun, Coursin, Riker, & Skrobik, 2013).
Detoxification entails a period of abstinence from the substance while providing support to manage
the physiological and psychological symptoms of withdrawal. It comprises three components:
1. an initial evaluation
2. a period of stabilisation, including medical support through withdrawal
3. linkage with treatment services.
After detoxification, most treatment can be undertaken on an outpatient
or non-residential basis whereby the individual attends sessions with a
health professional, often once or twice a week. The evidence suggests
that detoxification is not a sufficient treatment approach on its own
for entrenched substance use disorders since it produces relapse rates
equivalent to patients who have not received such help (McKetin et al.,
2012; Teesson et al., 2008). Substance use disorders are multi-determined
disorders associated with high rates of relapse. Effective treatment therefore
requires careful attention to the complex array of factors maintaining the
substance use and relapse prevention procedures to reduce the likelihood
of a return to substance misuse. However, while not sufficient on its own,
detoxification may be a useful first step in the process of ceasing drug or

alcohol misuse. In addition, even after detoxification, inpatient treatment
facilities have a role in the management of substance use disorders for some
patients. For instance, patients with minimal social support to discontinue
substance use often require housing separate from their usual environment
to minimise their drug use.
PHARMACOLOGICAL INTERVENTIONS
Not surprisingly, there has been considerable research on the use of
medications to treat substance use disorders. Effective medications for
several substance use disorders (e.g., for nicotine and heroin) are currently
DAL
available. In addition, pharmacotherapies for amphetamine use disorder

Most treatment for substance use disorders and cannabis disorder are being developed and are likely to be available
occurs on an outpatient basis, with the in the coming decade. Clinical trials have also commenced on vaccines
individual attending sessions with a health for specific drugs (cocaine and nicotine). These stimulate the production
professional such as a psychologist, usually on of antibodies so that when the drug is ingested, antibodies attach to the
a weekly basis to begin with. drug, making the molecule too large to cross the blood–brain barrier, hence
reducing the reinforcing properties of the drug (Shen, Orson, & Kosten,
2012). The effectiveness of this approach is yet to be demonstrated and there are potential ethical
concerns about offering vaccination in place of custodial sentences or of users later trying to overcome
the vaccine by using large quantities of the drug.
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Medications for substance use disorders serve three purposes. First, antagonist medications
can be used to block the rewarding effects of the substance. For example, some (though not all)
research suggests that naltrexone (which blocks the effects of opioids) can be effective in reducing
the rewarding effects of alcohol, craving for alcohol and consumption of alcohol (Lobmaier, Kunøe,
Gossop, & Waal, 2011). In contrast, oral naltrexone is not deemed to be a useful therapy for opioid
dependence, except for a very small proportion of highly motivated individuals who are willing to
keep taking a medication that will block the positive effects of heroin and other opioids (Kirchmayer,
Davoli, & Verster, 2004). A number of sustained-release medications have been evaluated for treating
opioid use disorder (Kunøe, Lobmaier, Ngo, & Hulse, 2014), but none has been approved for use in
Australia yet.
Second, agonist medications, such as buprenorphine or methadone, may be used as a substitute for
the abused substance in order to reduce the harms, such as deaths from overdose and infection through
shared needles, associated with substance misuse. Both methadone and buprenorphine outperform
placebo in keeping patients in treatment. While high doses of buprenorphine can reduce illicit opioid
use, it is not effective at low doses. In contrast, methadone is effective across a range of doses (Mattick,
Breen, Kimber, & Davoli, 2014). However, both medications typically need to be administered under
supervision to prevent their diversion into the illicit drug market.
Third, medication may be used to reduce the severity of withdrawal symptoms. For example,
nicotine replacement therapy in the form of patches, gum, spray, tablets or inhalers has been found to
be effective, improving the rate of quitting by 50–70 per cent (Stead et al., 2012).
MOTIVATIONAL APPROACHES: A FIRST STEP

Substance use disorders can also be treated with psychological interventions. These disorders are
essentially ‘appetitive’ disorders rather than aversive disorders, such as depression or anxiety. That is,
the individual seeks out the drug, whereas those with depression or anxiety would choose to avoid the
negative feelings associated with their disorders if possible. While some aspects of substance use are
aversive (e.g., hangover, social stigma, disrupted relationships, the cost of buying drugs and the threat
of criminal conviction), the essential feature of substance use disorders is that the substance provides
relief from unpleasant withdrawal symptoms, the cessation of craving, and the pleasure, euphoria or
intoxication that comes from using the substance. Given these perceived advantages of substance
use, the individual’s motivation to alter his/her use of a desired substance may be low (Saunders &
Wilkinson, 1990).
Motivational interviewing is an approach that is valuable for individuals experiencing low
motivation to change; in particular, it explores the client’s ambivalence about his/her drug use and
adopts a non-confrontational stance (Miller & Rollnick, 2013). In this approach, patients are helped
to increase both the value of changing their substance use (e.g., by considering the full range of
positive and negative consequences associated with their drug use) and their confidence that they can
successfully change. A systematic review and meta-analysis of motivational interventions in medical
settings found significant reductions in alcohol use, cannabis use and increased abstinence from
tobacco (Lundahl et al., 2013).
BRIEF AND EARLY INTERVENTIONS

The 1980s saw the recognition that by the time individuals presented to services for help, their problems
were frequently severe and well entrenched. This led to the development of shorter interventions
that aimed to detect and deal with substance use problems earlier, when they are more amenable to
change, with the view that severe and chronic disorders could be avoided. Thus, brief interventions
are generally considered most appropriate for those whose substance use is not yet severe (O’Donnell
et al., 2014).
These brief interventions entail only limited contact with a health professional such as a general
practitioner, usually comprising assessment and feedback regarding the effects of the individual’s
substance use on his/her health. Normative feedback, that is, information about the amount that other
people drink or use, is an important component of these interventions as those with problematic
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use are often unaware of how different their behaviour is from that of the general population.
Brief interventions can also include the provision of educational material explaining the negative
consequences of substance misuse and strategies for overcoming a substance use disorder. In addition,
brief interventions often draw on elements of motivational interviewing by helping individuals to
resolve their ambivalence about changing their substance use.
Ideally, a complete package comprises screening, brief intervention and, if needed, referral
for treatment. According to this approach, all patients should be screened for the target substance
(such as smoking in a general practice setting), receive a brief intervention and, for those with more
entrenched problems, referred for specialist treatment (Substance Abuse and Mental Health Services
Administration, 2013). This type of intervention has been shown to be cost effective, with a saving
of more than $5 for every $1 invested (Fleming et al., 2000). A model based on the National Health
Service in England estimated that screening all new registrants in general practice would save the
health system £120 million over 30 years, as well as conferring substantial benefits to individuals
(Purshouse et al., 2013).
Brief interventions have been developed that are tailored to an individual’s personality traits.
Specifically, the motivations to use and rewards from alcohol differ depending on whether the
individual is prone to: (1) anxiety, (2) depression, (3) impulsivity-reward or (4) sensation seeking. This
approach has been used in both school groups (Conrod, Stewart, Comeau, & Maclean, 2006) and those
accessing specialist mental health treatment, with significant reductions in both alcohol and cannabis
use plus improved mental health scores (Hides et al., 2013). A further important area for research in
this field is the examination of the ‘active ingredients’ in brief interventions so that the most effective
elements are used. In a review of the behavioural techniques used in alcohol brief interventions, only
prompting the self-recording of alcohol use was found to be effective (Michie et al., 2012).
SKILLS TRAINING APPROACHES

Training in a range of skills, and addressing unhelpful beliefs using cognitive behaviour therapy (CBT),
have been associated with beneficial outcomes in the treatment of alcohol use disorder (Shand, Gates,
Fawcett, & Mattick, 2003). As a general approach across different substances, CBT typically focuses
on helping the client to recognise situations where they are most likely to use drugs, aiding them in
avoiding these situations when appropriate and helping them cope with the problems and problematic
behaviour arising from their drug use. Training in communicating effectively with others, problem
solving, assertiveness skills (such as drink/drug refusal skills), challenging dysfunctional beliefs, and
relaxation and stress-management skills have all been effective for substance use problems. These
approaches aim to compensate for the skill deficits that have led to the use of alcohol or illicit drugs
as a method of enjoyment and as a coping strategy in difficult situations. While they have been most
extensively investigated in the context of alcohol use disorders, these techniques are also likely to be
of benefit in the management of other drug use disorders (Magill & Ray, 2009).
RELAPSE PREVENTION
Relapse prevention is an essential component of the management of substance use disorders and entails
both psychological and pharmacological approaches (Marlatt & Gordon, 1985; Marlatt & Donovan
2005). There is an extensive literature on the role of psychological therapy in relapse prevention with
substance use disorders, including the importance of anticipating high-risk situations for substance
use (e.g., negative mood or interpersonal conflict) and continuing to develop coping skills. The use of
medication to reduce cravings is also important as a means of helping patients to maintain the changes
they have made.
TECHNOLOGY-BASED INTERVENTIONS
More recently, psychological interventions have been adapted for delivery via the internet or mobile
phones. This approach has the potential to overcome some of the traditional barriers to accessing
treatment, such as cost, stigma, geographical location and the limited number of trained practitioners.
Furthermore, as these electronic resources are continuously available, individuals can access them at
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times of greatest need or motivation. Online interventions can also be used as standalone treatments or
as a resource to support those engaged in conventional psychotherapy or receiving pharmacotherapy
(Carroll et al., 2008).
These interventions typically draw on techniques from CBT and motivational interviewing to
change substance use behaviour. There is already robust evidence that this approach is successful in
helping those with alcohol use problems. Although most data have been collected from university
student populations (White et al., 2010), there have also been positive outcomes from general adult
samples (Riper et al., 2011) and adolescents (Tait & Christensen, 2010). In addition, there is initial
evidence to support their use among cannabis users (Tait, Spijkerman, & Riper, 2013) and for tobacco
cessation, albeit with smaller effects than for alcohol use problems (Rooke, Thorsteinsson, Karpin,
Copeland, & Allsop, 2010).
RECOVERY FROM SUBSTANCE USE DISORDERS

Substance use disorders are often referred to as ‘chronic relapsing conditions’. That is, a person may
spend years cycling in and out of drug use with intermittent periods of abstinence or controlled use
between periods of severe problems. In medicine, recovery is generally taken to refer to the end of
a disease. Within mental health, recovery is seen as a process. With respect to substance use, one
definition of recovery is ‘voluntarily sustained control over substance use, which maximises health
and wellbeing and participation in the rights, roles and responsibilities of society’ (UK Drug Policy
Commission, 2008). This moves away from just reducing the harms associated with substance use to
building positive outcomes. Recovery models also recognise that people start from different points,
that individuals have different goals for recovery and that the individual’s recovery goals may differ
from those of his/her family or society more broadly (White, 2007).
LO 10.2 Gambling disorder

Gambling is defined as an agreement between two or more parties to risk an item of value on the
outcome of an event determined in part by chance in order to obtain a larger return (profit). It is
attractive because it often offers individuals the opportunity to stake a small amount of money to win
a relatively substantial prize.

Gambling is a popular recreational activity in the Australian population, as shown by epidemiological
studies revealing that 15 per cent of adults gamble regularly (excluding lotto and scratch-cards), with
5 per cent playing gaming machines weekly or more often (Productivity Commission, 2009). Overall,
70–90 per cent of adults have gambled at some time (Petry, 2005). For many of these individuals,
gambling is a regular recreational activity that occurs on an affordable basis, while for others the
expenditure in time and money becomes excessive. The Australasian Gaming Council’s (2016) figures
for 2014–2015 indicate that, on average, Australian adults spend $1241 per year on gambling. The
total annual gambling expenditure for Australian adults was just over $22 billion.
In Australia, individuals aged 18 years and over can gamble on commercially available forms of
gambling that offer variable prizes from a few to many millions of dollars. These can be classified
into three major categories: gaming, which includes casino table games and electronic gaming
machines; wagering, which includes horse-racing, trotting, greyhounds and betting on sports and
other selected events; and lotteries such as lotto and scratch-cards. These can be played in land-based
venues or through the internet via smartphones, tablets, PCs or interactive televisions. The aggregate
amount of money spent by Australian adults involved in these various forms of gambling is shown
in Table 10.3.
‘Electronic gaming machines’ is a generic term encompassing electronic or computer-based reel-
type devices, video card games (blackjack and poker) and keno. Random number generators determine
the outcome of each play on these machines. Poker machines, slot machines, video lottery terminals
and fruit machines are terms used to describe variants of reel-based machines. Typically, they are
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TABLE 10.3 The annual aggregate expenditure in Australia (2015–2016)
ANNUAL EXPENDITURE (A$ MILLION)
Wagering 2814
Sports 814
Gaming machines 11 588
Lotteries 1993
Casinos 5169
Total 22 733 (inclusive of other forms)
Source: Australian Gambling Statistics, 32nd edition, Queensland Government Statistician’s Office, Queensland Treasury.
located in licensed premises—that is, hotels, clubs and casinos. In Australia in 2014–2015 there were
196 734 gaming machines located in 5207 venues (Australasian Gaming Council, 2016), with each
machine annually averaging a return of $60 000 to the operators of gambling venues (Productivity
Commission, 2010). Electronic gaming machines provide approximately 51 per cent of total gambling
takings. Just over half (58%) of machines are located in clubs, with 35 per cent and 7 per cent in hotels
and casinos respectively. In Western Australia, gaming machines are restricted to one casino.
Technological advances such as the internet have increased the availability and accessibility of
online simulated casino-table and poker-machine games using credit card facilities (Gainsbury, 2012;
Wood & Williams, 2011). Studies have also shown that the majority of interactive (online or internet)
gamblers are also land-based gamblers (Gainsbury, Wood, Russell, Hing, & Blaszczynski, 2012;
Wardle, Moody, Griffiths, Orford, & Volberg, 2011; Wood & Williams, 2011). However, Australia
and the United States have passed legislation to regulate and/or outlaw interactive internet games
to protect consumers against fraud, exploitation and underage gambling, as well as to limit loss of
revenue to overseas jurisdictions. Next generation games and gambling facilities are currently being
designed for mobile phones, again increasing the accessibility of gambling opportunities.
Competitive pressures from overseas online casinos, sports and newer forms offered by operators
are also likely to contribute to the continued promotion of gambling activities, as is the introduction of
virtual reality and the interest in fantasy and daily fantasy sports and eSports. Virtual-reality gambling
is an interactive form that involves the use of 3D computer-based goggles displaying high-resolution
graphics. The effect is to totally immerse a player in an artificial but realistic gambling environment.
Fantasy sports and daily fantasy sports refer to an online gambling activity characterised by
individuals paying a fee that is placed in a prize pool and picking a virtual team of real-world athletes
from professional and non-professional sports competitions. Points are accorded to specific levels of
performance, with the player accumulating the most points over a competitive season (fantasy sport)
or an event over a day (daily fantasy sport) winning the prize pool. ESports, in which bets are placed
on the outcome of online competitive real-time strategy or shooter-type video-game tournaments, is
growing in popularity, particularly in Asia.
In 2014–2015, there were 356 horse-race tracks conducting 2634 meetings, running a total of
19 123 races (Australasian Gaming Council, 2016). TAB and pubTAB facilities in local hotels and
clubs, combined with telephone and internet betting accounts, guarantee ease of access to sport
and horse/greyhound wagering. Horse-racing accounts for around 12 per cent of total takings from
gambling. Lotteries, lotto and scratch-cards are popular, with the largest provider reporting that
95 per cent of purchases are made through retail outlets and approximately 6 per cent made online.
Although 60 per cent of adults purchase such tickets, the expenditure on these forms of gambling
accounts for only approximately 9 per cent of total gambling takings.
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Some people regard activities such as participating in the stock-market as forms of risk taking
that share many characteristics with gambling. However, although rises in share values are difficult
to predict, their value is not influenced by chance. Generally, share trading is not regarded as a
recreational form of gambling and, apart from a few high-frequency day-traders, is not associated with
impaired control or psychological dysfunction.
It is important to understand the structure of commercial gambling. Operators of gambling
venues structure their games to have a slight statistical advantage over the player, called the ‘house-
edge’ or, for electronic gaming machines, the ‘return to player’. This house-edge represents the
long-term theoretical return (profit) to operators and effectively means that a person can win only
in the short term: statistically, the longer one plays, the greater the likelihood that losses will
eventuate.
What motivates most people to gamble when there is
a high risk of losing? People gamble recreationally for two
major reasons: for entertainment and to win money. The
attractiveness of risking relatively small amounts for the
possibility of a large prize is fuelled by frequent media reports
of multi-million-dollar lotto, Powerball or casino wins. Also
encouraging gambling are promotional marketing and media
coverage that glamorise gambling.
Types of gamblers
COURTESY A. BLASZCZYNSKI
There are several recognised categories of gamblers. People
who never gamble are referred to as non-gamblers. People
gambling within affordable limits are variably labelled
social, recreational or non-problem gamblers. This group
may be subdivided into regular (generally once a week) or
heavy gamblers depending on the frequency or intensity of
their behaviour. They may also be considered at-risk if they
are beginning to exhibit some of the features of problem In Australia, horse-racing accounts for 12 per cent of total
takings from gambling.

gambling.
‘Problem gambling’ implies the presence
of harm irrespective of the chronicity, severity
or impact of that harm. The South Australian
Centre for Economic Studies Report (2005)
recommended the following definition: ‘Problem
gambling is characterised by difficulties limiting
money and/or time spent on gambling which
leads to adverse consequences for the gambler,
others or for the community’ (p. i). ‘Disordered
gambling’ refers to the severe end of the problem
gambling spectrum, with impaired control
manifested by repeated, failed attempts to cease
or reduce gambling despite the development of
INGRAM PUBLISHING
significant negative personal, familial, financial,

occupational and/or legal difficulties. The term
is used to denote those individuals meeting
the formal diagnostic criteria for gambling
disorder as set out in the DSM-5 (APA, 2013)
or exceeding the clinical cut-off scores on People gamble recreationally for two major reasons: for entertainment and
gambling screening instruments. to win money.
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Historical approaches to gambling and problem gambling

Gambling and problem gambling are not new phenomena. Historical and archaeological evidence
shows that gaming and gambling have existed in almost every culture since antiquity. Early references
to board games are located in Egyptian murals dating from around 4000 years BCE and ‘astragals’
(knuckle-bones) were popular in ancient Egypt, Greece and India. Six-sided dice were used by the
Etruscans and introduced to Rome around 900 BCE. The term ‘dice’ originates from the Latin do or
datus, meaning ‘given’ in the sense of thrown or cast.
Greek and Roman soldiers wagered on the turn of numbered chariot wheels, which was a
predecessor of roulette (from the French for ‘small wheel’). This was refined by the mathematician
Blaise Pascal (1623–1662) and roulette was subsequently introduced to England in 1739, the United
States in the early 1800s and Australia in 1973 (Wrest Point Casino, Tasmania).
The oldest known Eastern games of Wei-ki in China and Go in Japan emerged around 2300 BCE.
Playing cards originated in twelfth-century China, reached Europe through Spain in the mid-1300s
and were taken to the Americas in 1492.
Horse-racing has a history dating to the times of Homer, Ovid, Herodotus and Xenophon.
Although public races were common in eleventh-century London, the sport of thoroughbred racing
evolved from the horse-breeding interests of Henry VIII (1491–1547). Horse-racing was common in
colonial Australia, with the first meetings held in Sydney’s Hyde Park in 1810. The establishment of
the Melbourne Cup in 1861 consolidated the sport as a national icon.
The origins of lotteries and their various derivatives are found in early religious and civil decision-
making processes. As Brenner and Brenner (1990) note, the drawing of lots was regularly used to
divine God’s will in guiding decisions related to resolving conflicts, selecting priests and civil servants,
determining innocence versus guilt and the division of property or distribution of gifts. Between the
fifteenth and eighteenth centuries, in the absence of banks and financial lending institutions in Europe
and North America, lotteries were commonly used to raise revenue to finance public works, military
ventures and town fortifications. This has continued to the present day, with lotteries financing the
building of Sydney’s Opera House.
The social acceptability of gambling has fluctuated over the years. The Koran and certain
fundamentalist Christian denominations regard gambling as sinful, while others, such as the Catholic
Church, are tolerant or actively utilise gambling for charitable purposes. Gambling has at various
times been condemned and prohibited by the state in response to public disorder; exploitation through
cheating; interference with military preparedness by soldiers wagering their weaponry and gambling
rather than training; protection of the aristocracy and the maintenance of social class structures by
ensuring that the lower classes did not win land and property; and the rise of the Protestant work ethic
(according to which gain through minimal work and idle pleasures is frowned upon).
Today, gambling is an integral part of the Australian cultural ethos. The first government-run
lottery began in Queensland in 1920. In 1956 poker machines were legalised in registered clubs,
but only in New South Wales. This changed in 1990, when gaming machines were permitted in all
other states except Western Australia, where they are limited to Burswood Casino. The first casino
opened in Wrest Point, Tasmania, in 1973, followed by casinos in the Northern Territory in 1979;
Queensland, South Australia and Western Australia in 1985; the Australian Capital Territory in 1992;
and New South Wales in 1995.
In terms of problem gambling, numerous anecdotal case histories of gambling behaviour leading
to financial and personal ruin are chronicled by historians. Notable among these cases of problem
gambling are the sixteenth-century Italian painter Guido, the seventeenth-century French poet Vincent
Voiture and French philosopher René Descartes, the eighteenth-century English writer and politician
Horace Walpole and the wife of Louis XIV of France, Marie Antoinette. Exemplary descriptions
of problem gambling are provided in Mikhail Lermontov’s (1841/1979) ‘The Fatalist’ (found in
his collection of short stories, A Hero of Our Times), Fyodor Dostoyevsky’s (1866/1978) novel The
Gambler and Alexander Pushkin’s (1834/1999) short story ‘The Queen of Spades’.
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The diagnosis of gambling disorder

Despite this early recognition of problem gambling in literature, it was only in the psychoanalytic
movement around 1914 that psychological interest in problem gambling emerged. The classification
of problem gambling as a psychological disorder is relatively recent, with pathological gambling
first appearing in the International Classification of Diseases in 1975 (ICD-9; World Health
Organization, 1975) and the third edition of the DSM (APA, 1980) as a behavioural habit and
an impulse control disorder respectively, and subsequently renamed as a gambling disorder in the
DSM-5 (APA, 2013).
DIAGNOSTIC CRITERIA FOR GAMBLING DISORDER

Instruments such as the South Oaks Gambling Screen (SOGS; Lesieur & Blume, 1987) and the
Problem Gambling Severity Index of the Canadian Problem Gambling Index (PGSI-CPGI; Ferris &
Wynne, 2001) are frequently used in large-scale studies and clinical populations to identify possible
cases of pathological gambling. The SOGS includes 20 questions assessing the severity of gambling
on several dimensions including financial (e.g., ‘Do you ever gamble more than intended?’),
emotional (e.g., ‘Have you ever felt guilty about the way you gamble or what happens when you
gamble?’), family/social (e.g., ‘Have people criticised your gambling?’) and occupational (e.g.,
‘Have you ever lost time from work due to gambling?’). A cut-off score of 5 is used to identify
the respondent as a ‘probable pathological gambler’. In contrast, the PGSI-CPGI has nine items
assessing gambling behaviours and consequences. It uses cut-off scores of zero for non-problem
gamblers, 1–2 for low-risk gamblers, 3–7 for moderate-risk gamblers and 8+ for problem gamblers,
out of a possible total score of 27. The PGSI-CPGI is now supplanting the SOGS as the screening
instrument of choice.
In the DSM-5 (APA, 2013), gambling disorder is included in the chapter ‘Substance-related and
Addictive Disorders’. It is defined as persistent and recurrent problematic gambling behaviour leading
to clinically significant impairment or distress as indicated by at least four of the following criteria in
a one-year period:
1. need to gamble with increasing amounts of money in order to achieve the desired excitement
(which is akin to the tolerance criterion for substance use disorder)
2. restlessness or irritability when attempting to cut down or stop gambling (which is akin to the
withdrawal criterion for substance use disorder)
3. repeated unsuccessful efforts to control, cut back or stop gambling
4. preoccupation with gambling (e.g., having persistent thoughts of reliving past gambling experiences,
handicapping or planning the next venture, thinking of ways to get money with which to gamble)
5. frequent gambling when distressed (e.g., feeling helpless, guilty, anxious, depressed)
6. after losing money, frequent return on another day to get even (‘chasing one’s losses’)
7. lying to conceal the extent of involvement in gambling
8. jeopardising or losing a significant relationship, job, education or career opportunity because of
gambling
9. relying on others to provide money to relieve a desperate financial situation caused by gambling.
These criteria refer to tolerance, withdrawal and a loss of control over gambling behaviour that are
akin to the criteria for substance use disorder. Indeed, the diagnostic criteria for gambling disorder
(and pathological gambling as it was referred to in previous editions of the DSM) were based on those
for substance use disorder. Lesieur and Rosenthal (1991) point out that, with the exception of chasing
losses, all of the diagnostic criteria for gambling disorder ‘have their counterpart in alcohol, heroin,
cocaine and other forms of substance dependence’ (p. 7).
Despite this, up until the DSM-5, pathological gambling was classified separately from drug
and alcohol problems as a disorder of impulse control, along with conditions such as kleptomania
(compulsive shoplifting), pyromania (compulsive fire-setting) and intermittent explosive personality
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disorder. These impulse control disorders are characterised by the repeated failure to resist an
urge to carry out behaviours that result in harm to the individual or to others. Individuals report
the presence of tension and arousal prior to the commission of an act and a sense of gratification
(positive reinforcement) and/or tension reduction (negative reinforcement) on its completion, followed
generally by an immediate sense of guilt or remorse. In the DSM-5 (APA, 2013), gambling disorder is
no longer defined as an impulse control disorder but as a non-substance behavioural addiction under
substance use disorder.
GAMBLING DISORDER AS AN ADDICTION

Historically, the diagnostic criteria for pathological gambling have undergone extensive revision
since the introduction of pathological gambling as a disorder in the DSM-III (APA, 1980), with the
criteria in the DSM-III-R (APA, 1986) modified to include symptoms paralleling those for substance
use disorder: preoccupation, tolerance, withdrawal and loss of control. This perspective persisted
with the DSM-IV-TR’s (APA, 2000) continued inclusion of aspects related to substance use disorder,
but the condition nevertheless remained classified separately from drug and alcohol problems as an
impulse control disorder. Despite continued debate and opposition by some researchers and clinicians,
the DSM-5’s (APA, 2013) reclassification of gambling disorder in the same chapter as substance
use disorder consolidates the tendency to conceptualise this behaviour as an addictive disorder. The
DSM-5 argues that research demonstrating the presence of significant similarities between
pathological gambling and substance addictions in respect to clinical phenomenology, aetiology,
comorbid conditions, treatment and neurophysiological functioning provides an evidence-based
justification for considering gambling to be an addiction. Whether other non-substance repetitive
behaviours (e.g., excessive eating, sexual behaviours, television watching and computer/internet
usage) will be included in this category remains to be seen.
The DSM-5’s (2013) approach reflects earlier historical and scientific influences that have shaped
the development of the addiction model of gambling. The formation of Gamblers Anonymous in
1957 and its adoption of the principles and philosophy of Alcoholics Anonymous set the general
foundation for the application of the addiction model to gambling. The collaborative relationship
between Gamblers Anonymous and Dr Robert Custer, a psychiatrist, was subsequently instrumental in
establishing the first hospital-based treatment centre for pathological gambling in the drug and alcohol
unit of the Veterans’ Administration facility in Ohio, USA. Following this, a number of hospital drug
and alcohol facilities established specialised gambling treatment programs.
Most importantly, as mentioned, the phenomenological similarities between gambling and
drug and alcohol problems have been used to support the addiction model of gambling (Lesieur &
Rosenthal, 1991). Gambling is conceptualised as an addiction on the basis that individuals repeatedly
engage in the behaviour to achieve a euphoric state of arousal equivalent to a drug-induced high or to
escape negative mood states. The repetitive nature of gambling, its persistence in the face of adverse
consequences, loss of control and features of tolerance and withdrawal appear consistent with the
symptoms manifested by drug-addicted individuals.
Beyond shared symptoms, research has found similarities between gamblers and those with
substance dependence in genetic abnormalities and neurobiological activity involving reward
pathways (e.g., similarities in brain responses to gambling and drug-related stimuli), suggesting a
common neurobiological process underlying these behaviours (Fauth-Buhler, Mann, & Potenza,
2016; Goudriaan, Oosterlaan, de Beurs, & van den Brink, 2004; Holden, 2001). That 40 per cent
of gamblers suffer comorbid alcohol abuse and 30 per cent of substance abusers meet criteria for
pathological gambling adds weight to the addiction model. Overall, these findings have led to
pathological gambling being described as a ‘behavioural addiction’—that is, an addiction without the
drug (Potenza, Steinberg, & McClaughlin, 2001) and classified within this category rather than as an
impulse control disorder (Fauth-Buhler, Mann, & Potenza, 2016).
Others, however, have highlighted differences between gambling and substance dependence,
thereby arguing that the two problems should be kept distinct. Walker (1992), for instance, points
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out a range of differences between problem gambling and substance dependence, such as the fact
that the withdrawal symptoms following cessation of gambling behaviour are typically mild and
psychological (e.g., irritability, restlessness, depressed mood, poor concentration and obsessional
thoughts) in contrast to the frequently more severe and physiological withdrawal symptoms associated
with substance dependence, as well as the fact that substances act directly on the reward pathways
of the brain. In addition, the ICD-10-CM (World Health Organization, 2017) continues to classify
pathological gambling alongside other conditions listed as impulse control disorders in the DSM-5,
such as kleptomania and pyromania. However, arguments have been advanced to support the notion
that the ICD-11, which is due to be released in 2018, should follow the DSM-5 by relocating gambling
within its addictive classification (Fauth-Buhler, Mann, & Potenza, 2016). Thus, debate continues
regarding the appropriate classification of pathological gambling as an addiction or a behavioural
habit, with the DSM-5’s reclassification strengthening the argument for the former over the latter.
It is expected that this reclassification by the DSM-5 (and potentially the ICD-11) will result in the
application of a wider range of modified substance abuse treatments being offered to those with
gambling disorder, including the use of pharmacological agents.
The epidemiology of problem gambling

The majority of adolescents gamble but do so infrequently and with minimal adverse consequences.
An estimated 24–40 per cent of adolescents gamble weekly, with 10–14 per cent being at-risk for
problem gambling and 2–9 per cent (median 5%) meeting criteria for pathological gambling (Hardoon
& Derevensky, 2002; Shaffer & Hall, 1996).
The 5 per cent figure for adolescent pathological gambling is approximately two to five times the
rate for adults (Shaffer, Hall, & Vander Bilt, 1997). The estimated rate of pathological gambling among
Australian adults using the South Oaks Gambling Screen was 2.1 per cent in 1997/98 (Productivity
Commission, 1999). The available data describing the distribution of pathological gambling using this
measure across Australian states and territories is presented in Table 10.4. Similar rates are reported
for New Zealand (2.7%), Spain (1.7–3.2%), the United States (0.8–4.0%), Canada (1.7%) and Hong
Kong (1.8%), although slightly lower rates are reported for Switzerland (0.8%) and Norway (0.6%). It
appears that internationally, an average of 1 per cent of adults meet criteria for pathological gambling.
Figures often vary due to differences in methodologies (face-to-face, telephone or online surveys) and
diagnostic measures used. The percentage of people with pathological gambling over the past year
across countries is 2.3% (Williams, Volberg, & Stevens, 2012).
Although not strictly comparable, more recent prevalence rates using the Problem Gambling
Severity Index show a decline across states and territories: 1.6 per cent for New South Wales,
0.7 per cent for Tasmania, 0.7 per cent for Victoria, 0.37 per cent for Queensland, 0.5 per cent in
the ACT, 0.64 per cent in the Northern Territory and 0.4 per cent in South Australia (Australasian
Gaming Council, 2012). In the only national prevalence study on interactive gambling (i.e., online or
internet-based gambling) conducted over the past decade and a half, Gainsbury et al. (2014) reported
a prevalence rate of 0.6 per cent using the Problem Gambling Severity Index.
Adolescent and adult males gamble more frequently and intensely than adolescent and adult females,
and older adolescents gamble more frequently than younger ones. Equal proportions of males and
females participate in using electronic gaming machines, lotteries and keno, but more males than females
wager on horses, casino-table games and sports betting. Bingo is played predominantly by females.
The ratio of male to female problem gamblers seeking treatment is 3:2. In Australia, the majority
of women, almost 100 per cent, presenting for treatment gamble on electronic gaming machines,
compared to around 80–90 per cent for males. Females report that they gamble predominantly as a
means of dealing with negative emotional states, in contrast to males who report being motivated by
factors related to winning, excitement and chasing losses (Mark & Lesieur, 1992).
In their review of the literature, Breen and Gainsbury (2013) found consistent evidence that
Indigenous populations in Australia, New Zealand and the United States manifested higher levels
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TABLE 10.4 State/territory prevalence studies for problem and moderate risk gambling in
Australia (2001–2015)
PROBLEM GAMBLING MODERATE RISK

JURISDICTION YEAR SAMPLE
(% OF ADULTS 18+) (% OF ADULTS 18+)
Australian Capital Territory 2009 5,500 0.5 1.5
2014 7,068 0.4 1.1
New South Wales 2006 5,029 0.8 1.6
2008-09 9,408 0.4 1.3
2011 10,000 0.8 2.9
Northern Territory 2006 2,000 0.64 Not collected
Queensland 2001 13,082 0.83 2.70
2003-04 30,373 0.55 1.97
2006-07 30,000 0.47 1.8
2008-09 15,000 0.37 1.6
2011-12 15,000 0.48 1.9
South Australia 2005 17,140 0.40 1.20
2012 9,402 0.6 2.5
Tasmania 2005 6,048 0.73 1.02
2007 4,051 0.54 0.86
2011 4,300 0.7 1.8
2013 5,000 0.5 1.8
Victoria 2003 8,479 0.97 0.91
2008 15,000 0.70 2.36
2014 13,554 08155 2.79
Western Australia N/A N/A N/A N/A
Australia 2009 N/A 0.7% 1.7%
2011 15,000 0.61% 3.7%
Source: Australasian Gaming Council, A Guide to Australasia’s Gambling Industries
of gambling involvement and prevalence

rates for problem gambling (up to 24%
in the Northern Territory, Australia)
compared to general population figures.
Among Indigenous communities in
Australia and elsewhere, cultural and
traditional beliefs, isolation associated
with living in remote areas, poor
integration in urban regions, lack of
social cohesion/dislocation, racism,
socioeconomic disadvantage and family
dysfunction are higher than in mainstream
COURTESY A. BLASZCZYNSKI
communities and therefore increase the

typical risk factors for the development of
gambling disorders.
The onset of problem and pathological
gambling varies extensively, although
females tend to report a shorter period
Pathological gambling behaviours are more likely to be during which gambling escalates to
exhibited by those gambling on multiple forms. problem gambling (1 year) compared
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to males (8–10 years) (Tavares, Zilberman, Beites, & Gentil, 2001). The average age at which most
people commence gambling is between 12 and 15 years. Ninety per cent of problem gamblers begin
before age 20 and maintain control for 1–10 years before gambling excessively and entering treatment
at a mean age of 35–39 years (Petry, 2005). Individuals gambling on multiple forms are more likely to
exhibit pathological gambling behaviours (Wood & Williams, 2011).
The course of problem gambling has been assumed to be chronic. However, recent longitudinal
studies have shown that, at least for the less severe cases, problem gambling is usually a transitory
condition, with 70 per cent ceasing their behaviour without treatment (Abbott, 2006; Slutske, Jackson,
& Sher, 2003). Unstable patterns of persistence over five years have also been reported for gamblers
meeting criteria for pathological gambling, with about half having a duration of one year (Williams
et al., 2015).
In 1984, the late American psychiatrist Robert Custer described the progression of pathological
gambling through several stages. In the early ‘winning phase’, people are motivated to continue
because of the excitement associated with occasional wins. About two-thirds of those who go on to
develop pathological gambling report that they experienced a relatively large win prior to developing a
gambling problem. This experience changes the affective salience of gambling (i.e., gambling-induced
mood changes attain a position of dominance over those produced by other activities) and results in
the emergence of specific cognitive beliefs (e.g., ‘I can win at gambling’). This leads to an increase in
the frequency and intensity of gambling behaviour. Heightened preoccupation with gambling, coupled
with accumulating losses, heralds entry into the ‘losing phase’, in which gambling escalates as the
individual attempts to recoup losses (the phenomenon of ‘chasing’). As debts accumulate, individuals
are unable to meet daily living costs and begin borrowing and lying to avoid detection. At this stage,
changes in personality emerge as the individual becomes stressed, irritable and withdrawn. This leads
to the ‘desperation phase’, where individuals might engage in illegal activities such as stealing as a
necessary means of financial and psychological survival.
Most individuals decide to seek treatment in response to a crisis related to their gambling (e.g.,
losing their home). However, the Productivity Commission (1999) conducted a national survey in
Australia and found that only about half of problem gamblers expressed a desire for treatment, with
one study cited in the Productivity Commission (1999) report estimating that only 3–10 per cent of
problem gamblers were in treatment at any one period.
A more chronic course of the disorder and worse response to treatment are associated with the
presence of comorbid psychological disorders (Hartmann & Blaszczynski, 2016). Of problem gamblers
in treatment, 75 per cent suffer major depression, 30–40 per cent have a substance use problem and
15–40 per cent display antisocial personality traits. Sixty per cent report having committed an offence
to finance their gambling. Using data from Blaszczynski and Farrell’s (1998) review of the State
Coroner’s records of gambling-related suicides in Victoria, the Productivity Commission (1999)
estimated that 1.7 per cent of the 2800 suicides during 1997 in Australia were gambling-related.
Suicide risk is greatest immediately prior to the disclosure of significant debts or criminal offence or
in the context of marital disintegration.
The aetiology of gambling disorder

Currently there is general consensus that multiple biological, psychological and sociocultural factors
are involved in the development of gambling disorder. The interaction between these is complex,
although most aetiological approaches tend to focus on a single component.
BIOLOGICAL FACTORS
Research into the biology of gambling disorder is still in its infancy. However, there is mounting but
inconclusive evidence for underlying neurobiological and genetic vulnerabilities that may be involved
in the aetiology of pathological gambling. Studies suggest that disturbances in the serotonin, dopamine
and noradrenaline neurotransmitter systems may play a role in the mechanism involved in behavioural
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inhibitory control, reward mechanisms and arousal in impulsive and addictive disorders (Petry,
2005). It has been proposed that the same neurobiological pathway underlying substance dependence
is also relevant for behavioural addictions such as gambling (Shaffer, LaBrie, & LaPlante, 2004;
Fauth-Buhler, Mann, & Potenza, 2016). Specifically, the dopaminergic pathway (which entails
activation of dopaminergic-enriched cells in the ventral tegmental area and subsequently in the
nucleus accumbens) is hypothesised to play a central role in regulating the positive affect or emotions
associated with behaviours such as gambling (Comings & Blum, 2000).
serotonin Serotonin is involved in specific impulsive behaviours. A number of studies have investigated
Drugs serotonergic activity in pathological gamblers, on the basis that low levels are associated with poor
manufactured impulse control such as suicide, violent impulsive behaviour, alcoholism and arson. In addition,
using artificial
decreased serotonergic activity has been consistently related to the personality traits of impulsivity and
or human-made
chemicals rather
sensation seeking. Support for the involvement of serotonin in gambling comes from pharmacological
than natural treatment studies demonstrating a positive response among those with pathological gambling to
ingredients. selective serotonin reuptake inhibitors (SSRIs) that increase the availability of serotonin. To date,
however, inconsistent results investigating differences in serotonergic activity between pathological
gamblers and controls have been reported, indicating the need for further research before the complex
relationship between impulsivity and serotonin is understood (Shah, Potenza, & Eisen, 2004).
dopamine The dopamine system, in particular the dopamine receptor D2 gene (DRD2), is associated with
Neurotransmitter impulsive-addictive disorders including drug and alcohol abuse and pathological gambling. Blum and
in the brain, colleagues (1996) report data indicating that a particular variant of the DRD2 gene (the D2A1 allele)
with excessive
may be a risk factor for pathological gambling, with 50.9 per cent of those with pathological gambling
function of the
dopaminergic
carrying the D2A1 allele. When severity of gambling was evaluated, 63.8 per cent of those in the
neurotransmitter upper range carried the D2A1 allele compared to 40.9 per cent in the lower range. Findings of higher
system theorised rates of problem gambling (5%) among patients suffering from Parkinson’s disease being treated with
to contribute to medications that increase dopamine activity is consistent with the dopamine dysregulation hypothesis
the development (Weintraub et al., 2010). Dopaminergic neurons are widely distributed throughout the mesolimbic,
of schizophrenia. mesocortical and orbital frontal brain structures and include the ventral tegmental area, nucleus
accumbens, orbitofrontal cortex, amygdala and hippocampus. These regions are involved in the
neurobiological substrates mediating reward sensitivity, associative learning, memory, expectancies,
cravings and the emotional and motivational changes occurring during withdrawal (Goldstein &
Volkow, 2002; Hisahara & Shimohama, 2011). As with serotonin, however, mixed results have been
reported in the limited number of studies comparing differences in dopaminergic activity between
pathological gamblers and controls. Thus the role of dopamine in the aetiology of problem gambling
awaits further investigation.
noradrenaline Noradrenaline is believed to be involved in arousal, excitement, impulsive behaviour and sensation
Neurotransmitter seeking and has therefore been implicated as a possible causal factor in pathological gambling. For
that is involved instance, several studies have found that pathological gamblers have significantly higher levels of
in the regulation
3-methoxy-4-hydroxyphenylglycol (MHPG, a metabolite or breakdown product of noradrenaline)
of mood (also
known as
compared to controls (Bergh, Eklund, Sodersten, & Nordin, 1997; Roy et al., 1988).
‘norepinephrine’).
PSYCHOLOGICAL FACTORS: PERSONALITY
Certain personality traits may predispose an individual to developing problem gambling.
Complementing the research on disturbances in neurotransmitters linked to impulsivity, the most
consistent finding is that of elevated levels of impulsivity in individuals with problem gambling. This
trait is manifested by spontaneous behaviour carried out without regard to its consequences and an
sensation inability to delay gratification. Steel and Blaszczynski (1998) found that severity of gambling-related
seeking
problems was significantly correlated with impulsivity.
Personality
trait entailing a
The relationship between the personality trait of sensation seeking and gambling is less clear-cut.
desire for novel Sensation seeking is defined as the desire for novel and stimulating experiences. It has been found to
and stimulating be elevated in both adolescent (Powell, Hardoon, Derevensky, & Gupta, 1999) and adult (Breen &
experiences. Zuckerman, 1999) gamblers and to be associated with placing larger bets and gambling in casinos
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(Coventry & Brown, 1993). However, sensation seeking has been unexpectedly shown to be lower
in pathological gamblers receiving treatment compared with healthy controls (Blaszczynski, Wilson,
& McConaghy, 1986). Partly explaining these discrepant findings is the varied sample used—that
is, community versus treatment-seeking populations (Raylu & Oei, 2002). As Zuckerman (1999)
suggests, low sensation seekers may be more likely to pursue treatment compared to high sensation
seekers (who tolerate risk and novel experiences to a greater extent) or treatment may reduce sensation
seeking. Thus, treatment-seeking gamblers may not reflect the true level of sensation seeking in those
with pathological gambling.
The majority (80–90%) of pathological gamblers have at least one personality disorder. The most personality
common comorbid personality disorders are the cluster B personality disorders (e.g., narcissistic, disorder
antisocial and borderline), which are found in approximately one-third of those with pathological Chronic pattern
gambling (Blaszczynski & Steel, 1998). Rather than simply being comorbid conditions, it has been of maladaptive
cognition,
suggested that these personality disorders may be causally related to pathological gambling. For
emotion and
instance, those with antisocial personalities respond differently to rewards and punishment, have behaviour
difficulty in delaying gratification and respond impulsively. People with borderline personality that begins in
disorders have immense difficulty in regulating emotions, act impulsively and have a tendency to adolescence or
engage in self-destructive behaviours, such that gambling may act as a form of self-directed punishment early adulthood
and an attempted means of coping with emotional distress. and continues
into later
PSYCHOLOGICAL FACTORS: LEARNING adulthood.
Operant (instrumental) conditioning approaches highlight the role of positive and negative operant
reinforcement in problem gambling. Participating in gambling produces states of subjective arousal (instrumental)
(elevated mood states such as excitement and euphoria) and physiological arousal (e.g., increases in conditioning
heart rate) that are positively reinforcing. On the other hand, the excitement helps the individual to Form of learning
escape emotional distress, thus negatively reinforcing gambling behaviour. in which
The schedule of reinforcement associated with gambling is also relevant in understanding the behaviours elicit
persistence of gambling in the face of mounting losses. The wins associated with gambling occur consequences
that either
occasionally (rather than on every instance of gambling) and at unpredictable times. These intermittent
reinforce or
(occasional) and variable (unpredictable) schedules of reinforcement associated with gambling are punish the
known to produce behaviours that are highly resistant to extinction. As such, gamblers are prone to organism, leading
persist in playing long after their gambling behaviour has been rewarded with a win. to an increased
Classical conditioning is also operative in gambling behaviour. Gambling-related environmental or decreased
cues (e.g., sights, sounds, time of the day and certain people) may be repeatedly paired with the probability
physiological arousal and subjective excitement associated with the act of gambling and winning. In respectively of
other words, these environmental cues become conditioned stimuli for eliciting arousal/excitement. the behaviour
occurring in
Subsequent exposure to these classically conditioned stimuli (e.g., seeing an advertisement for a
the future
club or hotel) triggers a state of arousal/excitement associated with the anticipation of winning (also known as
that is experienced as an urge or craving to gamble. This is similar to the process experienced by ‘instrumental
individuals with a substance dependence following exposure to drug-related paraphernalia (e.g., the conditioning’).
sight of a syringe).
PSYCHOLOGICAL FACTORS: COGNITIONS

Cognitive models emphasise the importance of erroneous perceptions and irrational beliefs about
randomness and probabilities in leading individuals to overestimate their chances of winning. A
number of key irrational beliefs have been elicited using the ‘thinking aloud’ technique, a procedure in
which participants are asked to verbalise without censorship all thoughts entering their mind as they
play electronic gaming machines. Studies consistently demonstrate that approximately 80 per cent of
people verbalise irrational or erroneous beliefs while gambling (Gaboury & Ladouceur, 1989; Petry,
2005). Interestingly, this appears to be independent of one’s level of statistical knowledge, in that
Pelletier and Ladouceur (2007) found no difference in perceptions and behaviours during a gambling
session between two samples of individuals with different levels of knowledge regarding mathematics.
Table 10.5 describes common cognitive distortions in those with problem gambling.
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TABLE 10.5 Common cognitive errors that are hypothesised to result in problem gambling
COGNITIVE ERROR ASSOCIATED BELIEFS
Illusion of control Belief and over-magnification of one’s skills and ability to influence
or predict the outcome of an event.
Gambler’s fallacy A series of losses must be followed by a win when, in fact, the
chances of winning/losing remain the same on each play (e.g., with
every toss of a coin, the probability of heads or tails is 50%).
Biased evaluation Successful outcomes are attributed to one’s skill; losses are
discounted as due to unforeseen external reasons.
Selective recall Selectively recalling wins and forgetting losses.
Cognitive regret Having invested considerable time and money in a session, a sense
of regret at missing out on the next, potentially winning, gamble.
Superstitious beliefs and luck Use of ‘lucky’ charms, objects, prayers or rituals to ‘improve’ the
chances of winning.
Luck as a personal quality Believing one has a special ‘lucky’ quality. May have cultural
associations with reference to ancestors looking after one’s
wellbeing.
Gambling as a source The belief that one can win at gambling—that is, that over the long
term one can come out ahead.
Illusory correlations Misinterpretation of a correlation between mutually independent

events.
Toneatto, Blitz-Miller, Calderwood, Dragonetti, and Tsanos (1997) classified common thinking
errors among gamblers into those relating to concepts of personal skill and judgment (illusions
of control), ability to influence outcomes (superstitious rituals and beliefs), selective recall and
erroneous perceptions regarding randomness and the independence of chance events (the so-called
‘gambler’s fallacy’). They found that the mean number of cognitive distortions per participant was
3.5. The most frequently reported cognitive errors were illusions of control and a superstitious belief
in certain behaviours (e.g., the use of charms) to influence the outcome. In summary, cognitive errors
are considered to play a crucial role in contributing to and maintaining gambling behaviours and
gambling disorders.
SOCIAL AND CULTURAL FACTORS

Adolescents whose parents have a gambling problem are three times more likely to develop gambling
problems themselves, a figure that increases to a magnitude of 12 times the risk when both parents
and grandparents are problem gamblers (Gambino, Fitzgerald, Shaffer, Renner, & Courtnage, 1993).
While studies show that gambling runs in families, it remains unclear whether this is due to an inherited
vulnerability or environmental factors. As an example of an environmental influence, parental
modelling of positive attitudes towards gambling may influence children’s own attitudes and behaviours
regarding gambling. Ladouceur and Mireault (1988) found that 90 per cent of a sample of high school
students in Quebec reported that their parents were aware of their gambling, 84 per cent stated that
their parents did not object, 61 per cent gambled in the company of their parents and 25 per cent
borrowed money from their parents or other relatives to gamble or pay gambling-related debts.
Early negative childhood experiences may also contribute to the development of problem gambling.
Adolescent pathological gamblers compared to non-pathological gamblers appear to be more likely
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to come from dysfunctional families, suffer low self-esteem and report gambling for excitement and
alleviating depression (Derevensky & Gupta, 2004). The finding that, for some young people, gambling
represents a means of escaping emotional pain and distress is consistent with Jacobs’ (1986) general
theory of addictions. Jacobs’ model asserts that childhood social and developmental experiences that
lead to feelings of inadequacy, worthlessness, low self-esteem and rejection predispose the individual
to engage in addictive behaviours. In this model, addictive patterns of behaviour originate in the
capacity of that behaviour to allow the individual to escape from emotionally painful realities and
experience esteem-enhancing fantasies of importance and success.
Cultural determinants of pathological gambling are important. For any biological or psychological
vulnerability towards the development of problem gambling to manifest itself, the individual needs
to be exposed to opportunities to gamble. Research demonstrates that as the availability of gambling
increases, so does the prevalence of problem gambling. For instance, one study assessed the rate of
problem gambling in the community at two time points separated by seven years (Ladouceur, Jacques,
Ferland, & Giroux, 1999). Corresponding to the increase in the availability of gambling activities
during this time period was a 75 per cent increase in the prevalence of problem gambling.
In addition to the increased availability of gambling, social attitudes encouraging gambling may,
for vulnerable individuals, result in problem gambling. From a social learning perspective, marketing
campaigns, newspaper and magazine coverage of prizes won and the glamorisation of gambling
through film and television foster media-based vicarious learning.
The exposure model postulates that as gambling opportunities increase within a community and
shifts in attitudes occur, there will be greater gambling participation rates (Shaffer, 2005). Abbott
(2006) concluded that early prevalence studies support the exposure model, with increased rates of
pathological gambling reported in Australia, New Zealand, Spain, Canada and the United States over
the past 30–40 years as gambling has become more available. However, in reviewing more recent
epidemiological surveys, Abbott (2006) concluded that there was now emerging evidence for a steady
or declining rate of pathological gambling. This conclusion is not at variance with the exposure model
but can be explained by reference to the social adaptation model, which suggests that populations
eventually learn to adapt to environmental changes and challenges (Shaffer et al., 2004). Protective
factors such as the promotion of responsible gambling (e.g., brochures regarding the risks of gambling
and problem-gambling support services), together with familiarity and loss of novelty appeal, may
have resulted in the adaptation of many community members to gambling within their environment
(Collins & Barr, 2006).
THE INTEGRATED PATHWAYS MODEL

Blaszczynski and Nower (2002) have advanced an integrated aetiological model that incorporates
biological, personality, learning, cognitive, social and cultural factors in differentiating three
subgroups of problem gamblers. These are the pathway 1 behaviourally conditioned, pathway 2
emotionally vulnerable, and pathway 3 biologically based problem gamblers. Each subgroup is
theorised to have common components related to exposure, cognitive schemas and reinforcement,
but also important additional variables contributing to different causal pathways, which have
implications for treatment.
Pathway 1 refers to ‘behaviourally conditioned problem gamblers’ who are characterised by
excessive gambling in the absence of any psychological disturbances that pre-dated their gambling
problem. These gamblers fluctuate between regular/heavy and problem gambling as a result of
classical and operant conditioning and distorted cognitions overestimating the probabilities of
winning. Accumulating financial problems motivate the individual to chase losses, with the
accompanying stresses causing depression and substance use. Thus psychological problems such
as mood disturbance and substance abuse are a consequence, rather than a cause, of excessive
gambling. Entry into this subgroup may occur at any age following exposure to gambling through
family or peer group interactions. Motivation for treatment is high and brief interventions appear to
be effective.
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Pathway 2 refers to ‘emotionally vulnerable problem gamblers’ who are also influenced by
conditioning, cognitive and social processes. However, mood disturbance, a history of poor coping
and problem-solving skills and dysfunctional family histories are additional risk factors for impaired
control. This subgroup gambles primarily to escape from emotional stresses. As a result of these
additional aetiological factors, treatment is more complex than that for behaviourally conditioned
gamblers and includes the enhancement of stress management and coping skills.
Pathway 3 refers to ‘biologically based problem gamblers’ with neurochemical dysfunctions
that result in high levels of impulsivity and differential responses to reward and punishment. This
group has a history of widespread impulsivity and risk taking, substance abuse, poor interpersonal
relationships, suicidality, irritability, low tolerance for boredom and engagement in criminal activities
that may or may not be gambling-related. Gambling commences at an early age and rapidly escalates
in intensity and severity. Motivation for treatment is poor, as is treatment outcome. In addition to
psychological treatments, this subgroup may benefit from pharmacological agents directed towards
decreasing impulsivity.
CASE STUDY: A BEHAVIOURALLY CONDITIONED PROBLEM GAMBLER

Steve, aged 32, was a keen basketball player since his early childhood. He played at local and state representative levels
and spent several years in the United States playing in the National Collegiate Athletic Association (NCAA) Division 1
basketball league. From age 18, Steve and his teammates would visit the local club after training and weekend games
to socialise, have a few drinks and discuss sport. He had no interest in playing electronic gaming machines but after
a few months succumbed to one of his friend’s constant requests to join him in a session of play. After the second or
third such occasion, Steve successfully hit a jackpot of $1500 after putting in $10. He felt elated and explained his good
fortune by saying that he was always lucky. He began to play the gaming machines more frequently and was delighted to
demonstrate his luck to his companions. Following a cluster of wins, he began to believe that he did indeed have luck on
his side. Although his gambling increased to the point where he played every time he entered a club or hotel, he limited
his betting to $20, losing no more than $50 at any one time.
At around the age of 22, Steve was invited to the wedding of a close friend. In the lead-up to the wedding, he and
a group of friends went out to a local hotel to celebrate. During the course of the evening, someone suggested that
they have a go at playing the electronic gaming machines. Steve boasted that he ‘always won’ on the machines and,
being teased by the group, put in $5. To everyone’s surprise, Steve won a $200 jackpot. He shouted a round of drinks
and then noticed the keno game being shown on the television screen. With a sense of bravado he decided to buy a
ticket and boasted that he would win again. On this occasion, he won $54, prompting him to further demonstrate his
luck by randomly selecting a dog race at the sports bar adjacent to where they were drinking. The group watched the
race televised on the screen. He not only managed to win again but also had some further small wins on the electronic
gaming machines later that night. The evening strongly reinforced his existing belief that somehow he was ‘blessed with
a personality trait of luck’.
Over the next few months, Steve began to frequent the local hotel and club to play the gaming machines and keno
and to bet on dogs in the greyhound races. He also decided to watch more sporting events and pick winners in his head.
He soon began to prefer dogs and sports betting but carried on playing keno on occasion. He experienced a run of small
returns on keno, and on a few relatively large bets on the greyhounds and a few basketball games. He consequently
developed the impression that not only was he lucky, he was skilful in picking winners. Using his skills, he came to
believe that he could turn his gambling into a profitable money-making activity. He discounted episodes where he lost
his bets on dog racing and sporting events on the basis that the outcome was influenced by the dogs being blocked or
unwell or biased refereeing: ‘The team would have won except the referees dictated the final result,’ he thought.
In response to seeing an advertisement promoting online sports betting on television, he decided to open an account
and bet via his smartphone. He became engrossed in reading sport columns in newspapers, watching basketball,
other sporting events and betting commentaries on television, and excitedly engaged in vigorous discussions and
debates with his teammates. His friends described him as being ‘totally preoccupied and obsessed with dogs and
sports betting’.
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By the end of the year, Steve was in substantial debt, and depressed and angry at the fact that his luck had changed.
He promised himself that he would stop gambling once he won back his losses and cleared his debt. Unfortunately,
however, his gambling escalated when he was inundated with sport advertising and promotions. He found himself
in serious debt with limited capacity to meet his repayments on the basis of his salary alone. Following a disastrous
weekend episode of losses on several sporting codes he became depressed and almost suicidal. After confiding in a
close friend, he decided to seek treatment and financial counselling to assist him overcome his problems.
The treatment of gambling disorder

Historically, the psychological treatment of pathological gambling can be categorised into three broad
timeframes. During the first period, from 1914–1957, psychoanalytic/psychodynamic interventions
were predominant. The 1960s to the 1980s witnessed the emergence of specific behavioural techniques
(such as aversion therapy) and peer counselling in the form of Gamblers Anonymous. From the 1980s
to the present, the treatment of pathological gambling has been dominated by cognitive-behavioural
approaches, while pharmacological interventions have also been explored. In addition, a public health
approach adopting a broad social policy perspective has emerged.
PSYCHOANALYTIC AND PSYCHODYNAMIC APPROACHES

Psychological interest in pathological gambling first emerged in conjunction with the advent of the
psychoanalytic movement at the turn of the twentieth century. Explanations emphasised the sexual
conflicts associated with gambling. Freud (1928), for instance, maintained that gambling was the
manifestation of a masturbation addiction, with masturbation considered the ‘primal addiction
for which all later addictions are substitutes’ (Herman, 1976, p. 94). Few clinicians currently use
psychoanalytic therapies in the treatment of gambling disorders.
GAMBLERS ANONYMOUS
Gamblers Anonymous, a self-help organisation, was established in 1957. Its philosophy, 12-step
recovery process and abstinence treatment objectives were derived from the principles and format
of Alcoholics Anonymous. The emphasis is
on shared common experiences provided by

mutually supportive peers in a group setting.
Gamblers Anonymous espouses the philosophy
that compulsive gambling is an illness that
is progressive in nature and cannot be cured
(Gamblers Anonymous, 1977). Since the
individual has an illness, this approach maintains
that participation in any form of gambling will
invariably lead to loss of control and a return
to pathological levels of gambling. Therefore,
the approach insists that abstinence is the only
valid treatment goal.
Stewart and Brown (1988) carried out
a systematic five-year retrospective and a
three-month prospective study of Gamblers
Anonymous treatment outcome results. In
DAL
the retrospective phase, only 7.3 per cent of

137 participants were abstinent over a two-year Gamblers Anonymous emphasises shared common experiences provided
period. The results also revealed high treatment by mutually supportive peers in a group setting. It espouses that compulsive
dropout rates, with 22.4 per cent of participants gambling is an illness that cannot be cured and that abstinence is the only
dropping out after one meeting and 70 per cent valid treatment goal.
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by the tenth meeting. The results from the prospective phase were similar, with a 12-month abstinence
rate of only 7.5 per cent and a 50 per cent dropout rate by the third week.
BEHAVIOURAL AND COGNITIVE INTERVENTIONS

The fundamental assumption of behavioural interventions is that gambling is a learned maladaptive
behaviour that can be unlearned through techniques based on the principles of learning. Skinner (1953)
suggested that the acquisition of gambling behaviour followed operant conditioning principles with
monetary reward delivered on intermittent variable ratio schedules acting as the primary reinforcement.
Later, Anderson and Brown (1984) postulated a two-factor model emphasising: (a) the role of
classical conditioning whereby environmental cues of gambling come to elicit arousal/excitement, and
(b) the negative reinforcement associated with a reduction in negative emotional states produced by
the narrowing of attention and hence distraction from awareness of life problems. Accordingly, most
behavioural treatments have used various techniques derived from operant or classical conditioning
techniques in an attempt to counter-condition the arousal/excitement associated with gambling
(e.g., aversion therapy) or to produce extinction of arousal through a process of repeated exposure to
gambling cues (exposure therapy).
Early behavioural interventions utilised aversive procedures, such as the pairing of electric shock
with gambling cues, to counter-condition the arousal. Covert sensitisation is one type of aversion
therapy in which the aversive stimuli are presented in the form of negative imagery (e.g., vividly
imagining oneself losing vast sums of money and its negative consequences). The small sample
sizes and lack of comparison groups involved in most early studies preclude an assessment of the
overall effectiveness of these interventions. However, they appear to have a success rate of around
20–30 per cent (McConaghy, Armstrong, Blaszczynski, & Allcock, 1983; McConaghy, Blaszczynski,
& Frankova, 1991).
In recent decades, behavioural techniques have been combined with cognitive techniques in
cognitive behavioural treatments (Dowling, Smith, & Trang, 2006; Gooding & Tarrier, 2009; de
Lisle, Dowling, & Allen, 2011). Cognitive therapy aims to challenge the dysfunctional beliefs that
are thought to result in problem behaviours. The majority of gamblers are realistic in that they hope
to win but expect to lose. Yet a small percentage of individuals gamble to excess due to a range of
irrational beliefs in which the likelihood of winning is overestimated. Cognitive therapy is designed
to identify common cognitive errors and to correct these by providing accurate information on the
nature, operation and probabilities of winning associated with specific forms of gambling.
While a number of psychological variables (such as depression, poor stress management and limited
coping skills) maintain patterns of gambling behaviour, the primary motivation for gambling is linked
to winning. Many gamblers offer the explanation that they gamble for fun, for social reasons or as an
escape from emotional distress. However, it is the possibility of winning that generates excitement
leading to changes in negative mood states: playing games or picking winners rapidly dissolves into
boredom if there is no prize offered. Cognitive therapy, therefore, targets the core belief that gambling
represents a source of income and that one can win back losses.
A key technique of cognitive therapy is cognitive restructuring, which aims to map out the major
cognitive distortions held by the individual with a gambling problem and to replace these irrational
beliefs with rational ones. Irrational beliefs targeted in therapy include a lack of awareness regarding
the concept of randomness and the mutual independence of chance events (i.e., the gambler’s fallacy).
Here, individuals with a gambling problem may fail to realise that the outcome of a dice throw or coin
toss, for example, has absolutely no influence on the outcome of the next dice throw or coin toss. Thus
they may continue to gamble after a series of tails, for example, believing that a coin toss of heads
is highly likely on the next toss. Another common error is the illusion of control in which people
overestimate their level of skill and consequently their likelihood of winning. While the level of skill
involved in games and events may vary from absolutely no skill (as in electronic gaming machines)
to some skill (as in knowledge of the form in horse-racing and sports betting), chance, by definition,
plays a significant part in determining the outcome of any gamble.
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The following dialogue between a therapist and patient with problem gambling provides an
illustration of cognitive restructuring. The therapist and patient have identified that one of the patient’s
dysfunctional beliefs is an illusion of control. The therapist seeks to challenge the irrational nature of
this belief and help the patient to replace it with a more rational belief.
Patient: The way I press the button on a gaming machine increases my chance of winning. It’s a
skill that gives me an advantage over other players.
Therapist: If pressing the button the way you do is a skill that leads to your winning, is there any
evidence that your skill has improved with practice? Like any skill, I would presume
that the more you practised the better your skill would become?
Patient: Well, now that you mention it, I don’t seem to be getting any better at it. In fact, I’m still
losing more than I win and falling behind.
Therapist: That’s because the outcome of each game is determined by a random number
generator—that is, pure chance. Nothing that a player does can influence the random
outcome.
Echeburua, Baez, and Fernandez-Montalvo (1996) sought to investigate the benefits of behavioural
techniques, cognitive techniques and their combination in the treatment of pathological gambling.
Sixty-four participants with pathological gambling who were electronic gaming machine players were
randomly assigned to six weeks of exposure therapy, cognitive restructuring, a combination of these
two interventions or a wait-list control. The exposure therapy involved in vivo (real-life) exposure
to a gambling situation in the absence of placing bets or acting on other impulses, while cognitive
restructuring entailed identifying and challenging irrational beliefs related to excessive gambling. The
results indicated that most patients improved following treatment, with the highest success rate in
the exposure therapy condition. Specifically, participants allocated to the wait-list control achieved a
six-month success rate of 25 per cent compared to a rate of 62 per cent for cognitive therapy, 75 per cent
for exposure therapy and 37 per cent for a combination of both approaches. The authors acknowledged
that the combined program may not have given participants sufficient time to adequately learn either
the cognitive or the behavioural skills, given that the intervention was brief (only six weeks). A
follow-up conducted 12 months later indicated that the exposure therapy and combined approaches
maintained their original proportions of participants reporting success. However, the proportion of
participants in the cognitive restructuring group reporting success reduced to 37 per cent, indicating
that future cognitive approaches need to include strategies designed to maintain treatment gains
(e.g., extending the length of treatment to allow individuals more time to learn the skills of cognitive
restructuring on their own without the assistance of a therapist).
A systematic review of therapies for gambling disorder indicates clear support for the effectiveness
of cognitive behavioural interventions (Cowlishaw et al., 2012). Similar to the treatment of substance
use, motivational interviewing also forms an important intervention with demonstrated effectiveness
in reducing problem gambling (Hodgins, Currie, & el-Guebaly, 2000) and in retaining gamblers in
treatment (Wulfert, Blanchard, Freidenberg, & Martell, 2006).
PHARMACOLOGICAL INTERVENTIONS
Although currently there is no approved pharmacological treatment specific to pathological gambling,
several types of medication have shown the potential to be effective in some cases. These include
serotonin reuptake inhibitors (SSRIs; fluvoxamine and paroxetine), opioid antagonists (naltrexone)
and mood stabilisers (lithium).
However, the small number of trials conducted to date have shown mixed outcomes (Hollander,
Kaplan, & Pallanti, 2004; Petry, 2005). Contributing to this confusion are the high treatment dropout
rates, short follow-up periods (so that the maintenance of treatment improvements over time remains
unknown) and varied measures used to assess treatment outcome (which makes it difficult to compare
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the findings across studies). In general, it is recommended that SSRIs be used for individuals with
pathological gambling who have comorbid depression, mood stabilisers where there is evidence of
cyclothymic or bipolar mood disturbances, and naltrexone in cases of concurrent alcohol dependence. By
improving these comorbid conditions, the individual may be more able to overcome problem gambling.
THE PUBLIC HEALTH MODEL

Korn and Shaffer (1999) and Korn (2002) applied the public health model to gambling. The public
health model is predominantly concerned with the external societal determinants of gambling and less
with individual biological and psychological variables. It adopts a consumer-protection approach to
problem gambling by pursuing strategies designed to restrict the availability of gambling within the
community and by changing sociocultural attitudes and government policies.
The core premise of the public health approach is that exposure to gambling (by analogy, equivalent
to exposure to germs) is a necessary but not sufficient factor that ‘infects’ or shapes an individual’s
pattern of gambling behaviour. It is argued that the risk for problem gambling is related to: (a) the
duration of exposure to gambling, and (b) the addictive quality of the type of available gambling, in
that some forms of gambling, (e.g., electronic gaming machines) are more ‘addictive’ than others
(e.g., lotteries) as a result of their structural characteristics. That is, electronic gaming machines allow
high-frequency continuous play over extended periods of time, in contrast to a lottery, which is a
single event that is generally drawn weekly.
In general, the public health approach is designed to reduce population-based risk factors by
implementing strategies designed to restrict exposure to gambling and to promote a climate of
responsible gambling. This is achieved by policies limiting the number of gambling venues, placing
caps on the total number of electronic gaming machines, restricting trading hours and educating and
informing the public of the risks associated with gambling.
Public health initiatives appear to be effective in increasing the awareness of the risks of
gambling and in promoting responsible gambling practices, but more research is needed before a
clear understanding can be achieved of which strategies are most beneficial. Educating children on
probabilities and the nature of gambling, as well as teaching resilience skills (e.g., enhancing self-
esteem), have been shown to influence attitudes and participation in gambling among samples of
adolescents (Derevensky & Gupta, 2004).
CASE STUDY: COGNITIVE THERAPY FOR A PROBLEM GAMBLER

Rowan, a 32-year-old married electrician, first began wagering on his favourite football team during his apprenticeship
ten years ago. He and his fellow apprentices would discuss upcoming games and debate which team would be ahead at
the final whistle. Initially, it was friendly chatting, but at one point one apprentice challenged the group ‘to put their money
where their mouth is’ for the weekend’s games, with the winner taking all. On the Monday, Rowan successfully picked
seven winners from the eight games and won the pool. The group repeated the competition the following weekend,
and this soon became a regular activity. He found that he enjoyed this and quickly developed a reputation for being a
very good judge of team outcomes. This bolstered his self-esteem and he found himself looking forward to each week’s
football competition round.
This pattern of weekly betting continued for two years, with any wins frequently reinforcing his belief that he had
above-average skills in picking winners. Rowan then decided to apply his skills to betting with bookies. This decision
was fuelled by his increasing confidence that he could win more than was possible from just betting with his workmates.
He opened up an account with one of the online sports betting operators that he noticed from frequent advertisements
on television and on the playing field. He was happy with the free bonus bets offered when he first opened the account.
Initially, he restricted his betting to the weekend games. Eventually, after a few big wins, he decided to increase the size
of his bets on the online account. Given the ease with which he could now bet on midweek games using his smartphone,
even when at work, he also began to increase the frequency of his betting. He reported that he usually won and was
ahead by several thousand dollars.
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Rowan soon found it more and more difficult to focus on his work as he became preoccupied with reading the latest
news on the teams’ performances. As a consequence, his work performance deteriorated. This resulted in conflicts
with his fellow workers and supervisors, particularly given that all he spoke about was sports and betting during breaks
at work.
Rowan began to experience some minor depression in response to the conflict with his supervisor. However,
he continued experiencing excitement in anticipation of the outcome of football games, and as his interest in other
sporting events began to increase, the time and money he spent soon escalated. He found his involvement in sports
betting enabled him to ‘zone out’ and forget about daily stresses at work and home. While his wife was completely
unaware of his sports betting given that all of his activities were confined to betting via his smartphone, he tended to
feel guilty when betting, knowing that she would be angry if she found out what he was doing and how much money
was being lost.
Interestingly, Rowan held the strong belief that he was ahead with his sports betting despite his increasing losses. He
selectively remembered wins over losses and therefore believed that he was a good gambler since he often picked the
winning team. He stated that he would be well ahead if it were not for the fact that referees influenced play and resulted
in the team he selected losing.
Eventually Rowan’s debts became excessive and his wife finally discovered that he had lost his money gambling. He
reluctantly acquiesced to her pressure and sought treatment but persisted in betting on some sports. He maintained that
he had great skills in picking winning teams so his therapist decided to challenge his beliefs. He was asked to select
teams but refrain from gambling for two weeks and to monitor the outcome of his selections. This monitoring established
the fact that, on average, most teams he selected lost and that his belief in his skills were over-rated and unfounded. He
realised in therapy that his mistaken belief that he won money was partly based on his faulty tendency to recall wins and
not losses.
SUMMARY
Both substance use disorders and gambling disorder entail persistent engagement in the behaviour despite the multiple and
severe problems the individual encounters as a result of this behaviour. It is this characteristic that renders these disorders a
challenge both in terms of understanding their aetiology and in developing effective treatments.
Numerous substances are recognised in the DSM-5 as potentially entailing a substance use disorder, including alcohol,
amphetamines, cocaine, cannabis, hallucinogens, inhalants, nicotine, opioids and sedatives. The comorbid medical and
psychological disorders, as well as elevated mortality (e.g., through overdose, accidents or infectious diseases), among those with
a substance use disorder highlight the importance of research on these conditions.
Substance use disorders predominantly affect young men. Understanding the aetiology of these conditions continues to be
an area of development. Research to date suggests that substance use disorders occur due to a wide variety of factors, including
genes, neurobiological processes, learned behaviours, personality factors, cognitive processes, family and peer influences and
cultural norms.
The need for accurate diagnosis, early intervention, treatment and relapse prevention is paramount for individuals with a
substance use disorder to benefit both themselves and the broader community. There is a range of effective treatments that draw
on psychological approaches (such as motivational interviewing, brief interventions and skills training) and pharmacological options.
Gambling is a popular recreational activity, with the majority of individuals gambling within affordable limits. However,
approximately 0.2–4.0 per cent of the adult population experience a gambling disorder depending on the criteria and methodologies
applied, with a higher rate of 5 per cent exhibited by adolescents. The twelve-month prevalence rate across countries is
2.3 per cent. In Australia, the rate hovers just under 1 per cent. In addition to financial problems, this group suffers high rates of
depression, substance use disorders, employment difficulties and criminal offences motivated by a drive to maintain their gambling.
Multiple factors are involved in the aetiology of gambling disorder. Most aetiological models of gambling focus on one component
but recognise that complex interactions exist between biological, personality, cognitive, behavioural and environmental variables.
The integrated pathways model is a conceptual model that integrates the multitude of aetiological factors into a coherent framework
that recognises different subtypes among those with pathological gambling and thereby guides treatment. To date, cognitive
behaviour therapy has received the strongest support in the management of pathological gambling, with success rates in the vicinity
of 75 per cent.
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KEY TERMS
classical conditioning . . . . . . . . . . . . . 294 instrumental (or operant) personality disorder. . . . . . . . . . . . . . . 311
disease model of addiction . . . . . . . . 292 learning model. . . . . . . . . . . . . . . . . 294 sensation seeking . . . . . . . . . . . . . . . . 310
dopamine. . . . . . . . . . . . . . . . . . . . . . . . 310 noradrenaline. . . . . . . . . . . . . . . . . . . . 310 serotonin. . . . . . . . . . . . . . . . . . . . . . . . 310
endogenous opioid system . . . . . . . . 293 operant (instrumental) synthetic drugs. . . . . . . . . . . . . . . . . . . 287
impulsivity. . . . . . . . . . . . . . . . . . . . . . . 295 conditioning . . . . . . . . . . . . . . . . . . . 311
REVIEW QUESTIONS
LO 10.1
10.1 Describe the criteria required for the diagnosis of a substance use disorder.
10.2 Appraise the notion that alcohol use is a more important health problem than heroin use in Australia.
10.3 Describe the problems associated with substance use by older people.
10.4 Compare the explanations for relapse offered by two theories regarding substance use disorders.
10.5 Contrast detoxification and pharmacological treatments for substance use disorders.
LO 10.2
10.6 What is the difference between ‘pathological’ and ‘problem’ gambling, and what are the diagnostic criteria for
gambling disorder?
10.7 Contrast the different aetiological models explaining pathological gambling.
10.8 Pathological gamblers represent a heterogeneous group of individuals. What are the various subtypes of
gamblers?
10.9 What are the most common comorbid conditions found among gamblers?
10.10 What are the implications of technological advances on the prevalence of pathological gambling?
REFERENCES
Abbott, M. (2006). Do EGMs and problem gambling go together like Australian Gaming Council (2007). A database on Australia’s
a horse and carriage? Gambling Research, 18, 7–38. gambling industry 2006/07. Melbourne: Author.
Agrawal, A., & Lynskey, M. T. (2008). Are there genetic influences Australasian Gaming Council (2012). A database on Australia’s
on addiction: Evidence from family, adoption and twin studies. gambling industry 2011/12. Melbourne: Author.
Addiction, 103, 1069–1081. Australasian Gaming Council (2016). A guide to Australasia’s
American Psychiatric Association (1980). Diagnostic and gambling industry 2015/16. Melbourne: Author.
statistical manual of mental disorders (3rd ed.). Washington, DC: Australian Government Department of Health (2016). Post-
Author. implementation review: Tobacco plain packaging. Retrieved from
American Psychiatric Association (1986). Diagnostic and statistical http://ris.pmc.gov.au/sites/default/files/posts/2016/02/Tobacco-
manual of mental disorders (3rd ed. revised). Washington, DC: Plain-Packaging-PIR.pdf.
Author. Australian Institute of Health and Welfare (2011). Drugs in Australia
American Psychiatric Association (2000). Diagnostic and statistical 2010: Tobacco, alcohol and other drugs. Drug statistics series no.
manual of mental disorders (4th ed. text revision). Washington, 27 (cat. no. PHE 154). Canberra: Author.
DC: Author. Australian Institute of Health and Welfare (2014). 2013 National
American Psychiatric Association (2013). Diagnostic and statistical Drug Strategy Household Survey. Drug statistics series no. 25 (cat.
manual of mental disorders (5th ed.). Arlington: Author. no. PHE 183). Canberra.
Anderson, G., & Brown, R. I. F. (1984). Real and laboratory Australian Medical Association (2016). Alcohol-related violence
gambling: Sensation-seeking and arousal. British Journal of [updated 2016; cited 31 Mar 2017. Retrieved from https://ama
Psychology, 75, 401–410. .com.au/ausmed/alcohol-related-violence.
rie66620_ch10_281-326.indd 320 07/31/17 05:22 PM

Australian Psychological Society (2013). The increasing harm from Colliver, J. D., Compton, W. M., Gfroerer, J. C., & Condon, T.
advertising and promotion of gambling in sport. Retrieved from (2006). Projecting drug use among aging baby boomers in 2020.
https://www.psychology.org.au/publications/inpsych/2013/june/ Annals of Epidemiology, 16, 257–265.
gambling/. Comings, D. E., & Blum, K. (2000). Reward deficiency syndrome:
Awissi, D.-K., Lebrun, G., Coursin, D. B., Riker, R. R., & Skrobik, Y. Genetic aspects of behavioural disorders. Progress in Brain
(2013). Alcohol withdrawal and delirium tremens in the critically Research, 126, 325–341.
ill: A systematic review and commentary. Intensive Care Medicine, Commonwealth of Australia Department of the Prime Minister
39, 16–30. and Cabinet (2015). Final report of the National Ice Taskforce.
Begg, S., Vos, T., Barker, B., Stevenson, C., Stanley, J. C., & Lopez, A. Canberra: Author.
D. (2007). The burden of disease and injury in Australia 2003 (cat. Conrod, P. J., Stewart, S. H., Comeau, N., Maclean, A. M. (2006).
no. PE 82). Canberra: Australian Institute of Health and Welfare. Efficacy of cognitive–behavioral interventions targeting personality
Bergh, C., Eklund, T., Sodersten, P., & Nordin, C. (1997). Altered risk factors for youth alcohol misuse. Journal of Clinical Child and
dopamine function in pathological gambling. Psychological Adolescent Psychology, 35, 550–563.
Medicine, 27, 473–475. Coventry, K. R., & Brown, R. I. F. (1993). Sensation seeking,
Blaszczynski, A., & Farrell, E. (1998). A case series of 44 completed gambling and gambling addictions. Addiction, 88, 541–554.
gambling-related suicides. Journal of Gambling Studies, 14, Cowlishaw, S., Merkouris, S., Dowling, N., Anderson, C., Jackson,
93–109. A., & Thomas, S. (2012). Psychological therapies for pathological
Blaszczynski, A., & Nower, L. (2002). A pathways model of problem and problem gambling. Cochrane Database Systematic Reviews,
and pathological gambling. Addiction, 97, 487–499. 11, CD008937.
Blaszczynski, A., & Steel, Z. (1998). Personality disorders among Custer, R. L. (1984). Profile of the pathological gambler. Journal of
pathological gamblers. Journal of Gambling Studies, 14, 51–71. Clinical Psychiatry, 45, 35–38.
Blaszczynski, A., Wilson, A. C., & McConaghy, N. (1986). Sensation Darke, S., Degenhardt, L., & Mattick, R. P. (2007). Mortality
seeking and pathological gambling. British Journal of Addictions, amongst illicit drug users: Epidemiology, causes and intervention.
81, 113–117. Cambridge: Cambridge University Press.
Blum, K., Sheridan, P. J., Wood, R. C., Braverman, E. R., Chen, T. J., Degenhardt, L., Roxburgh, A., & McKetin, R. (2007). Hospital
Cull, J. G., & Comings, D. E. (1996). The D2 dopamine receptor separations for cannabis- and methamphetamine-related psychotic
gene as a determinant of reward deficiency syndrome. Journal of episodes in Australia. Medical Journal of Australia, 186,
the Royal Society of Medicine, 89, 396–400. 342–345.
Breen, H., & Gainsbury, S. (2103). Aboriginal gambling and problem Degenhardt, L., Larney, S., Dobbins, T., Chan, G., Weier, M.,
gambling: A review. International Journal of Mental Health and Roxburgh, A., Hall, W., & McKetin, R. (2016). Estimating the
Addiction, 11, 75–96. number of regular and dependent methamphetamine users in
Breen, R. B., & Zuckerman, M. (1999). ‘Chasing’ in gambling Australia, 2002–2014. Medical Journal of Australia, 204, 153.
behaviour: Personality and cognitive determinants. Personality and de Lisle, S., Dowling, N., & Allen, J. (2011). Mindfulness-based
Individual Differences, 27, 1097–1111. cognitive therapy for problem gambling. Clinical Case Studies, 10,
Brenner, R., & Brenner, G. A. (1990). Gambling and speculation: 210–228.

A theory, a history, and a future of some human decisions. Derevensky, J., & Gupta, R. (Eds.) (2004). Gambling problems in
Cambridge: Press Syndicate University of Cambridge. youth: Theoretical and applied perspectives. New York: Kluwer
Budney, A. J., & Hughes, J. R. (2006). The cannabis withdrawal Academic/Plenum Publishers.
syndrome. Current Opinion in Psychiatry, 19, 233–288. Dostoyevsky, F. (1866/1978). The gambler. London: Penguin Books.
Bujarski, S., O’Malley, S. S., Lunny, K., & Ray, L. A. (2013). The Dowling, N., Smith, D., & Trang, T. (2006). Treatment of female
effects of drinking goal on treatment outcome for alcoholism. pathological gambling: The efficacy of a cognitive-behavioural
Journal of Consulting and Clinical Psychology, 81, 13–22. approach. Journal of Gambling Studies, 22, 355–372.
Carroll, K. M., Ball, S. A., Martino, S., Nich, C., Babuscio, T. A., Echeburua, E., Baez, C., & Fernandez-Montalvo, J. (1996).
Nuro, K. F., . . . Rounsaville, B. J. (2008). Computer-assisted Comparative effectiveness of three therapeutic modalities in the
delivery of cognitive-behavioral therapy for addiction: A psychological treatment of pathological gambling: Long-term
randomized trial of CBT4CBT. American Journal of Psychiatry, outcome. Behavioural and Cognitive Psychotherapy, 24, 51–72.
165, 881–888. Edwards, G., & Gross, M. M. (1976). Alcohol dependence:
Chang, C.-K., Hayes, R. D., Perera, G., Broadbent, M. T. M., Provisional description of a clinical syndrome. British Medical
Fernandes, A. C., Lee, W. E., . . . Stewart, R. (2011). Life Journal, 1, 1058–1061.
expectancy at birth for people with serious mental illness and other Fauth-Buhler, M., Mann, K., & Potenza, M. (2016). Pathological
major disorders from a secondary mental health care case register gambling: A review of the neurobiological evidence relevant
in London. PLoS ONE, 6, e0019590. for its classification as an addictive disorder. Addiction Biology.
Cloninger, C. R. (1987). A systematic method for clinical description doi:10.1111/adb.12378
and classification of personality variants. Archives of General Ferris, J., & Wynne, H. (2001). The Canadian Problem Gambling
Psychiatry, 44, 573–588. Index: Report to the Canadian Inter-Provincial Advisory
Collins, P., & Barr, G. (2006). The National 2006 Prevalence Study: Committee. Ottawa: Canadian Centre for Substance Abuse.
Gambling and problem gambling in South Africa. Cape Town: Fleming, M. F., Mundt, M. P., French, M. T., Manwell, L. B.,
National Centre for the Study of Gambling. Stauffacher, E. A., & Barry, K. L. (2000). Benefit-cost analysis
rie66620_ch10_281-326.indd 321 07/31/17 05:22 PM

of brief physician advice with problem drinkers in primary care Herman, R. D. (1976). Gamblers and gambling. New York: Harper
settings. Medical Care, 38, 7–18. & Row.
Frei, M., Berends, L., Kenny, P. A. S., Jenner, L., Hunter, B., & Hides, L., Carroll, S., Scott, R., Cotton, S., Baker, A., & Lubman, D.
Mugavin, J. (2012) Alcohol and other drug withdrawal: Practice I. (2013). Quik Fix: A randomized controlled trial of an enhanced
guidelines (2nd ed.). Fitzroy: Turning Point Alcohol and Drug brief motivational interviewing intervention for alcohol/cannabis
Centre. and psychological distress in young people. Psychotherapy and
Freud, S. (1928). Dostoyevsky and parricide. In Complete Psychosomatics, 82, 122–124.
psychological works of Sigmund Freud (standard edition). London: Hing, N. (2014). Sports betting and advertising (AGRC Discussion
Hogarth Press. Paper No. 4). Melbourne Australian Gambling Research
Gaboury, A., & Ladouceur, R. (1989). Erroneous perceptions and Centre. Retrieved from: https://aifs.gov.au/agrc/sites/default/files/
gambling. Journal of Social Behavior and Personality, 4, 411–420. publication-documents/agrc-dp4-sports-betting.pdf.
Gainsbury, S. (2012). Internet gambling: Current research findings Hing, N., Cherney, L., Blaszczynski, A., Gainsbury, S. M., &
and implications. New York: Springer. Lubman, D. I. (2014). Do advertising and promotions for online
Gainsbury, S. M., Russell, A., Hing, N., Wood, R., Lubman, D. I., gambling increase gambling consumption? An exploratory study.
& Blaszczynski, A. (2014). The prevalence and determinants of International Gambling Studies, 14, 394–409. doi:http://dx.doi.org/
problem gambling in Australia: Assessing the impact of interactive 10.1080/14459795.2014.903989
gambling and new technologies. Psychology of Addictive Hisahara, S., & Shimohama, S. (2011). Dopamine receptors and
Behaviors, 28, 769–779. doi:10.1037/a0036207 Parkinson’s disease. International Journal of Medicinal Chemistry,
Gainsbury, S., Wood, R., Russell, A., Hing, N., & Blaszczynski, 16, 1–16.
A. (2012). A digital revolution: Comparison of demographic Hodgins, D. C., Currie, S. R. & el-Guebaly, N. (2000). Motivational
profiles, attitudes and gambling behaviour of internet and enhancement and self-help treatments for problem gambling.
non-internet gamblers. Computers in Human Behavior, 28, Journal of Consulting and Clinical Psychology, 69, 50–57.
1388–1398. Holden, C. (2001). ‘Behavioral’ addictions: Do they exist? Science,
Gambino, B., Fitzgerald, R., Shaffer, H., Renner, J., & Courtnage, P. 294, 980–982.
(1993). Perceived family history of problem gambling and scores Hollander, E., Kaplan, A., & Pallanti, S. (2004). Pharmacological
on SOGS. Journal of Gambling Studies, 9, 169–184. treatments. In J. E. Grant & M. N. Potenza (Eds.), Pathological
Gamblers Anonymous (1977). Gamblers Anonymous Leaflet. Los gambling: A clinical guide to treatment (pp. 189–206). Washington,
Angeles: Gamblers Anonymous Publishing. DC: American Psychiatric Association.
Gilligan, S. B., Reich, T., & Cloninger, C. R. (1987). Etiologic Humensky, J. L. (2010). Are adolescents with high socioeconomic
heterogeneity in alcoholism. Genetic Epidemiology, 4, 395–414. status more likely to engage in alcohol and illicit drug use in early
Goldstein, R., & Volkow, N. (2002). Drug addiction and its adulthood? Substance Abuse Treatment, Prevention, and Policy,
underlying neurobiological basis: Neuroimaging evidence for the 5, 19.
involvement of the frontal cortex. American Journal of Psychiatry, Jacobs, D. F. (1986). A general theory of addictions: A new theoretical
159, 1642–1652. model. Journal of Gambling Behavior, 2, 15–31.
Gooding, P., & Tarrier, N. (2009). A systematic review and meta- Kirchmayer, U., Davoli, M., & Verster, A. (2004). Naltrexone
analysis of cognitive-behavioural interventions to reduce problem maintenance treatment for opioid dependence. Chichester: John
gambling: Hedging our bets. Behaviour Research and Therapy, 47, Wiley.
592–607. Knight, B., Hichens, C., & Worthington, E. (2016). Rehab Inc:
Goudriaan, A. E., Oosterlaan, J., de Beurs, E., & van den Brink, The high price parents pay to get their kids off ice. Four Corners,
W. (2004). Pathological gambling: A comprehensive review of 12 September. Retrieved from http://www.abc.net.au/4corners/
biobehavioral findings. Neuroscience and Biobehavioral Review, stories/2016/09/12/4535254.htm.
28, 123–141. Korn, D. (2002). Examining gambling issues from a public health
Gracey, M., & King, M. (2009). Indigenous health part 1: perspective. Electronic Journal of Gambling Issues. Retrieved
Determinants and disease patterns. The Lancet, 374, 65–75. from http://www.collectionscanada.gc.ca/eppp-archive/100/202/
Hardoon, K. K., & Derevensky, J. (2002). Child and adolescent 300/e-gambling/html/2004/no10/archive/pdf/Egambling-All7.pdf.
behaviour: Current knowledge. Clinical Child Psychology and Korn, D. A., & Shaffer H. J. (1999). Gambling and the health of the
Psychiatry, 7, 263–281. public: Adopting a public health perspective. Journal of Gambling
Hartmann, M., & Blaszczynski, A. (2016). The longitudinal Studies, 15, 289–365.
relationship between psychiatric disorders and gambling disorders. Kunøe, N., Lobmaier, P., Ngo, H., & Hulse, G. K. (2014). Injectable and
International Journal of Mental Health and Addiction. doi:10.1007/ implantable sustained release naltrexone in the treatment of opioid
s11469-016-9705-z addiction. British Journal of Clinical Pharmacology, 77, 264–271.
Hawton, K., & Harriss, L. (2007). Deliberate self-harm in young Kushner, M. G., Abrams, K., Thuras, P., & Hanson, K. L. (2000).
people: Characteristics and subsequent mortality in a 20-year Individual differences predictive of drinking to manage anxiety
cohort of patients presenting to hospital. Journal of Clinical among non-problem drinkers with panic disorder. Alcoholism:
Psychiatry, 68, 1574–1583. Clinical and Experimental Research, 24, 448–458.
Heather, N. (2006) Controlled drinking, harm reduction and their Ladouceur, R., Jacques, C., Ferland, F., & Giroux, I. (1999).
roles in the response to alcohol-related problems. Addiction Prevalence of problem gambling: A replication study seven years
Research and Theory, 14, 7–18. later. Canadian Journal of Psychiatry, 44, 802–804.
rie66620_ch10_281-326.indd 322 07/31/17 05:22 PM

Ladouceur, R., & Mireault, C. (1988). Gambling behaviors among McConaghy, N., Blaszczynski, A., & Frankova, A. (1991).
high school students in the Quebec area. Journal of Gambling Comparison of imaginal desensitisation with other behavioural
Behavior, 4, 3–12. treatments of pathological gambling: A two to nine year follow-up.
Laslett, A. M., Catalano, P., Chikritzhs, T., Dale, C., Doran, C., British Journal of Psychiatry, 159, 390–393.
Ferris, J., . . . Wilkinson, C. (2010). The range and magnitude of McKetin, R., Lubman, D. I., Lee, N. M., Ross, J. E., & Slade, T.
alcohol’s harm to others. Melbourne: AER Centre for Alcohol N. (2011). Major depression among methamphetamine users
Policy Research, Turning Point Alcohol and Drug Centre, Eastern entering drug treatment programs. Medical Journal of Australia,
Health. 195, S51.
Lermontov, M. (1841/1979). The fatalist. In G. C. Blakey (Ed.), The McKetin, R., McLaren, J., Lubman, D. I., & Hides, L. (2006). The
gambler’s companion (pp. 309–317). New York: Paddington Press. prevalence of psychotic symptoms among methamphetamine
Leshner, A. I. (1997). Addiction is a brain disease, and it matters. users. Addiction, 101, 1473–1478.
Science, 278, 45–47. McKetin, R., Najman, J. M., Baker, A. L., Lubman, D. I., Dawe, S.,
Lesieur, H. R., & Blume, S. B. (1987). The South Oaks Gambling Ali, R.,  . . 
. 
Mamun, A. (2012). Evaluating the impact of
Screen (SOGS): A new instrument for the identification of community-based treatment options on methamphetamine use:
pathological gamblers. American Journal of Psychiatry, 144, Findings from the Methamphetamine Treatment Evaluation Study
1184–1188. (MATES). Addiction, 107, 1998–2008.
Lesieur, H. R., & Rosenthal, R. J. (1991). Pathological gambling: A McKetin, R., Quinn, C., Groves, G., McLaren, J., & Kelly, E. (2005).
review of the literature. Journal of Gambling Studies, 7, 5–39. Methamphetamine: Physical forms, purity and terminology.
Li, M. D., & Burmeister, M. (2009). New insights into the genetics of In R. McKetin, J. McLaren, & E. Kelly (Eds.), The Sydney
addiction. Nature Review Genetics, 10, 225–231. methamphetamine market: Patterns of supply, use, personal harms
Lingford-Hughes, A. R., Davies, S. J. C., McIver, S., Williams, T. M., and social consequences. NDLERF Monograph Series No. 13
Daglish, M. R. C., & Nutt, D. J. (2003). Addiction. British Medical (pp. 16–24). National Drug Law Enforcement Research Fund.
Bulletin, 65, 209–222. Michie, S., Whittington, C., Hamoudi, Z., Zarnani, F., Tober, G., &
Lobmaier, P. P., Kunøe, N., Gossop, M., & Waal, H. (2011). West, R. (2012). Identification of behaviour change techniques
Naltrexone depot formulations for opioid and alcohol dependence: to reduce excessive alcohol consumption. Addiction, 107,
A systematic review. CNS Neuroscience and Therapeutics, 17, 1431–1440.
629–636. Miller, W. R., & Rollnick, S. (2013). Motivational interviewing:
Lubman, D. I., Yucel, M., & Pantelis, C. (2004). Addiction, a condition Helping people change (3rd ed.). New York: Guilford Press.
of compulsive behaviour? Neuroimaging and neuropsychological Mills, K. L., Teesson, M., Ross, J., & Peters, L. (2009). Trauma,
evidence of inhibitory dysregulation. Addiction, 99, 1491–1502. PTSD, and substance use disorders: Findings from the Australian
Lundahl, B., Moleni, T., Burke, B. L., Butters, R., Tollefson, D., National Survey of Mental Health and Well-Being. American
Butler, C., & Rollnick, S. (2013). Motivational interviewing in Journal of Psychiatry, 163, 652–658.
medical care settings: A systematic review and meta-analysis of Ministry of Health (2010) Drug use in New Zealand: Key results
randomized controlled trials. Patient Education and Counseling, of the 2007/08 New Zealand Alcohol and Drug Use Survey,
93, 157–168. Wellington, Ministry of Health.

Magill, M., & Ray, L. A. (2009). Cognitive-behavioral treatment with Ministry of Health (2015). Annual update of key results 2014/15:
adult alcohol and illicit drug users: A meta-analysis of randomized New Zealand Health Survey Wellington, Ministry of Health.
controlled trials. Journal of Studies on Alcohol and Other Drugs, O’Donnell, A., Anderson, P., Newbury-Birch, D., Schulte, B.,
70, 516–527. Schmidt, C., Reimer, J., & Kaner, E. (2014). The impact of brief
Mark, M. E., & Lesieur, H. R. (1992). A feminist critique of problem alcohol interventions in primary healthcare: A systematic review
gambling research. British Journal of Addiction, 87, 549–565. of reviews. Alcohol & Alcoholism, 49, 66–78.
Marlatt, G. A., & Donovan, D. M. (2005). Relapse prevention, second O’Farrell, B. (2015). Review of illegal offshore wagering. Canberra:
edition: Maintenance strategies in the treatment of addictive Commonwealth of Australia (Department of Social Services).
behaviors, New York: Guilford Press. Parliamentary Joint Select Committee on Gambling Reform (2013).
Marlatt, G. A., & Gordon, J. R. (1985). Relapse prevention: The advertising and promotion of gambling services in sport.
Maintenance strategies in the treatment of addictive behaviors. Canberra: Commonwealth of Australia.
New York: Guilford Press. Pelletier, M., & Ladouceur, R. (2007). The effect of knowledge of
Martin, G., Swannell, S. V., Hazell, P. L., Harrison, J. E., & Taylor, A. mathematics on gambling behaviours and erroneous perceptions.
W. (2010). Self-injury in Australia: A community survey. Medical International Journal of Psychology, 42, 134–140.
Journal of Australia, 193, 506–510. Petry, N. M. (2005). Pathological gambling: Etiology, comorbidity, and
Mattick, R. P,. Breen, C., Kimber, J., & Davoli, M. (2014). treatment. Washington, DC: American Psychological Association.
Buprenorphine maintenance versus placebo or methadone Potenza, M. N., Steinberg, M. A., & McClaughlin, S. D. (2001).
maintenance for opioid dependence. Cochrane Database of Gender-related differences in the characteristics of problem gamblers
Systematic Reviews, 2. using a gambling helpline. American Journal of Psychiatry, 158,
McConaghy, N., Armstrong, M. S., Blaszczynski, A., & Allcock, C. 1500–1505.
(1983). Controlled comparison of aversive therapy and imaginal Powell, J., Hardoon, K., Derevensky, J., & Gupta, R. (1999).
desensitisation in compulsive gambling. British Journal of Gambling and risk-taking behaviour among university students.
Psychiatry, 142, 366–372. Substance Use and Misuse, 34, 1167–1184.
rie66620_ch10_281-326.indd 323 07/31/17 05:22 PM

Productivity Commission (1999). Australia’s gambling industries. Shaffer, H. J., Hall, M. N., & Vander Bilt, J. (1997). Estimating the
Canberra: Commonwealth of Australia. prevalence of disordered gambling behavior in the United States
Productivity Commission (2009). Gambling: Draft report. Canberra: and Canada: A research synthesis. American Journal of Public
Commonwealth of Australia. Health, 89, 1369–1376.
Productivity Commission (2010). Gambling: Report No. 50. Canberra: Shaffer, H. J., LaBrie, R. A., & LaPlante, D. (2004). Laying the
Commonwealth of Australia. foundation for quantifying regional exposure to social phenomena:
Purshouse, R. C., Brennan, A., Rafia, R., Latimer, N. R., Archer, R. J., Considering the case of legalised gambling as a public health toxin.
Angus, C. R., Preston, L. & Meier, P. S. (2013). Modelling the Psychology of Addictive Behaviors, 18, 40–48.
cost-effectiveness of alcohol screening and brief interventions in Shah, K., Potenza, M., & Eisen, S. (2004). Biological basis for
primary care in England. Alcohol and Alcoholism, 48, 180–188. pathological gambling. In J. E. Grant & M. N. Potenza (Eds.),
Pushkin, A. (1834/1999). The Queen of Spades. In The complete Pathological gambling: A clinical guide to treatment (pp. 127–142).
works of Alexander Pushkin. Norfolk: Milner & Company. Washington, DC: American Psychiatric Association.
Raylu, N., & Oei, T. (2002). Pathological gambling: A comprehensive Shand, F., Gates, J., Fawcett, J., & Mattick, R. P. (2003). The
review. Clinical Psychology Review, 22, 1–53. treatment of alcohol problems: A review of the evidence. Canberra:
Reich, R. R., Goldman, M. S., & Noll, J. A. (2004). Using the false Commonwealth of Australia.
memory paradigm to test two key elements of alcohol expectancy Shen, X. Y., Orson, F. M., & Kosten, T. R. (2012). Vaccines against
theory. Experimental and Clinical Psychopharmacology, 12, drug abuse. Clinical Pharmacology and Therapeutics, 91, 60–70.
102–110. Skinner, B. F. (1953). Science and human behaviour. New York: Free
Riper, H., Spek, V., Boon, B., Conijn, B., Kramer, J., Martin-Abello, Press.
K., & Smit, F. (2011). Effectiveness of e-self-help interventions Skog, O. J. (2000). Addicts’ choice. Addiction, 95, 1309–1314.
for curbing adult problem drinking: A meta-analysis. Journal of Slade, T., Johnston, A., Teesson, M., Whiteford, H., Burgess, P.,
Medical Internet Research, 13, e42. Pirkis, J., & Saw, S. (2009). The Mental Health of Australians
Robinson, T. E., & Berridge, K. C. (2003). Addiction. Annual Review 2. Report on the 2007 National Survey of Mental Health and
of Psychology, 54, 25–53. Wellbeing. Canberra: Department of Health and Ageing.
Roche, A. M., & McEntee, A. (in press). Ice and the outback: Patterns Slutske, W., Jackson, K. M., & Sher, K. J. (2003). The natural history
and prevalence of methamphetamine use in rural Australia. of problem gambling from age 18 to 29. Journal of Abnormal
Australian Journal of Rural Health. Psychology, 112, 263–274.
Rooke, S., Thorsteinsson, E., Karpin, A., Copeland, J., & Allsop, D. Sobell, M., & Sobell, L. (1993). Problem drinkers: Guided self-
(2010). Computer-delivered interventions for alcohol and tobacco change treatment. New York: Guilford Press.
use: A meta-analysis. Addiction, 105, 1381–1390. Sorock, G. S., Chen, L.-H., Gonzalgo, S. R., & Baker, S. P. (2006).
Rossow, I., & Kuntsche, E. (2013). Early onset of drinking and risk of Alcohol-drinking history and fatal injury in older adults. Alcohol,
heavy drinking in young adulthood—A 13-year prospective study. 40, 193–199
Alcoholism: Clinical and Experimental Research, 37, E297–E304. South Australian Centre for Economic Studies (2005). Problem
Roxburgh, A., Ritter, A., Grech, K., Slade, T., Burns, L. (2011). gambling and harm: A national definition. Adelaide: Author.
Trends in drug use and related harms in Australia, 2001 to 2011. Stead, L. F., Perera, R., Bullen, C., Mant, D., Hartmann-Boyce, J.,
Drug Policy Modelling Program. Sydney: National Drug and Cahill, K., & Lancaster, T. (2012). Nicotine replacement therapy
Alcohol Research Centre. for smoking cessation. The Cochrane Library 2012.
Roy, A., Adinoff, B., Roehrich, L., Lamparski, D., Custer, R., Steel, Z., & Blaszczynski, A. (1998). Impulsivity, personality disorders
Lorenz, V., . . . Linnoila, M. (1988). Pathological gambling: and pathological gambling severity. Addictions, 93, 895–905.
A psychobiological study. Archives of General Psychiatry, 45, Stewart, R., & Brown, R. I. F. (1988). An outcome study of Gamblers
369–373. Anonymous. British Journal of Psychiatry, 152, 284–288.
Saunders, B., & Wilkinson, C. (1990). Motivation and addiction Stone, A. L., Becker, L. G., Huber, A. M., & Catalano, R. F. (2012).
behaviour: A psychological perspective. Drug and Alcohol Review, Review of risk and protective factors of substance use and problem
9, 133–142. use in emerging adulthood. Addictive Behaviors, 37, 747–777.
Scholes-Balog, K. E., Hemphill, S., Reid, S., Patton, G. C., & Substance Abuse and Mental Health Services Administration (2013).
Toumbourou, J. W. (2013). Predicting early initiation of alcohol Systems-level implementation of screening, brief intervention,
use: A prospective study of Australian children. Substance Use and and referral to treatment. Rockville: Technical Assistance
Misuse, 48, 343–352. Publications.
Semple, D. M., McIntosh, A. M., & Lawrie, S. M. (2005). Cannabis Tait, R. J., Caldicott, D., Mountain, D., Hill, S. L, & Lenton, S.
as a risk factor for psychosis: Systematic review. Journal of (2016). A systematic review of adverse events arising from the use
Psychopharmacology, 19, 187–194. of synthetic cannabinoids and their associated treatment. Clinical
Shaffer, H. J. (2005). From disabling to enabling the public interest: Toxicology, 54, 1–13.
Natural transitions from gambling exposure to adaptation and self- Tait, R. J., & Christensen, H. (2010). Internet-based interventions
regulation. Addiction, 100, 1227–1229. for young people with problematic substance use: A systematic
Shaffer, H. J., & Hall, M. N. (1996). Estimating prevalence of review. Medical Journal of Australia, 192, S15–21.
adolescent gambling disorders: A quantitative synthesis and guide Tait, R. J., Spijkerman, R., & Riper, H. (2013). Internet and computer
toward standard gambling nomenclature. Journal of Gambling based interventions for cannabis use: A meta-analysis. Drug and
Studies, 12, 193–214. Alcohol Dependence, 33, 295–304.
rie66620_ch10_281-326.indd 324 07/31/17 05:22 PM

Tavares, H., Zilberman, M. L., Beites, F. J., & Gentil, V. (2001). A systematic review. Journal of Medical Internet Research,
Gender difference in gambling progression. Journal of Gambling 12, e62.
Studies, 17, 151–159. White, W. L. (2007). Addiction recovery: Its definition and
Teesson, M., Mills, K., Ross, J., Darke, S., Williamson, A., & Havard, conceptual boundaries. Journal of Substance Abuse Treatment, 33,
A. (2008). The impact of treatment on 3 years’ outcome for heroin 229–241.
dependence: findings from the Australian Treatment Outcome Wilcox, H. C., Conner, K. R., & Caine, E. D. (2004). Association
Study (ATOS). Addiction, 103, 80–88. of alcohol and drug use disorders and completed suicide: An
Thomas, S., Lewis, S., Duong, J., & McLeod, C. (2012). Sports empirical review of cohort studies. Drug and Alcohol Dependence,
betting marketing during sporting events: A stadium and broadcast 76 ( Supp.), S11–S19.
census of Australian Football League matches. Australian and New Williams, R. J., Hann, R. G., Schopflocher, D., West, B., McLaughlin,
Zealand Journal of Public Health, 36, 145–152. P., White, N., King, K., & Flexhaug, T. (2015). Quinte longitudinal
Toneatto, T., Blitz-Miller, T., Calderwood, K., Dragonetti, R., & study of gambling and problem gambling. Report prepared for the
Tsanos, A. (1997). Cognitive distortion in heavy gambling. Journal Ontario Problem Gambling Research Centre. Guelph, Ontario.
of Gambling Studies, 13, 253–266. Williams, R., Volberg, R., & Stevens R. (2012). The population
Trigo, J. M., Martin-García, E., Berrendero, F., Robledo, P., & prevalence of problem gambling: Methodological influences,
Maldonado, R. (2010). The endogenous opioid system: A common standardized rates, jurisdictional differences, and worldwide
substrate in drug addiction. Drug and Alcohol Dependence, 108, trends. Ontario: Ontario Problem Gambling Research Centre and
183–194. Ontario Ministry of Health and Long Term Care.
UK Drug Policy Commission (2008). The UK drug policy commission Wilson, M., Stearne, A., Gray, D., & Saggers, S. (2010). The harmful
recovery consensus group: A vision of recovery. London: Author. use of alcohol amongst Indigenous Australians. Retrieved from
United Nations Office on Drugs and Crime (2015). The challenge of www.healthinfonet.ecu.edu.au/alcoholuse_review.
synthetic drugs in East and South-East Asia and Oceania. Vienna: Winger, G., Woods, J. H., Galuska, C. M., & Wade-Galuska, T.
Global SMART Program, UNDOC. (2005). Behavioral perspectives on the neuroscience of drug
Victorian Responsible Gambling Foundation. (2015). The changing addiction. Journal of the Experimental Analysis of Behavior, 84,
gambling environment. Gambling Information Resource Office. 667–681.
Retrieved from https://www.responsiblegambling.vic.gov.au/__data/ Wise, R. A. (2002). Brain reward circuitry: Insights from unsensed
assets/pdf_file/0020/17705/GIRO-info-The-changing-gambling- incentives. Neuron, 36, 229–240.
environment.PDF. Wood, R., & Williams, R. (2011). A comparative profile of the
Volkow, N. D., Fowler, J. S., Wang, G. J., Baler, R., & Telang, F. internet gambler: Demographic characteristics, game play
(2009). Imaging dopamine’s role in drug abuse and addiction. patterns, and problem gambling status. New Media & Society, 13,
Neuropharmacology, 56 ( Supp. 1), 3–8. 1123–1141.
Walker, M. B. (1992). The psychology of gambling. Sydney: World Health Organization (1975). International classification of
Butterworth-Heinemann. diseases—revision 9. Retrieved from http://www.wolfbane.com/
Wardle, H., Moody, A., Griffiths, M., Orford, J., & Volberg, R. icd/icd9h.htm.
(2011). Defining the online gambler and patterns of behaviour World Health Organization (1992). The ICD-10 international
integration: Evidence from the British Gambling Prevalence statistical classification of diseases and related health problems.
Survey 2010. International Gambling Studies, 11, 339–356. V.1. Geneva: World Health Organization
Weintraub, D., Koester, L., Potenza, M. N., Siderowf, A. D., Stacy, World Health Organization (2017). International classification
M. A., Voon, V., . . . Lang, A. E. (2010). Impulse control disorders of diseases, tenth revision, clinical modification (ICD-10-CM).
in Parkinson disease: A cross sectional study of 3,090 patients. Geneva: World Health Organization. Retrieved from https://www.
Archives of Neurology, 67, 589–595. cdc.gov/nchs/icd/icd10cm.htm.
Wells, J. E., Baxter, J., & Schaaf, D. (2007). Substance use disorders Wulfert, E., Blanchard, E. B., Freidenberg, B. M., & Martell, R. S.
in Te Rau Hinengaro: The New Zealand Mental Health Survey. (2006). Retaining pathological gamblers in cognitive behavior
Wellington. Wellington: Alcohol Advisory Council of New therapy through motivational enhancement. Behavior Modification,
Zealand. 30, 315–340.
West, R. (2001). Theories of addiction. Addiction, 96, 3–13. Zheng, W., McLerran, D. F., Rolland, B. A., Fu, Z., Boffetta, P.,
West, R. (2013). The PRIME theory of motivation. Retrieved from He, J., . . . Tamakoshi, A. (2014). Burden of total and cause-
www.primetheory.com. specific mortality related to tobacco smoking among adults aged ≥
West, R., & Brown, J. (2013). Theory of addiction (2nd ed.). 45 years in Asia: A pooled analysis of 21 cohorts. PLoS Medicine,
Chichester: Wiley. 11, e1001631.
White, A., Kavanagh, D. J., Stallman, H., Klein, B., Kay-Lambkin, F., Zuckerman, M. (1999). Vulnerability to psychopathology: A biosocial
Proudfoot, J., . . . Young, R. (2010). Online alcohol interventions: model. Washington, DC: American Psychological Association.
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CHAPTER 11
Sexual and relationship

problems
Marita McCabe
CHAPTER OUTLINE
● Sexual problems: sexual dysfunctions
● Sexual problems: the paraphilic disorders
● Relationship problems
● Summary

11.1 Describe the different types of sexual dysfunction for males and females and the range of treatments for these
disorders.
11.2 Specify the diagnostic criteria for the paraphilic disorders outlined in the DSM-5 and describe current
understandings regarding the aetiology and treatment of these disorders.
11.3 Describe the factors associated with the development of relationship problems and the various treatments that
have been used to treat these problems.
SEXUAL AND RELATIONSHIP PROBLEMS: AN AUSTRALASIAN FOCUS

In 2013, a Royal Commission was established by the Australian Government to investigate cases of child sexual abuse
by institutions within Australia (see www.childabuseroyalcommission.gov.au). The Royal Commission into Institutional
Responses to Child Sexual Abuse was allocated $434.1 million to fund its operations and Supreme Court Judge Justice
Peter McClellan was appointed to act as its head, with six commissioners appointed in total. The brief of the Royal
Commission is to inquire into how institutions with a responsibility for children have managed and responded to
allegations and instances of child sexual abuse and to make recommendations about the required changes to laws,
policies and practices in order to prevent and respond appropriately to cases of child sexual abuse in institutions. The
institutions include schools, foster care settings, churches, orphanages and government agencies.
The appointment of the Royal C ommission has been widely applauded by both institutions and people who have
been the victims of child sexual abuse. This development is seen as providing an opportunity for past practices to be
reviewed so as to ensure that children are protected in the future. It is also an opportunity for survivors of child sexual
abuse in institutions to be given a voice to assist with the healing of their past experiences of abuse. The final report of
the Royal Commission is due to be delivered to the Governor-General by the end of 2017.
The Royal Commission has called for submissions from all interested parties and has so far received inquiries from
thousands of people who claim to have been the victims of child sexual abuse, as well as from institutions outlining
their procedures to respond to child sexual abuse. People who wish to make a complaint are called on to make a
written statement but they are not required to appear before the Royal Commission unless they want to. They can also
request a private session with only one or two Commissioners in attendance, something over 5000 individuals have
continued
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done so far, sharing their distressing stories (some of which

can be accessed at http://www.childabuseroyalcommission.
gov.au/share-your-story/your-stories). Trained counsellors
attend these private sessions, given the risk that individuals
may experience significant distress as they recall their
experiences of abuse. The Royal Commission travels around
Australia, providing all citizens with the opportunity to tell
their story in a private setting, if this is what they desire.
The Royal Commission delivered a report on ‘Redress
and Civil Litigation’ at the end of 2015, stating that, ‘Our case
studies and private sessions to date leave us in no doubt
that many people, while children, were injured by being
subjected to child sexual abuse in institutions. In some cases,
AAP
their injuries are severe and long-lasting. People can be
affected by these injuries for the rest of their lives . . . In spite The sexual abuse of children within institutions, and the
of the severity of the injuries many survivors have suffered, responses of these institutions to reports of child sexual
many survivors have not sought or obtained compensation’ abuse, have been the focus of a Royal Commission
(p. 91). Barriers for survivors of institutional child sexual abuse established by the Australian Government.
seeking some form of reparation for the injuries done to
them include: (1) the years and even decades it can take for
survivors to disclose the abuse they have experienced even to those to whom they are close; (2) the years it may take
people to recognise the links between the abuse they experienced as children and the difficulties they experienced
in later life (such as drug and alcohol problems, depression or relationship difficulties); and (3) the significant power
imbalance that usually exists between the institution and the survivor of the abuse.
The aim of the ‘Redress and Civil Litigation’ report is to make recommendations as to what institutions and the
government should do to offer reparation to those who have experienced institutional child sexual abuse and to prevent
future child sexual abuse from occurring in institutional contexts. It includes 93 recommendations to government. Just
one of these recommendations states that appropriate redress for survivors of institutional child sexual abuse should
include the following:
. Access for survivors to counselling and psychological care throughout their life as needed.
1
2. The provision of monetary payments to survivors as a tangible way of acknowledging the ill-treatment and suffering
they have experienced, with a minimum payment of $10 000 and a maximum payment of $200 000 for the most
severe cases.
3. A direct personal response from the institution in which the abuse occurred (if the survivor wants this), including
an opportunity for the survivor to meet with a senior representative of the institution, informing the survivor of
the steps the institution has taken to prevent further abuse from occurring, and an apology. An apology can
offer some healing: ‘What makes an apology work is the exchange of shame and power between the offender
and the offended. By apologising, you take the shame of your offence and redirect it to yourself. You admit to
hurting or diminishing someone and, in effect, say that you are really the one who is diminished—I’m the one who
was wrong, mistaken, insensitive or stupid. In acknowledging your shame you give the offended the power to
forgive. The exchange is at the heart of the healing process’ (Lazare, as cited in Royal Commission into Institutional
Responses to Child Sexual Abuse, 2015, pp. 140–141). Attesting to the healing power of a genuine and effective
apology, one of the survivors quoted in the report wrote that: ‘I received a formal letter of apology from Bishop
Jarratt. I have realised now how important it is to myself and my siblings. Bishop Jarratt apologised unreservedly
for the “unconscionable and disgraceful conduct of a priest who betrayed every standard of decency and of the
spiritual and moral trust expected of him” and “the singular failure of concern and pastoral care when you most
needed to be believed and helped”. He said, “we can’t undo the past but the church must make drastic change.
Those responsible must be accountable”. And they must’ (p. 142).
The sexual abuse of children is just one of the issues that will be addressed in this chapter. It will provide a description
of the main problems experienced by men and women in their sexual and relationship functioning. The aetiology and
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Chapter 11 Sexual and relationship problems 329
treatment approaches to address these problems will be considered, and current challenges in each of the areas
highlighted. The vast bulk of research on sexual and relationship problems has focused on heterosexual men and
women. While many of the same problems are also experienced by homosexual men and women, some of the issues
that are more specific to gay and lesbian individuals will also be described.
sexual
LO 11.1 Sexual problems: sexual dysfunctions dysfunctions
Disorders
There are two broad categories of sexual problems: sexual dysfunctions and the paraphilias. Sexual characterised
dysfunctions, which will be considered first, generally involve problems in the desire, arousal or orgasm by some type of
phases of sexual functioning. The paraphilias refer to deviant types of sexual behaviours that lead to disturbance in the
sexual gratification through sexual activity with inanimate objects or behaviours that do not involve phases of sexual
functioning
consent. The paraphilias include exhibitionistic disorder, fetishistic disorder, frotteuristic disorder, including desire,
paedophilic disorder, sexual masochistic disorder, sexual sadism disorder, transvestic disorder and arousal and
voyeuristic disorder. orgasm.
The definition of sexual dysfunction desire phase

Stage of sexual
Sexual dysfunction generally consists of an impairment or disturbance in one or more of the three functioning
stages of sexual functioning identified by Kaplan (1979): desire, arousal and orgasm. The desire phase characterised
refers to the individual’s experience of thoughts and feelings to engage in sexual activity. The aim of by the urge or
inclination to
the arousal phase is to produce physiological changes that allow intercourse to take place (such as
engage in sexual
erection of the penis and lubrication of the vagina). The orgasmic phase refers to the experience of activity.
orgasm, which entails rhythmic contractions of the penile urethra and muscles at the base of the penis
for men and of the muscles around the base of the vagina and pelvic floor for women. arousal phase
This three-stage model of the sexual response cycle is compatible with the current diagnostic Stage of sexual
scheme for men of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (American functioning
characterised by
Psychiatric Association [APA], 2013). However, for the first time, in this current edition of the DSM, the subjective
the desire and arousal phases have been combined into a single disorder for women. Thus, the DSM-5
experience of
includes four male and two female sexual dysfunctions that fit within this three-stage model of sexual pleasure and
functioning and also includes an additional genito-pelvic pain/penetration disorder for women. These excitement
disorders are outlined in Table 11.1. as well as
physiological
changes (such
TABLE 11.1 The DSM-5 (APA, 2013) classification of sexual dysfunction as the tensing
of muscles and
STAGE OF SEXUAL RESPONSE MEN WOMEN enlargement of
blood vessels).
Desire Male hypoactive sexual Female sexual interest/arousal
desire disorder disorder orgasm
Stage of sexual
Arousal Erectile disorder functioning
characterised by
Orgasm Delayed ejaculation Female orgasmic disorder the discharge of
Premature ejaculation neuromuscular
Pain Genito-pelvic pain/penetration tension built up
during sexual
disorder
activity; in men,
entails rhythmic
contractions of
Three dimensions are used by the DSM-5 to specify subtypes of these disorders. The first dimension the prostate,
is used to indicate the nature of the onset of sexual dysfunction as either lifelong or acquired. Lifelong seminal vesicles,
dysfunctions are those that have been present since the individual became sexually active, whereas vas deferens
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and penis, acquired sexual dysfunctions are those that develop after a period of normal functioning. The
and seminal second dimension is used to indicate the context in which the sexual dysfunction occurs. This can
discharge; in be either generalised (where the dysfunction is not limited to a certain context) or situational (where
women, entails
the dysfunction is limited to certain types of stimulation, situations or partners). Third, the DSM-5
contractions of
the orgasmic specifies subtypes of sexual dysfunction on the basis of the severity of the dysfunction, which may
platform and be mild, moderate or severe. This classification of mild, moderate or severe generally relates to the
uterus. level of distress experienced by the man or woman; the exception is premature ejaculation, where the
severity is specified by time to ejaculation.
In contrast to the DSM-5 classification of female sexual dysfunctions, both the International
Consultation on Sexual Medicine (ICSM) (McCabe et al., 2016a) and the International Classification
of Diseases (ICD-11) (Parish & Hahn, 2016) have maintained the separation of the desire and arousal
phase for women, and accordingly have separate classifications for hypoactive sexual desire disorder
and female sexual arousal disorder. In this way, these classification systems of sexual dysfunction
have maintained a parallel between the phases of the sexual response cycle for men and women.
METHODOLOGICAL ISSUES
Before discussing each of the disorders listed in Table 11.1, it is important to highlight some of the
methodological flaws of research in this area. First, one of the greatest problems in the literature on
sexual dysfunction is the wide range of different sub-populations from which samples are drawn. While
large-scale epidemiological studies utilising participants from the general population have been carried
out, studies often assess and compare groups that vary considerably in their dysfunctional nature. For
instance, studies have variously included sexually dysfunctional participants who have sought treatment
for their sexual problem, sexually dysfunctional participants from the community who have not sought
treatment, participants from the general population who do not have a sexual problem, dysfunctional
and functional participants from various medical settings, and students. Second, studies vary greatly in
the age groups that they examine. Some studies look only at men and women aged over 40, others at
respondents aged over 18, and others look at people only up to age 70. Finally, the existing literature is
plagued by inconsistency in the manner in which the various dysfunctions are defined and measured.
Where samples are composed of clinically (i.e., treatment-seeking) dysfunctional participants, the
measures used to assess the presence of sexual dysfunction (such as clinical diagnosis) are much more
reliable than those used to measure and assess dysfunction in non-clinical populations (generally one-
item self-report measures) and where the severity and duration of the dysfunction may not be assessed.
One result of these methodological shortcomings is that the prevalence rates of sexual dysfunctions
across studies are often substantially different, depending on the type of participants included and the
hypoactive different criteria used to diagnose sexual dysfunction. For example, McCabe and Goldhammer (2013)
sexual desire found that among Australian women, the prevalence of sexual desire disorders varied from 3–31 per
disorder cent, depending on whether strict DSM criteria, responses to questionnaire measures of sexual desire
Sexual
or self-classification measures were used to define desire problems. A recent Danish study reported
dysfunction
in which an
prevalence rates for each of the separate dysfunctions in a sample of 4415 sexually active men and
individual’s women aged 16–95 years (Christensen et al., 2011). This study found that 11 per cent of both men and
desire for sex women reported at least one sexual dysfunction. In terms of specific problems, the prevalence rates
is diminished to were: premature ejaculation, 7 per cent; erectile dysfunction, 5 per cent; arousal disorder, 7 per cent;
the point that and anorgasmia, 6 per cent. No data were reported on sexual desire disorders or sexual pain disorders.
it causes him/
her significant SEXUAL DESIRE DISORDERS
distress or Sexual desire is the interest one has in being sexual and engaging in sexual activity alone or with a partner
interpersonal (Goldhammer & McCabe, 2011; Wincze & Carey, 2001). Individuals who are persistently and recurrently
difficulties and
uninterested in sexual expression, who report the absence of sexual fantasies altogether, and who are
is not due to
transient life
distressed by their lack of interest, are said to be experiencing low sexual desire. In the DSM-5, hypoactive
circumstances or sexual desire disorder is a distinct classification for males but is combined with sexual arousal disorder
another sexual for females, due to the high levels of overlap in the prevalence and aetiology of these two disorders for
dysfunction. women. Estimates of the one-year prevalence rate (i.e., the number of individuals with the disorder in any
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one-year period) of hypoactive sexual desire disorder in community samples have been up to 7 per cent erectile disorder
(Schiavi, Stimmel, Mandeli, & White, 1995). In Australian research, McCabe and Connaughton (2014) Sexual
dysfunction in
found that 8 per cent of men experienced sexual desire problems, whereas 55 per cent of women were
men entailing
reported by Giles and McCabe (2009) to experience desire problems. Laumann, Paik, and Rosen (1999) recurrent inability
found that lack of sexual desire was the most common sexual dysfunction for women, with 33 per cent to attain or
of women experiencing this sexual dysfunction. In terms of the prevalence of sexual desire disorders in maintain an
women across the lifespan, a review of studies found that the prevalence ranges from 8.9 per cent at 18–44 erection until the
years to 12.3 per cent at 45–64 years to 7.4 per cent at over 65 years (Parish & Hahn, 2016). completion of
sexual activity.
CASE STUDY: A MALE WITH HYPOACTIVE SEXUAL DESIRE DISORDER

Jim is a 45-year-old married man who had been experiencing low sexual desire for two years by the time he discussed
the problem with his GP. A medical evaluation revealed no physical problems, and Jim had no history of previous mental
health treatment, psychiatric medications or substance abuse. Jim reported good erectile functioning, but a diminished
interest in sexual activity, as well as a diminished sensation with orgasm. He was highly distressed about these sexual
changes.
It was only after further questioning by the GP that it became apparent that Jim had been feeling quite depressed. He
reported that he was very stressed at work and that he had been spending less time in the past couple of years with his
wife and family. His two children were going through adolescence and his wife was becoming impatient with him because
she was largely having to manage the children on her own. It was further discovered through the GP’s assessment that
at about the time Jim’s sexual difficulties began, his best friend from childhood passed away unexpectedly from an
undiagnosed cardiac condition. Since that time, Jim had become preoccupied with thoughts of his own mortality, and had
often found himself thinking that his own death might be just around the corner.
One focus of therapy was Jim’s grief regarding the death of his best friend and his subsequent death anxiety.
Couple sessions were also included in order to deal with the relationship stress that had resulted from Jim’s sexual and
relationship withdrawal. These sessions focused on Jim and his wife spending more time together and improving their
communication so that they could rebuild the intimacy they had experienced earlier in their marriage. Therapy led to a
substantial improvement in all of Jim’s symptoms, including his level of interest in sex and his orgasmic sensation.
female sexual
According to Wincze and Carey (2001), sexual arousal refers to ‘the physiological, cognitive arousal disorder
Sexual
and affective [emotional] changes that serve to prepare men and women for sexual activity’ (p. 23).
dysfunction
Inadequate sexual arousal in men is generally experienced as the inability (which may be further in women
classified as either partial or complete) to attain or maintain an erection that is sufficient for sexual characterised
intercourse (APA, 2013). This dysfunction is labelled erectile disorder by the DSM-5. Female sexual by recurrent
arousal disorder is experienced as difficulty in attaining or maintaining adequate lubrication until inability to attain
the completion of the sexual act (APA, 2013). As noted earlier, in the DSM-5 arousal disorder and or maintain
sexual desire disorder have been combined for women. However, as previously stated, both the ICSM the swelling-
and ICSD-11 have maintained the separation of hypoactive sexual desire disorder and female sexual lubrication
response
arousal disorder (McCabe et al., 2016a; Parish & Hahn, 2016). of sexual
Early prevalence estimates for erectile disorder suggested that as many as 50 per cent of men excitement.
will experience erectile difficulties at some stage in their life (Frank, Anderson, & Rubenstein, 1978; hypertension
Kaplan, 1974). Australian prevalence estimates indicate that erectile disorder increases substantially Condition in
with age, ranging from 3 per cent of men aged 40–49 years to 64 per cent of men aged 70–79 years in a which the blood
community sample (Pinnock, Stapleton, & Marshall, 1999). In a more recent study of Australian men, supply through
the prevalence rate was found to be 40 per cent (McCabe & Connaughton, 2014). The prevalence of the blood vessels
erectile disorder is also higher among men who smoke and who have a range of medical conditions such is excessive
and is a major
as heart disease, diabetes and hypertension (high blood pressure) (Feldman, Goldstein, Hatzichristou,
risk factor for
Krane, & McKinlay, 1994; Mannino, Klevens, & Flanders, 1994; Panser et al., 1995; Ventegodt, 1998). heart disease
Compared to erectile disorder, less is known about the prevalence of female sexual arousal disorder and stroke (also
and it is difficult to accurately estimate the prevalence of this disorder given its overlap with other known as high
sexual dysfunctions among women. However, it has been estimated that between 30 and 50 per cent blood pressure).
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delayed of women experience dysfunction in the desire, arousal or orgasm phases of the sexual response cycle
ejaculation (Laumann, Paik, & Rosen, 1999; Spector & Carey, 1990). An Australian study found that 52 per cent
When an of women experienced arousal problems (Giles & McCabe, 2009).
individual
experiences a ORGASMIC DISORDERS
marked difficulty
The DSM-5 identifies two types of orgasmic disorders in men: delayed ejaculation and premature
or inability to
ejaculate.
ejaculation. Delayed ejaculation is diagnosed when the individual experiences a marked difficulty or
inability to ejaculate, despite the apparent presence of adequate stimulation and a desire to ejaculate (APA,
premature 2013). It is a disorder that most commonly refers to men who are not able to ejaculate with their partner,
ejaculation but are able to ejaculate during sleep or masturbation (Wincze & Carey, 2001). This disorder is relatively
Sexual rare, with estimates of its prevalence ranging between 0 per cent (Schiavi, Stimmel, Mendeli, & White,
dysfunction
1995) and 3 per cent (Ventegodt, 1998) in community samples. An Australian study found that delayed
characterised
by a man’s
ejaculation was experienced by 4 per cent of a community sample of men (McCabe & Connaughton, 2014).
inability to delay Premature ejaculation is identified in the DSM-5 as a sexual dysfunction characterised by a persistent
ejaculation after or recurrent pattern of ejaculation within approximately one minute following vaginal penetration and
minimal sexual happening before the man wishes it. Community estimates of the one-year prevalence of premature
stimulation or ejaculation have generally been about 5 per cent (Schiavi, Stimmel, Mendeli, & White, 1995; Ventegodt,
until he wishes to 1998). McCabe and Connaughton (2014) found the prevalence to be 8 per cent. A more recent study has
ejaculate, causing found a global prevalence rate of 5 per cent (Althof et al., 2014), but there have been substantial differences
significant
across different cultures, with the prevalence rate being 11.3 per cent in Korean men (Lee et al., 2016).
distress or
interpersonal Female orgasmic disorder is defined by the DSM-5 as a marked delay or absence of orgasm or
problems. reduced intensity of orgasmic sensations. The woman must experience clinically significant distress
about her symptoms. A woman may experience lifelong anorgasmia (when she has never experienced
female orgasmic an orgasm) or acquired anorgasmia (the existence of orgasmic problems in a woman who was
disorder previously able to experience orgasm). Female orgasmic disorder may occur in some situations but
Sexual
not in others (e.g., problems with one sexual partner but not with a different partner). Laumann, Paik,
dysfunction
in women and Rosen (1999) estimate that the prevalence of anorgasmia in women is 24 per cent, although an
characterised by Australian study found the prevalence to be 51 per cent (Giles & McCabe, 2009).
recurrent delay Genito-pelvic pain/penetration disorder involves persistent or recurrent difficulties in one or more
or absence of of the following: vaginal penetration during intercourse, vaginal or pelvic pain during intercourse/
orgasm following attempted intercourse, fear or anxiety about vaginal penetration and/or tensing or tightening of the
a normal pelvic floor muscles during attempted vaginal penetration. Genito-pelvic pain/penetration disorder is
excitement period
rarely included in large-scale studies of sexual dysfunction, although one study found that sexual pain
(also termed
‘anorgasmia’). affected up to 4 per cent of women (Giles & McCabe, 2009).
CASE STUDY: A MALE WITH PREMATURE EJACULATION

Marco and Anita are a couple in their late 40s who have been married for 20 years. Marco was recently diagnosed
by his GP as having premature ejaculation. During the assessment process it became clear that Marco had probably
had the disorder his entire adult life but had never realised it because he usually had an alcoholic drink or two to slow
himself down before intercourse. It was only recently that he became fully aware of his problem, in part because he
stopped using alcohol to relax him prior to having sex. A physical examination from his urologist cleared Marco of any
medical problems.
Marco never experienced premature ejaculation during oral and manual sex. But with intercourse he could last only
a maximum of three thrusts (or a few seconds) before ejaculating. ‘There is something about intercourse that gives me
problems,’ he said. Both partners were frustrated by this situation because Anita was capable of experiencing orgasms
through sexual intercourse, provided the stimulation lasted long enough. Marco often brought her to orgasm prior to
intercourse, but both partners wanted intercourse to last longer.
There was a difficult relationship dynamic between the couple, with Anita criticising Marco because he was not
assertive enough with his business colleagues, his friends or their children. He felt powerless and angry with himself
about his lack of control in his life. He was ambitious, but his desire to please others led to his ambition being undermined.
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Marco also felt his masculinity to be compromised in his relationship with Anita. This was part of their day-to-day
interaction, as well as being expressed in their sexual interactions.
Because the couple reported that affection and foreplay were not issues, the stop-start method was prescribed in
the second session. This method involves using manual stimulation to bring Marco to the point of ejaculation, stopping
stimulation to allow the level of arousal to reduce and then starting stimulation again; this occurs three or four times before
eventual ejaculation. The couple used the stop-start method and reached the point where it was time for intercourse.
Marco then began to experience premature ejaculation, and, in turn, Anita began to punish him verbally, making comments
such as ‘It’s important to take control over your life; here is yet another area in which you’re not achieving this control.’
Marco also contributed to difficulties with the stop-start exercises in that he could be passive-aggressive: he would quietly
resist Anita’s demands by trying to ignore them, but avoided confronting her regarding the negative effect her demands
were having on him. However, each partner eventually gained insight into these behaviours and succeeded in overcoming
the premature ejaculation. The treatment took approximately six months, providing what Marco and Anita considered a
long-term cure to their relationship and sexual problems.
The conceptualisation of sexual dysfunctions

Two broad models have been proposed in understanding sexual dysfunction: the linear and circular
models. The linear model assumes that individuals progress through a sequence of stages from an
initial awareness of sexual desire that triggers engagement in sexual activity. This activity results in
arousal with a focus on genital swelling and lubrication, and culminates in orgasmic release (Basson,
2000; Charlton & Quatman, 1997; Kaplan, 1979). The dysfunctions of hypoactive sexual desire,
sexual arousal and orgasmic disorders are based on these three stages respectively.
Rather than conceptualising sexual dysfunction
as occurring in a linear fashion, Basson (2000) has
proposed that a circular model is a more accurate
description of sexual dysfunctions occurring in
women. In this model, Basson (2000) maintains
that women have various reasons to initiate or
agree to sexual activity that may not be related to
the experience of sexual desire. For instance, a
woman may begin engaging in sexual activity as

an expression of love for her partner, to experience
pleasure, or to enhance emotional closeness with
her partner. Given these various reasons to engage
in sex, a woman is willing to become receptive to
sexual stimuli. If the woman finds the sexual stimuli
to be sexually exciting, arousal is experienced.
DAL
Continued stimulation will facilitate further arousal
and ultimately trigger a desire for sex. Thus sexual Relationship difficulties can be both a cause and a consequence of
activity and arousal trigger an experience of sexual dysfunction.
desire that motivates continued sexual activity and
facilitates the experience of further arousal. In short, there is a circular relationship between arousal
and desire, and desire may not be the first phase in this sequence of events.
Basson (2000) also emphasises the critical influence of contextual factors, and not just sexual
stimulation, on a woman’s sexual arousal. These contextual factors include feeling accepted and
desired by her partner, the partner’s behaviour, and the woman’s body satisfaction and mood. The
model thus highlights the need to consider psychological and relationship factors that are involved in
the development, maintenance and treatment of female sexual problems.
A final difference between the linear and circular models is that, according to Basson (2000), the
occurrence of orgasm is not considered essential. Instead, a woman will experience a phase of sexual
satisfaction (with or without orgasm) if the sexual stimulation is of sufficient duration.
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While this model has been developed to explain female sexual dysfunction, there has been limited
research on an equivalent model for men and may be unnecessary if the linear model suffices. For
women, recent studies show that many aspects of women’s sexual problems are inconsistent with the
linear model and tend to support Basson’s (2000) re-conceptualisation of women’s sexual response
in terms of a circular model (Leiblum, 2001). For instance, most women (41 per cent) presenting
for treatment of a sexual dysfunction report experiencing problems in multiple phases, lending
support to the circular notion of women’s sexual problems in which problems in the different phases
influence one another rather than existing as separate stages (Laumann, Paik, & Rosen, 1999). Studies
in both the United States and Australia have demonstrated that Basson’s model is most useful in
explaining the response cycle of dysfunctional women, but that for women who are not experiencing
sexual dysfunction the linear model is most useful in explaining their sexual response cycle (Giles &
McCabe, 2009; Sand & Fisher, 2007). These findings would suggest that sexually functional women
seem to go through the process of experiencing sexual desire, which is followed by feelings of sexual
arousal, which then escalate and lead to the experiences of orgasm if the women experiences a high
enough level of sexual arousal. In contrast, women who experience sexual dysfunction are less likely
to experience spontaneous sexual desire and may experience desire only when actually engaged in a
sexual activity. Their levels of desire and arousal are much more likely to be tied into contextual cues
and the relationship rather than the enjoyment of the sexual act for its own sake.
The aetiology of sexual dysfunction

Current understandings of the causes of sexual dysfunction acknowledge the contribution of biological,
psychological and social factors consistent with a biopsychosocial approach. For example, a study by
Kontula and Haavio-Mannila (2009) found evidence for the role of biological and psychosocial factors
in sexual functioning in that, among both men and women, positive sexual functioning was associated
with good health, positive sexual self-esteem and a sexually skilful partner. McCabe et al. (2016b)
completed a comprehensive evaluation of the biopsychosocial factors associated with both male and
female sexual dysfunction.
BIOLOGICAL FACTORS
The biological causes of sexual dysfunction, in particular erectile disorder, have received a great
deal of research attention in recent years. This literature has established the role of several variables
including age, disease and drug use in creating male sexual dysfunction. There has been much more
limited research on the biological causes of sexual dysfunction in women.
As the Australian population ages, it is important to focus on how the ageing process affects and
interacts with sexual health. It is widely regarded in society that as men and women age, their capacity
for successful sexual performance diminishes (Mulligan, Retchin, Chinchilli, & Bettinger, 1988). The
evidence for this view has come from both clinical observations (Kaplan, 1974; Masters & Johnson,
1970) and a number of empirical studies showing that the incidence of sexual dysfunction increases as
men and women age (Laumann, Paik, & Rosen, 1999; Rhoden, Teloken, Sogari, & Souto, 2002). This
reduction in sexual activity is likely to be due to a complex interplay of contributing factors including
general health, a natural slowing down of most physical activities as one ages, and the quality of the
person’s relationship. Since older adults will differ greatly from one another on each of these factors,
there will subsequently be large individual differences among older adults in the degree to which
sexual activity decreases with age. For example, older individuals who remain generally physically
active are more likely to remain sexually active compared to those individuals experiencing increasing
physical frailty. In addition, age does not appear to increase the risk of all sexual dysfunctions, with
one study finding that age was a significant factor predicting erectile and sexual desire problems but
not problems with premature or delayed ejaculation (McCabe & Connaughton, 2014).
Early work into the biological causes of sexual dysfunction noted a vast array of medical conditions
that impacted upon sexual functioning (Kaplan, 1974; Masters & Johnson, 1970). More recently, an
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Australian study also found that men with delayed ejaculation or sexual desire disorders experienced
a higher level of medical problems than men without sexual problems (McCabe & Connaughton,
2014). Among these medical problems, vascular conditions (disorders of the blood circulation system)
are frequently associated with sexual dysfunction. In men, sexual dysfunction can arise from these
conditions because decreased penile blood pressure is insufficient to achieve and sustain an erection
(Graber, 1993). Erectile dysfunction also occurs in 25 per cent of men treated for hypertension
(Monga & Rajasekaran, 2003), which may be a result of the medication used to treat the disease. For
example, Dunn, Croft, and Hackett (1999) found that while erectile problems were associated with
self-reported hypertension (high blood pressure), this finding was limited only to those participants
who were taking antihypertensive drugs.
Numerous other drugs have been implicated in the development of sexual dysfunction.
Pharmacological agents used for treating non-sexual disorders, such as antidepressant medication,
have been found to be associated with sexual dysfunction (Kennedy, Eisfeld, Dickens, Bacchiochi,
& Bagby, 2000; Segraves, 1988; Wincze & Carey, 2001). In addition, recreational drugs, cigarette
smoking and alcohol have been found to negatively affect sexual functioning (McVary, Carrier, &
Wessells, 2001; Mirin, Meyer, Mendelson, & Ellingboe, 1980).
PSYCHOLOGICAL AND SOCIAL FACTORS

A comprehensive review of the psychological and interpersonal factors that contribute to sexual dysfunction
has been published by McCabe et al. (2010). This review considers each of the dimensions outlined in
the model developed by McCabe (1991). The model includes developmental, individual and relationship
factors, and the interaction between them, in contributing to the aetiology of sexual dysfunction. The model
begins with the premise that both individuals in a relationship bring a range of personal characteristics
into their relationship. These characteristics may stem from a variety of sources, including developmental
experiences (i.e., past experiences in the individual’s life, especially experiences relevant to sexual activity
such as a history of sexual abuse) and current aspects of the individual’s functioning (e.g., depression, body
image and stress). These factors influence what each individual brings to the relationship generally and the
sexual relationship specifically. For example, an individual may experience depression, which has a negative
impact on the relationship that may in turn reduce the individual’s sexual desire for his/her partner. As a
result of this withdrawal, the partner may feel rejected from both the relationship and from sexual interaction,
which exacerbates both the relationship and sexual problems. Once this occurs, treatment focused on one
individual may not be successful in resolving the sexual problems as both individuals in the relationship are
now affected. As a result, therapy is most likely to be effective if it involves both partners in the relationship.
In the interactional model of developmental, individual and relationship factors influencing one
another, cognitions—that is, the interpretations that individuals place on events in the relationship—
are crucial (Nobre, 2009). The meaning individuals give to sexual events (e.g., interpreting a partner’s
erectile dysfunction as rejection) is seen to be more important in predicting sexual dysfunction than the
event itself. Also important is the meaning individuals give to non-sexual aspects of the relationship
(e.g., interpreting a partner’s depression-related withdrawal as rejection). Most importantly, if these
evaluations are negative and are not expressed to the partner directly, the model proposes that they
might be expressed indirectly in the form of a sexual dysfunction (e.g., a loss of sexual desire for the
partner). The model developed by McCabe (1991) is presented in Figure 11.1.
Research supports various aspects of McCabe’s (1991) model of the causes of sexual dysfunction.
There has been little research carried out to identify the importance of developmental factors related to
sexual dysfunction. However, one exception is that of previous sexual experiences, whether occurring
in childhood, adolescence or adulthood. In many clinical reports, sexual trauma or negative sexual
messages are noted as childhood sources of sexual dysfunction in both men and women (McCabe &
Connaughton, 2014; Seibel, Rosser, Horvath, & Evans, 2009; Swaby & Morgan, 2009; Wincze &
Carey, 2001). However, McCabe and Cobain (1998) point out that many of the studies examining the
impact of childhood experiences on sexual dysfunction are methodologically flawed. For instance,
they rely on retrospective recall of childhood events that may not reflect what actually occurred at
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Developmental
Cognitive Emotional Sexual

Individual evaluation Individual
response dysfunction
Relationship
FIGURE 11.1 McCabe’s (1991) model to explain the development of sexual dysfunction within a relationship
Source: McCabe, M. P. (2001). Evaluation of a cognitive behavior therapy program for people with sexual dysfunction. Journal of Sex and
Marital Therapy, 27, 259–271.
this stage of development (e.g., due to memory loss or biased recall). In contrast, methodologically
sound research that has sought to explore this relationship has shown no association between events in
childhood or adolescence and later adult sexual functioning in men (McCabe & Cobain, 1998). Thus,
further research is needed to explore the possible impact of both sexual and non-sexual developmental
experiences on adults’ later sexual functioning.
anxiety
State
Anxiety is one of the individual factors that people bring to their relationships and is generally
characterised regarded as a psychological variable that interferes with the sexual response (Kaplan, 1974). Anxiety
by negative in sexual situations may take numerous forms including performance anxiety, fear of success, fear
affect and bodily of pleasure and fear of injury (Letourneau & O’Donohue, 1993). Most clinical evidence for the
symptoms detrimental effect of anxiety on sexual desire and arousal focuses on performance anxiety—that is,
of tension anxiety in response to perceived sexual performance demands (e.g., concerns regarding whether
accompanied by or not the person will become aroused and experience an orgasm) (Levine, 2003). McCabe and
the anticipation of
Connaughton (2014) found that performance anxiety was a significant factor predicting low sexual
future danger or
misfortune. desire, premature ejaculation and delayed ejaculation among Australian men. Patterson and O’Gorman
(1989) conducted a study of sexually functional and dysfunctional women and men and found that
performance general sexual anxiety was higher in dysfunctional men and women than it was in functional men and
anxiety women. This suggests that dysfunctional men and women display greater anxiety towards a broader
Anxiety
range of sexual situational variables (such as fear of being in a sexually intimate situation) rather than
regarding sexual
performance performance concerns alone. There is some suggestion that anxiety may be more strongly related to
that interferes sexual activity in some relationships than others. For instance, Beaber and Werner (2009) found that
with sexual anxiety was negatively correlated with overall sexual functioning among heterosexual women, but
functioning. that there was no association between these two variables in homosexual women. These researchers
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suggested that one possibility accounting for this finding may be that lesbian partners communicate
their anxieties with one another in ways that facilitate, rather than impair, sexual functioning.
Another individual factor that a person might bring to the relationship is that of stress. Although
the role of stress in sexual functioning is less well understood than that of anxiety, the presence of
financial difficulties, work stress or stress that arises from illness have all been associated with an
increased incidence of sexual dysfunction (Wincze & Carey, 2001). Clinicians also report that major
life stressors are common in patients presenting with sexual dysfunction (Morokoff & Gilliland, 1993).
Morokoff, Baum, McKinnon, and Gilliland (1987) assessed the effects of both chronic, longstanding
stressors and acute, immediate stressors in erectile difficulties. Their data showed that erectile
impairment results from a combination of both forms of stress. Further, Morokoff and Gilliland
(1993) conducted a study on the sexual functioning of men and women from the general population.
Their results showed that the rate of increase in erectile difficulties associated with increasing age
was significantly faster in unemployed men than in employed men. Overall, however, the relationship
between psychosocial stressors and sexual dysfunction has received very little research attention.
A key component of the model proposed by McCabe (1991) is the role of relationship factors
in sexual dysfunction. Most men and women who seek treatment for sexual dysfunctions are in
established heterosexual relationships (Riley, 2002). However, partner issues in the aetiology and behaviour
maintenance of sexual dysfunction have not been extensively studied (Riley, 2002). Where relationship therapy
issues have been examined, most published reports are clinical observations or uncontrolled Array of
studies (Metz & Epstein, 2002). Nevertheless, the existing body of literature has indicated a strong treatment
association between numerous relationship variables and sexual dysfunction. These variables have techniques,
often based on
included partner rejection and marital conflict (Kaplan, 1974; Schiavi, 1981; Snyder & Berg, 1983),
the principles
communication problems (McCabe, 2007; McCabe & Cobain, 1998; McCabe & Connaughton, 2014; of learning, that
Schiavi, 1981; Snyder & Berg, 1983; Speckens, Hengeveld, Lycklama à Nijeholt, van Hemert, & aim to change
Hawton, 1995; Spector & Boyle, 1986), and a lack of intimacy (McCabe, 1997; McCabe & Matic, an individual’s
2007). Relationship difficulties can be both a cause and a consequence of sexual dysfunction. For specific
example, while relationship conflict may interfere with desire, arousal and intimate behaviour and behaviours
thus contribute to the development of sexual dysfunction, the sexual dysfunction may itself give rise by replacing
to increased conflict and distress in a couple’s overall relationship (Metz & Epstein, 2002). unwanted
behaviours with
desired ones.
The treatment of sexual dysfunction sensate focus
Treatments for sexual dysfunctions have primarily entailed behavioural, cognitive-behavioural and exercises
medical approaches. Treatment
for sexual
dysfunctions in
BEHAVIOUR THERAPY
which partners
Behaviour therapy attempts to alleviate sexual difficulties through a combination of techniques alternate
including education, communication skills training and sensate focus exercises (Sarwer & Durlak, between giving
1997). Sensate focus exercises were the cornerstone of the famous Masters and Johnson (1970) and receiving
approach to the treatment of sexual problems. These exercises are designed to assist the couple to stimulation
re-experience sexual pleasure by focusing on the pleasurable sensations that accompany body and in a relaxed
genital stimulation in the absence of performance demand (e.g., ‘I must experience an orgasm’) or atmosphere in
excessive monitoring of oneself during sexual activity, known as ‘spectatoring’ (e.g., ‘I am not yet which sexual
intercourse is
becoming aroused’), which are believed to interfere with sexual functioning. This is accomplished
forbidden so as to
through a graded series of mutual body-touching exercises beginning with general body pleasuring reduce pressure;
(known as the sensate focus I exercise) and later introducing genital body pleasuring in the absence of partners
intercourse (known as the sensate focus II exercise). These exercises aim to: communicate
openly with each
∙ help partners learn to communicate with one another about their preferred sensual and sexual other regarding
experiences their preferred
∙ provide pleasurable sensual and sexual experiences for both partners in the absence of anxiety or types of bodily
pressure to perform sexually (e.g., experience orgasm) pleasuring.
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∙ help individuals to focus on their physical sensations rather than negative thoughts
∙ provide an experience of positive interaction between the partners (Allgeier & Allgeier, 2000;
Sarwer & Durlak, 1997; Spence, 1991; Wiederman, 1998).
Sensate focus exercises are often applied in the treatment of all sexual dysfunctions because of
their ability to help the couple broaden their approach to sexuality beyond a focus on intercourse while
reducing the threatening emphasis on performance and the need to achieve orgasm. An example of the
instructions for the sensate focus I exercise is presented in Table 11.2.
TABLE 11.2 A section of the handout provided to patients practising the sensate focus I exercise
GUIDELINES FOR SENSATE FOCUS I: NON-GENITAL BODY PLEASURING
The aim of this exercise is to help you to improve your ability to enjoy the experience of physical contact with
your partner and to learn more about the types of touch that you and your partner like. Hopefully the exercise
will allow both of you to feel more relaxed and to become aware of and concentrate on pleasurable feelings.
You should also find that the task helps you to build better communication with your partner.
Remember that the aim of this exercise is not to be sexual but to enjoy pleasurable feelings. The
sensations experienced in all parts of your body (and not just your sexual parts) are important in the
giving and receiving of physical pleasure. Examples of non-sexual body parts include the face, neck,
shoulders, back, stomach, arms and legs.
You and your partner should take it in turns to give and receive pleasure. The person who is giving
pleasure should try to explore different types of touch (e.g., stroking, massaging and tickling) in order to
learn more about the type of contact that his/her partner finds pleasurable. The giver needs to focus on
the partner’s, and not his/her own, pleasure. The person who is receiving pleasure should just relax and
concentrate on the pleasurable sensations. It is also important that the receiver gives feedback to the
partner regarding the types of touch and parts of the body that are enjoyable.
After 10 minutes in the role of giver or receiver, it’s time to change over. Then repeat both roles again.
The whole exercise should take 40 minutes. Occasionally you may feel tempted to break the rules and
move on to include sexual areas of the body. Please try not to do this since it goes against the aim of
the exercise. The aim is not to become sexually aroused but to allow you to practise these exercises in a
relaxed way where you do not feel pressured to take part in sexual activities.
Source: Adapted from Spence, S. H. (1991). Psychosexual therapy: A cognitive-behavioural approach. Melbourne: Chapman & Hall.
Outcome studies reveal overall improvement in only about two-thirds of people with sexual
dysfunction who have participated in behavioural approaches (Wiederman, 1998). The main premise
of these approaches is that the removal of performance anxiety will lead the couple to a healthy, more
enjoyable sexual relationship. However, this is probably too narrow in its focus and fails to address
many of the other factors contributing to sexual dysfunction (Charlton, 1997). A more complex view of
human nature and sexual dysfunction suggests that factors other than performance anxiety may need to
be addressed if treatment is to be successful (Beitchman et al., 1992; Clayton, 2003; Kelly, Strassberg,
cognitive & Turner, 2006; Rosen, Taylor, Leiblum, & Bachmann, 1993; Tiefer, Hall, & Travis, 2002). These
behaviour factors include the broad array of developmental, individual and relationship factors noted in the section
therapy (CBT) on aetiology. While behavioural approaches are still an integral part of sex therapy, the expansion of
Type of
aetiological factors, and the recognition that anxiety may not be the major causal factor in the development
psychological
treatment that
of sexual dysfunction, particularly for women, has led to more comprehensive treatments.
combines both
cognitive and COGNITIVE BEHAVIOUR THERAPY
behavioural A major focus of cognitive behaviour therapy (CBT) is to challenge any unrealistic beliefs that may
concepts and be contributing to sexual problems. For example, individuals may be making cognitive errors such as
techniques. ‘all-or-none’ thinking (e.g., ‘If our sexual relationship is poor it means our whole relationship is poor’),
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personalisation (e.g., ‘My partner mustn’t find me attractive because she has difficulty reaching orgasm
with me’) or catastrophising (e.g., ‘My relationship is doomed if I don’t fix my erectile problem’) (Spence,
1991). Initially with the help of the therapist, the patient learns to identify and challenge the unrealistic
beliefs that trigger negative behaviours and emotions regarding sexual activity. An example form in which
the patient is required to monitor and challenge any unrealistic beliefs is shown in Table 11.3.
TABLE 11.3 An example of a thought-monitoring and challenging form for a patient with a sexual
dysfunction
WHAT WOULD BE
WHAT WERE HOW DID THIS A MORE REALISTIC HOW DO YOU
DAY SITUATION YOU THINKING? MAKE YOU FEEL? THOUGHT? FEEL NOW?
Friday Putting off I’m just not Ashamed at myself It’s understandable Still a bit
going to interested in sex. for not being that I’m too tired for nervous about
bed—I know normal. sex after juggling going to bed
Paul will want work and looking but I can do it.
sex. after the kids all day.
I know that Paul Under a lot of Paul loves me and is Less anxious
enjoys sex and I pressure, anxious unlikely to have an and guilty.
feel like I’m letting about having sex, affair. We just need
him down—also but even more to take time out
he might seek it anxious if I don’t. from the rest of our
out elsewhere. lives to reignite my
desire for sex.
A study by McCabe (2001) evaluated the effects of a short-term CBT program on male and female
sexual dysfunction. The participants comprised 95 males and 105 females who attended a clinic for the
treatment of their sexual dysfunction. The program consisted of 10 sessions of individual therapy in which
cognitive and behavioural strategies were used to enhance communication in the relationship, increase
positive sexual behaviours and lower sexual anxiety. Problem solving was used to identify barriers to
engaging in and enjoying sexual activities. Homework exercises included both cognitive strategies
(e.g., monitoring and challenging unrealistic beliefs) and behavioural exercises (e.g., sensate focus
exercises). Partners were involved in therapy sessions when appropriate in order to ensure compliance
with the treatment program; this generally occurred for two or three sessions for most couples.
The results demonstrated that, after therapy, women and men reported experiencing lower levels of
sexual dysfunction in their relationship, more positive attitudes towards sex, and increased perceptions
that sex was enjoyable. Despite these improvements, a large percentage of men and women (40.8%)
still experienced sexual dysfunction most of the time at the completion of treatment. As the majority
of men and women in the study had multiple dysfunctions that had been in place for a lengthy period
of time, the sexual problems were likely to be resistant to a short-term treatment approach. It is also
possible that targeting a broader range of issues (such as McCabe’s [2009] suggestion to incorporate
broader aspects of the woman’s life to address anorgasmia) may have improved the treatment outcome
results (Meana, 2009). Another problem with this study is that it did not include a control group for
comparison so it is not clear whether the improvements were due to the CBT techniques that were
used or to some other aspect of the intervention (e.g., receiving support from the therapist).
INTERNET-BASED TREATMENTS FOR SEXUAL DYSFUNCTION

There are many barriers to seeking treatment for sexual problems for men and women, including
geographical barriers (e.g., for people living in rural and regional areas), lack of time, difficulty in
identifying a suitable therapist and the embarrassment people may feel in seeking help for a sexual
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dysfunction. As a result, the use of the internet is developing as a means of treatment for sexual
dysfunction. A team of Australian researchers have developed internet-based programs for the treatment
of sexual problems in men (McCabe, Price, Piterman, & Lording, 2008) and women (Hucker & McCabe,
2014; Jones & McCabe, 2011). A description of the content of the program for women is shown in
Table 11.4. These programs were developed for heterosexual couples and although they are primarily
focused on one partner, they involve both partners in the process of therapy. The programs are delivered
online, and for women they have included online therapist assistance and chat groups. Men were less
likely to respond to this online therapist contact, preferring instead to work through the therapy program
without this assistance. The outcome in terms of both sexual and relationship functioning from these
programs is very encouraging, leading to improvements equivalent to those from face-to-face therapy.
However, the dropout rate from therapy was high, and the patient profile indicated that these programs
are probably most suitable for patients who do not have major relationship problems.
TABLE 11.4 Pursuing Pleasure: an internet-based program to treat sexual dysfunction among heterosexual women
Module 1
This module is intended to allow couples to emotionally reconnect before beginning touch exercises and to encourage women to
start thinking about their attitudes towards sex. A ‘no sex rule’ is explained to couples. Psychoeducation is provided on the different
types of female sexual dysfunction and common myths about sex. Women complete a written exercise to explore the usefulness of
their current beliefs about sex and couples begin communication exercises in the form of discussion letters. Non-sexual mindfulness
(meditating on the breath) is introduced to help women learn the skill of staying present and focused.
Module 2
This module includes psychoeducation on female sexual anatomy and possible causal, perpetuating and protective factors
involved in female sexual dysfunction. Women complete a written exercise to explore the development and maintenance of
their sexual difficulties. Couples continue the communication exercises and women are introduced to sensual mindfulness
(mindfulness in the shower) to draw attention to the pleasurable sensations of their bodies. Sensate focus is introduced to
couples with non-sexual body touching sessions.
Module 3
This module provides psychoeducation on female sexual desire/interest and factors that may negatively or positively affect
this. Women are introduced to the CBT model and complete a written exercise focused on factors that may be having an
impact on their sexual desire/interest. Couples continue the communication exercises, and mindfulness is incorporated into
sensate focus in self-touching sessions. Couples continue non-sexual massages.
Module 4
This module includes psychoeducation on male sexual anatomy and the relationship between body image and sexual
enjoyment. Information is also provided on sexual pain disorders and orgasmic disorders. Women complete a written exercise
on body image and sex. Couples continue communication exercises. Genital touching is introduced to sensate focus sessions
and the use of mindfulness skills is encouraged to facilitate present moment awareness and manage difficult thoughts and
feelings that may have a negative impact on sexual experience.
Module 5
Module 5 contains psychoeducation on sexual intercourse with a focus on developing a broad and flexible definition of ‘sex’.
Women complete a written exercise focused on thoughts and feelings during intercourse. Couples continue communication
exercises and are given the option of continuing the letters or alternatively discussing the questions without the use of letters.
Penetration is introduced to the sensate focus sessions and the use of mindfulness skills is encouraged to increase present
moment awareness and manage difficult thoughts and feelings that may have a negative impact on sexual experience.
Module 6
This final module provides psychoeducation on sexual erotica, toys and aids, as well as an explanation of medical interventions
for female sexual dysfunction. Couples continue the communication exercises. Couples continue intercourse in sensate
focus sessions and the use of mindfulness skills is encouraged to increase present moment awareness and manage difficult
thoughts and feelings that may have a negative impact on sexual experience. Women complete a written exercise focusing on
the gains made throughout their participation in the program, anticipating potential difficulties in sexual function that may arise
following the end of the program, and use this information to create a relapse prevention plan.
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MEDICAL TREATMENTS FOR MALE SEXUAL DYSFUNCTION

An implicit assumption underlying the medical model of erectile disorder is that it can be cured by
providing the patient with a penis rigid enough for sexual intercourse. Medical treatments typically
entail the use of vacuum devices, penile injections, oral medications or penile implants. Since the late
1990s the first-line medical treatment has been oral medications such as sildenafil, commonly known
as Viagra® and belonging to the category of phosphodiesterase type 5 inhibitors (PDE5i). Sildenafil
results in muscle relaxation and hence increased blood flow to the penis, thereby producing an
erection. There is a substantial body of literature that PDE5i medications are effective treatments for
men to obtain an erection (e.g., Conaglen, Williamson, & Conaglen, 2009). It also appears that men
are more likely to seek these treatments if they have experienced erectile problems for a long period
of time (Matic & McCabe, 2008) and if they experience severe erectile problems (McCabe & Matic,
2007). However, the medical model of erectile disorder minimises the importance of psychological
variables and suggests that exclusively targeting the physical component of the disorder is an adequate
treatment (Bancroft, 1970; Carpiano, 2001; Rosen, 1996). Challenging this assumption, Delizonna,
Wincze, Litz, Brown, and Barlow (2001) assessed whether the mere presence of an erection would
prompt subjective feelings of sexual arousal in a sample of non-sexually dysfunctional men. Their
findings suggested that men who experienced mechanically induced erections did not report any
subjective state of physical or mental sexual arousal. However, men who obtained self-stimulated
erections did report subjective feelings of arousal.
Medical treatments for erectile
disorder do not address the psychosexual
SHUTTERSTOCK.COM/SEAN NEL
components of an individual’s sexual
experience (such as subjective arousal)
and this failure may lead men to become
dissatisfied with the result of using
these approaches (Matic & McCabe,
2007). The medical approach to the
treatment of erectile disorder overlooks
other important patient, partner and Oral medications such as sildenafil, commonly known as
relationship factors (e.g., levels of Viagra®, have been the first-line medical treatment for
intimacy and conflict), which may result erectile disorder.

in dissatisfaction and a discontinuation of
therapy (Althof, 2002). Consistent with this, Aubin, Heiman, Berger, Murallo, and Yung-Wen (2009)
found that a combination of psychological therapy and Viagra® for erectile dysfunction was more
effective than Viagra® alone in terms of both erectile functioning and treatment satisfaction. Similar
findings have been obtained for the treatment of premature ejaculation (Li, Zhu, Xu, Sun, & Wang,
2006). Related to the importance of relationship factors, McCabe, Conaglen, Conaglen, and O’Connor
(2010) found that female partners played a major role in encouraging the male to seek treatment for
his sexual problems.
MEDICAL TREATMENTS FOR FEMALE SEXUAL DYSFUNCTION

In recent years, the focus of treatment for female sexual dysfunction has shifted from predominantly
androgen
psychologically based techniques towards a more medical approach (Kleinplatz, 2003; McCarthy, Substance (such
2004; Segraves & Balon, 2005; Tiefer, 2002). For instance, a review of behavioural and cognitive- as testosterone)
behavioural treatments for female sexual dysfunction indicated that there have been some recent producing male
studies, but that most treatment outcome studies have focused on medical interventions (Stinson, characteristics.
2009). The discovery of effective pharmacological agents for male erectile dysfunction has led
oestrogen
researchers to attempt to develop similar agents for females (Segraves, 2006). As a result, regardless Group of female
of the psychological and relationship factors that may contribute to a woman’s sexual dysfunction, sex hormones
researchers have begun focusing on possible medical causes and medical interventions. Examples of produced by the
medical treatments for female sexual dysfunction include hormonal (androgen and oestrogen) therapy. ovary.
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An extensive review of the literature on the effectiveness of pharmacological treatments for

women found mixed results, although in the majority of cases, these approaches were found to be
largely unsuccessful (Basson et al., 2003; Heiman, 2002; Segraves & Balon, 2005). The female sexual
response is vastly different from that of males and, unlike their male counterparts, the potential role of
hormonal factors and various medical treatments on the sexual interest and activity of women remains
unclear (McCarthy, 2004; McConaghy, 1993). A medical approach to the treatment of sexual disorders
in women fails to take into account the many individual factors (e.g., body image) and the quality of
the relationship described by women as being related to the development of their dysfunction (Basson,
2000; 2003; Kleinplatz, 2003).
Only one published clinical trial supports the use of sildenafil for the treatment of female sexual
arousal disorder in a sample of 51 young pre-menopausal women (Caruso, Intelisano, Lupo, & Agnello,
2001). In contrast, a well-controlled clinical trial involving 583 women showed no difference in levels
of sexual arousal between those who received this drug and a placebo group (Basson et al., 2002). The
medical model of female sexual dysfunction tends to emphasise quantity, performance and objective
measures (e.g., frequency of orgasm and adequate lubrication) over the quality of sex and measures
of subjective experience (e.g., pleasure, satisfaction and intimacy), which women describe as being
particularly relevant in their motivation to engage in sexual activity (Kleinplatz, 2003; McCarthy, 2004).
Undoubtedly, pharmacotherapy may play a role in the treatment of a limited number of sexual disorders
(particularly for men), but the use of these treatments for women requires further development.
In 2015, the US Food and Drug Administration (FDA) approved a medical treatment called
flibanserin for hypoactive sexual desire disorder among pre-menopausal women. It is expected, as
occurred when sildenafil was first approved for the treatment of men with erectile dysfunction, that
this approval will legitimise female sexual dysfunctions and encourage more women to seek treatment
for these sometimes debilitating conditions. This medication has not been approved for the treatment
of sexual dysfunction in Australia; indeed, no approach to approve this medication has yet been made
to the Therapeutic Goods Administration (TGA) in Australia.
LIMITATIONS OF TREATMENT RESEARCH

While the high prevalence of sexual dysfunction is widely recognised in the literature, research on
the effectiveness of psychological treatment approaches is limited. Treatment programs for sexual
dysfunction have frequently lacked adequate research methodology, making it difficult to evaluate
their effectiveness. For instance, studies often fail to include a control condition against which to
compare the treatment condition, making it difficult to know what to attribute any improvements to
(e.g., with the passage of time, sexual problems may resolve themselves). Also, long-term follow-up
data are lacking in the majority of studies, so it is not known whether treatment gains persist over time
(Hawton, Catalan, Martin, & Fagg, 1986; McCabe, 2001; O’Donohue, Dopke, & Swingen, 1997).
As well as methodological problems, the treatments evaluated thus far appear to be limited in their
approach. In many of the studies reported to date, a large majority of the men and women who received
therapy failed to show improvements in their sexual functioning, suggesting a need to develop new
approaches (McCabe, 2001). There are several ways in which treatments could be improved. First, with
debate in recent years surrounding the conceptualisation of female sexual functioning in terms of the
circular-sex-response model (Basson, 2000), treatments need to incorporate broader aspects of emotional
and interpersonal functioning that may be especially relevant for the sexual functioning of women.
Second, Althof and colleagues (2005) highlight the need to expand the focus beyond just the patient to
include the partner and their relationship. This need is underscored by the finding that sexual dysfunction
in one partner may lead to sexual dysfunction in the other partner. For example, approximately half of the
women whose partners experience erectile disorder also report having a sexual dysfunction. Such results
suggest that treatment for sexually dysfunctional men and women should be completed by both partners,
rather than just the partner labelled as dysfunctional.
In addition to studies that are methodologically flawed and treatments that are limited in their focus,
research studies on treatments for sexual dysfunctions are few in number. An extensive review of the
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literature on psychological treatment approaches for sexual dysfunction found very few published
studies, and those located were generally conducted in the 1970s and 1980s, when the focus was
mainly on a limited set of psychological factors (e.g., performance anxiety) (Delizonna, Wincze, Litz,
Brown, & Barlow, 2001).
CASE STUDY: A FEMALE WITH SEXUAL INTEREST DISORDER AND A MALE WITH
ERECTILE DISORDER
Mary and Fred are a couple in their early 40s. They were referred to a clinical psychologist for treatment of the sexual
difficulties they had been experiencing over the past few years. Mary had previously been married to someone else, but
they divorced after two years of marriage. She began her relationship with Fred eight years ago. They live in separate
apartments but date each other exclusively. During their initial session with the clinical psychologist, when an assessment
was undertaken, the couple described themselves as intellectually compatible but with an almost non-existent sex life for
the past few years. They both appeared anxious and embarrassed when discussing their problems during the initial visit.
On inquiry, it emerged that Mary has had problems intermittently with a degree of vaginismus. While this was not
severe, it did undermine her interest in sexual activity since she feared this would result in pain. Mary’s difficulties have
dominated their sexual relationship. She described an abusive relationship with her first husband and attributed some of
her sexual problems to this time. Fred felt increasingly frustrated, impatient and angry that Mary had refused counselling
in the past for her sexual problems. It was only when he began losing his erection consistently that Mary finally agreed
to seek help.
Treatment focused on communication issues and reducing the level of performance demand that both partners were
experiencing. For example, in terms of performance demand, Mary would have thoughts such as ‘If we don’t have sex,
Fred will get angry with me’, while Fred would criticise himself and become anxious at the first sign that he was losing
his erection. In accordance with sensate focus exercises, the couple were encouraged to refrain from intercourse and
to focus on non-demand touching for a period of four weeks. The strong emphasis on Mary having complete control in
each of the sessions helped to maintain a low level of anxiety for her. Kegel exercises were also recommended so as
to strengthen Mary’s pelvic floor muscles in order to assist with orgasm and the experience of sexual pleasure. These
exercises entailed squeezing the muscles that stop urination for about three seconds, relaxing and then squeezing again.
Four weeks into the treatment, the couple attempted intercourse for the first time since starting treatment. Although
Mary felt some anxiety immediately after penetration, she reported telling herself to ‘relax’ and was able to experience
an orgasm soon after. She noted that this was the first time she had experienced an orgasm during intercourse for more
than six months. Fred experienced no erectile difficulties during the experience.
LO 11.2 Sexual problems: the paraphilic disorders

Historical and current approaches to understanding paraphilias
paraphilias
The second broad category of sexual problems is the paraphilias. The behaviours that are currently
Atypical sexual
referred to as paraphilias have been described throughout history in the literature, art and mythologies activities that
of many different cultures. During the Middle Ages, many behaviours were explained by reference involve one of
to the supernatural. For example, a person who behaved in unusual or unacceptable ways sexually or the following:
otherwise was believed to be possessed by the devil or cast under a spell by witchcraft. (a) nonhuman
Yet it was not until the nineteenth century that the paraphilias began to be classified as legal or objects; (b)
psychiatric conditions. In 1886, Richard von Krafft-Ebing first referred to aberrant sexual behaviours non-consenting
adults; (c) the
and his views influenced Freud, who was of the opinion that any form of sexual behaviour that took
suffering or
precedence over heterosexual intercourse indicated that the individual had experienced a defect in his/ humiliation of
her psychosocial development. oneself or one’s
Since the turn of the twentieth century, there have been many views about various forms of sexual partner; and
expression, with many researchers pointing out the difficulty in defining the difference between normal (d) children.
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variants of sexual expression and the paraphilias. There have also been changes in behaviours classified
as a paraphilia, with homosexuality being removed from the DSM classification system in 1987. In
fact, Silverstein (2009) has suggested that most of the paraphilias will be removed from the DSM in
the next 50 years. In contrast, Blanchard and colleagues (2008) have suggested an expansion of the
paraphilias listed in the DSM to include a diagnosis for hebephilia (for individuals who are mostly
erotically attracted to 11–14-year-olds). De Block and Adriaens (2013) provide an extremely interesting,
well-articulated and persuasive argument for the proposal that the DSM classification of paraphilic
behaviours as mental disorders is based on moral, ethical and legal views rather than psychiatric
concerns. Although paraphilias are usually considered to be sexually deviant behaviour (Balon, 2013),
we are not clear what sexual deviance means, and the border between normal or acceptable sexual
behaviour and abnormal sexual behaviour is difficult to determine. Balon (2013) also emphasises
the role of value judgments in the diagnosis of paraphilic disorders. For example, homosexuality was
originally listed in the DSM classification system but was then removed as it was no longer considered
to be a psychiatric disorder but rather a normal variant of the expression of sexuality. Consistent
with these views, Bhugra, Popelyuk, and McMullen (2010) highlight the fact that there is significant
variation across different cultures in terms of the legality of various paraphilic behaviours, which again
highlights the moral, ethical and legal contributions in classifying these behaviours as aberrant.
A method of distinguishing between a normal variant of sexual expression and a paraphilia is to
consider whether the object that causes sexual excitement has a negative effect on others. Another
factor used to identify a paraphilia is the level of interference with the person’s daily functioning,
including his/her interpersonal functioning. In addition, paraphilias are usually diagnosed only when
the sexual behaviour is the individual’s preferred or exclusive form of sexual gratification. As such,
fantasies and occasional sexual experiments would not be classified as a paraphilia since many people
experience fantasies of mild paraphilic behaviours but these are not the preferred or exclusive form of
sexual outlet. In general, a condition is classified as a paraphilia only if it causes significant distress,
is obligatory (i.e., the person feels compelled to engage in the behaviour and is unable to resist
this compulsion), harms others, results in the person engaging in illegal activity or interferes with
relationships.
It is difficult to determine the prevalence of paraphilias due to the private nature of these behaviours.
For example, individuals may be ashamed of their behaviour or fear punishment, given the often
illegal nature of these behaviours, which prevents them from disclosing their problem. Furthermore,
the behaviours are sexually satisfying, which reduces the person’s motivation to seek treatment, again
making it difficult to determine the prevalence of these conditions.
The diagnosis of paraphilic disorders

Paraphilic disorders involve sexual activities or interest in engaging in behaviours other than genitally
focused sexual activities with mature consenting partners. However, it should be noted that Ahlers et
al. (2011) found that 62.4 per cent of men in their study reported sexual arousal to either a fantasy or
exhibitionistic experience of paraphilic situations, indicating that such experiences are common and not necessarily
disorder a disorder. Details on these patterns are summarised in Table 11.5. The paraphilias included in the
A paraphilic DSM-5 (APA, 2013) are exhibitionistic disorder, fetishistic disorder, frotteuristic disorder, paedophilic
disorder that disorder, sexual masochistic disorder, sexual sadism disorder, transvestic disorder and voyeuristic
involves a person disorder. The characteristics of each of these disorders are outlined below.
obtaining intense
sexual arousal EXHIBITIONISTIC DISORDER
from exposing Exhibitionistic disorder is a paraphilic disorder that involves a person obtaining intense sexual arousal
his/her genitals from exposing his/her genitals to an involuntary observer, generally a complete stranger. In order to be
to an involuntary
observer,
classified as a paraphilic disorder, the person needs to have engaged in these behaviours for a period of at
generally a least six months and it is also necessary that the person has experienced marked distress or interpersonal
complete problems as a result of the exhibitionistic fantasies or behaviours. Most exhibitionists are males and a
stranger. large percentage of females have observed exhibitionistic behaviours on at least one occasion.
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TABLE 11.5 Frequency of paraphilia-associated sexual arousal patterns in a community sample

of men (n = 367)
MASTURBATION
PARAPHILIC SITUATION FANTASY n (%) FANTASY n (%) REALITY n (%)
Fetishistic 110 (30.0) 97 (26.4) 90 (24.5)
Transvestic fetishistic 18 (4.9) 21 (5.7) 10 (2.7)
Masochistic 58 (15.8) 50 (13.6) 45 (12.3)
Sadistic 80 (21.8) 73 (19.9) 57 (15.5)
Voyeuristic 128 (34.9) 90 (24.5) 66 (18.0)
Exhibitionistic 13 (3.5) 12 (3.3) 8 (2.2)
Frotteuristic 49 (13.4) 26 (7.1) 24 (6.5)
Paedophilic 35 (9.5) 22 (6.0) 14 (3.8)
Other* 23 (6.3) 23 (6.3) 12 (3.3)
Presence of at least one of 215 (58.6) 175 (47.7) 163 (44.4)

the above categories
*Other includes wearing diapers, sex with babies, sex with elderly, sex with amputees, asphyxia, necrophilic, urophilic, koprophilic or zoophilic.
Source: From Ahlers, C. J., Schaefer, G. A., Mundt, I. A., Roll, S., Englert, H., Willich, S. N., & Beier, K. M. (2011). How unusual are the contents of
paraphilias? Paraphilia-associated sexual arousal patterns in a community-based sample of men. Journal of Sexual Medicine, 8, 1362–1370.
The exhibitionist obtains sexual gratification from the shock, fear or disgust that the victim
displays. If the victim does not react, there is no sexual gratification. There is rarely sexual contact
with the victim. The offender often repeats the exhibitionistic act, which is in a public place, a number
of times. It is not at all uncommon for these offenders to be arrested for repeat offences as the acts are
generally repeated in the same location.
FETISHISTIC DISORDER fetishistic

Fetishistic disorder involves the use of non-living objects or a highly specific non-genital body part disorder
The use of non-
(e.g., feet, toes, hair) to obtain sexual arousal. For heterosexual men, these are commonly women’s
living objects or
clothing (e.g., bras, underpants, shoes or stockings). The difference between a fetish and being aroused a highly specific
by a woman wearing these items of clothing is that for a person with a fetish the sexual arousal is non-genital body
focused on the clothing, whereas for other heterosexual men the clothing simply enhances the sexual part (e.g., feet,
appeal of the woman wearing the apparel. toes, hair) to
For a person with a fetish, the person has difficulty in becoming sexually aroused without it being obtain sexual
present. The items generally have greater appeal if they have been used. The person may hold, rub arousal.
or smell the fetish object and may either masturbate with the object or use it during their sexual frotteuristic
encounter with their sexual partner. disorder
A paraphilia
FROTTEURISTIC DISORDER that leads the
Frotteuristic disorder is a paraphilia that leads the person, usually a younger male, to obtain sexual person, usually
gratification from touching or rubbing against a non-consenting person. The behaviour frequently occurs a younger male,
to obtain sexual
in crowded places (e.g., trains, footpaths or queues). The person may rub his genitals against the legs or
gratification
thighs of the victim or fondle her breasts. He (most people with this paraphilia are male) often fantasises from touching or
that he is in a romantic relationship with the victim but then feels that he needs to escape after touching rubbing against a
the victim before he is detected. Generally people who engage in the behaviour are in the late adolescence non-consenting
period or in their early 20s, and the behaviour generally declines in frequency as the person gets older. person.
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PAEDOPHILIC DISORDER
paedophilic Paedophilic disorder involves intensive, recurrent sexual fantasies, urges or sexual activity with a
disorder prepubescent child or children of either sex, although the paedophile is frequently more attracted to
When a person one sex. The prime form of sexual gratification for a paedophile comes from sexual activity with a
has intensive, prepubescent child (13 years or younger). The paedophile needs to be at least 16 years of age and at
recurrent sexual
least five years older than the child.
fantasies,
urges or sexual Most paedophiles are men and most of them sexually abuse female children. They may also have
activity with a sexual relationships with adult women. The average age of abuse for girls has been reported to be
prepubescent 10 years and for boys to be 11 years (Finkelhor, 1984). Many paedophiles have an immature
child or children personality and poorly developed interpersonal skills. Most acts of child sexual abuse are perpetrated
of either sex. in the home (either the victim’s home or that of the perpetrator) and the paedophile is known to the
victim (frequently a relative or friend of the family).
Trust is established with the child and coercive strategies are used to engage the child in
sexual acts (e.g., ‘This is our little game’ or ‘I will look after you if you do this’). The child is
frequently sworn to secrecy and threatened to remain silent about the sexual abuse. The sexual acts
perpetrated by the paedophile include touching of the child’s genitals, exposure of the perpetrator’s
genitals, and coerced or forced fondling of his genitals. Actual sexual intercourse occurs in about
10 per cent of cases. Many paedophiles have been abused themselves in childhood, although the
vast majority of victims of paedophilia do not become paedophiles in adulthood. For those who
do develop paedophilia in adulthood, it is possible that they are attempting to resolve their own
negative experiences and sort through the feelings of guilt, anger and hurt that have stemmed from
this experience. In an attempt to describe the factors associated with paedophilic disorder, Kruger
and Schiffer (2011) found that paedophiles were more likely than controls to demonstrate higher
levels of psychopathology (such as paranoia), as well as signs of sexual obsessiveness and sexual
dysfunction. However, the sample size in this study was small, so these results need to be treated
with caution.
When the victim is a close relative of the paedophile, the act is one of incest, which refers to sexual
relationships between close relatives. As with paedophilia more generally, it is difficult to determine
the actual prevalence of incest. The victims often feel powerless and are sworn to secrecy so they tend
not to report the crime. Further, even if they do tell someone else about what is happening, they may
not be believed or the act may not be reported to legal authorities. Therefore the level of incest (and
other forms of paedophilia) reported to the authorities is likely to be a gross underestimation of the
prevalence of the condition.
Incest occurs in a wide range of situations and it is difficult to specify the type of perpetrator,
victim or family for which it is likely to occur. However, Finkelhor (1984) identified a number of
factors that are likely to increase the occurrence of the behaviour: the presence of a step-father; a
traditional role structure to the family (i.e., a dominant father figure, a submissive mother, and the
expectation of obedient children); a distant non-affectionate mother who is frequently absent from the
family; low socioeconomic status; and the victim having few friends. Having said this, incest has been
found to occur in a very broad range of family situations.
There has been limited well-controlled research on the long-term effects of incest. This is partly
due to the fact that describing the experience is dependent upon retrospective recall and so there may
be many intervening experiences that influence the accuracy of the recall of the incest or child abuse
experience. For instance, the way in which the child is treated at the time of the abuse (e.g., the extent
to which the child is believed and not blamed for the abuse), the level of support provided for the child,
the quality of the child’s relationships both in childhood and in adulthood, as well as the severity and
length of time of the abuse are all likely to influence the impact of the abuse both immediately in
childhood and later in adulthood. Higgins, McCabe, and Ricciardelli (2003) found that if the sexual
abuse was associated with high levels of physical abuse, it was the physical abuse that explained most
of the maladjustment in adulthood.
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SEXUAL SADISTIC AND SEXUAL sexual sadistic

MASOCHISTIC DISORDER disorder
The experience
Sexual sadistic disorder involves the
of sexual arousal
experience of sexual arousal from the from the physical
physical or psychological suffering of another or psychological
person. Sexual masochistic disorder is the suffering of
erotic excitement that comes from being another person.
the recipient of such activities as being
sexual
humiliated, beaten, bound or otherwise made
masochistic
to suffer. These activities often involve both
disorder
dominance and aggression. In bondage and The erotic
domination situations, a victim is bound, excitement
gagged and immobilised at the mercy of the a person
master or mistress. This bondage occurs using experiences from
chairs, shackles, harnesses and whips. The such activities as
aggression then involves verbal humiliation being humiliated,
SAUL LOEB/GETTY IMAGES

beaten, bound or
and whippings, which can vary in intensity.
otherwise made
The victim can either be non-consenting or a to suffer.
willing collaborator.
As with the other paraphilias, males are
more likely to engage in sexual masochism and transvestic
sadism than females. Prevalence figures are disorder
again difficult to determine, particularly since The popular book Fifty Shades of Grey features elements When men who
couples may buy some of the paraphernalia of sexual practices involving sadism and masochism. view themselves
(e.g., handcuffs) associated with these as male become
sexually aroused
activities and occasionally experiment with these behaviours while not having a paraphilia.
by the process of
cross-dressing.
TRANSVESTIC DISORDER
This paraphilia involves the experience of recurrent and intense sexual arousal from cross-dressing. gender identity
Sexual arousal results from the associated images that the man has of being a female. Transvestic disorder
disorder is not diagnosed in an individual with gender identity disorder—that is, an individual who Disorder in which
the individual
perceives that s/he is actually a member of the opposite sex (e.g., a man trapped in a female body). believes that s/he
Instead, transvestic disorder is confined to men who view themselves as male but become sexually was born with
aroused by the process of cross-dressing. This cross-dressing may involve a few items of women’s the wrong sex’s
clothing or may entail dressing entirely as a female and using make-up. genitals and is
Although men with this disorder are generally heterosexual, they tend to have had few sexual partners. fundamentally
The condition is likely to have commenced in childhood or early adolescence, and to have initially a person of the
involved partial cross-dressing, which then developed into more complete and public cross-dressing in opposite sex.
adulthood. Also, gender dysphoria (i.e., confusion about one’s gender identity and a discomfort with voyeuristic
one’s biological gender) may eventually develop in some men who initially display this disorder. disorder
The experience
VOYEURISTIC DISORDER of being sexually
Voyeuristic disorder involves looking at unsuspecting individuals, who are usually strangers, as they aroused by
are undressing, in the act of sexual activity or when they are naked. This activity is sexually arousing secretly watching
and the voyeur engages in masturbation while viewing the activity or masturbates to the memory of another person,
the activity at a later point in time. Frequently the person has a fantasy about having a relationship usually a stranger,
undressing,
with the watched person, but this relationship very rarely actually occurs. This condition generally bathing,
develops prior to 15 years of age, although the minimum age for a diagnosis is 18 years. engaging in
It is important to distinguish voyeurism from voyeuristic behaviour, where sexual arousal is sexual activity or
achieved by looking at naked photographs or strip shows. Voyeurism is repetitive and compulsive being naked.
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and the person being observed does not know that this is occurring. It is the secret nature of the
observation that is sexually arousing.
The aetiology of paraphilic disorders

There is little data on the origins of most of the paraphilias. However, it is generally believed that
the causes originate in childhood or adolescence. Both psychoanalytic and learning explanations
have been developed to explain paraphilias. Using fetishism as an illustration of these two accounts,
people with a fetish may report childhood experiences involving the fetishist object. For example,
from a psychoanalytic perspective, a boy’s mother may have worn black high-heeled shoes and his
unacceptable sexual fantasies about her transferred to less threatening fantasies about her shoes
(Stoller, 1977). Within the learning framework, this same fetish may be seen as an instance of classical
conditioning. That is, the boy may have become sexually aroused in a situation that featured black
high-heeled shoes and, through this pairing, the shoes subsequently became a conditioned stimulus for
eliciting sexual arousal.
The treatment of paraphilic disorders

Just as the aetiology of the paraphilias remains unclear, the treatment of these conditions also
requires further research. Various types of treatment approaches have been used. Biological
treatments have been used to reduce the sex drive of perpetrators. Both chemical castration
(i.e., the use of hormones to reduce the sexual drive) and surgical castration (i.e., removal of
the testes) have been employed. The actual effectiveness of these treatment strategies has been
questioned and it is now recommended that, even if they are used, they should be employed in
conjunction with psychological therapy so that the person with the disorder engages in rehabilitation
(Kelley & Byrne, 1992). Further, most participants in paraphilia studies are recruited from prisons
or legally mandated treatment groups, and they primarily focus on paedophilia, exhibitionism and
rape (Balon, 2013).
Various types of behaviour therapy are frequently employed in the treatment of paraphilias. These
approaches typically employ strategies involving aversion therapy and exposure therapy. In aversion
therapy, an unpleasant or painful stimulus is paired with the inappropriate behaviour. For example, a
transvestite may be instructed to engage in fantasies that include waves of nausea and vomiting as part
of a sexual scene in which he is dressed as a woman, whereas a shoe fetishist might imagine shoes as
foul smelling, covered with fungus and coated with faeces rather than as a source of sexual excitement.
While aversion therapy aims to reduce sexual associations with paraphilic situations, exposure therapy
aims to reduce anxiety associated with non-paraphilic situations. Various forms of exposure therapy
are frequently used to assist the person to feel less anxious about non-paraphilic sexual interactions.
For instance, in systematic desensitisation, the individual is asked to imagine non-paraphilic sexual
interactions and to pair these with a relaxation response.
social skills Another behavioural approach that is also receiving some support is social skills training. Given
training that most people with paraphilias seem to have marked social deficits, this may be an area worth
Behavioural exploring in future treatment approaches. Social skills training aims to help teach people with a
technique that paraphilia how to interact with others in a comfortable and pleasant way. Although these skills can be
aims to help
learnt by people experiencing paraphilias, Seto (2009) suggests that, at least for paedophilia, there is
clients with
problems in no evidence to suggest that these treatments are effective.
interacting and Recent treatment approaches for the paraphilias are outlined by Marshall and Marshall (2015).
communicating The authors divide the targets of treatment into those that have been present over a long period of
with others. time (e.g., insecure attachment, lack of intimacy, loneliness, poor self-regulation and lack of concern
for others) and acute factors that arose in the offender’s life just prior to the onset of offending. It
is recommended that treatment focuses on both sets of factors. However, there has been limited
evaluation of the differences between the various paraphilias in these predisposing factors as well as
the effectiveness of treatments to address them.
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LO 11.3 Relationship problems

In addition to sexual problems, couples may also experience problems in their relationship more
generally. Mention has already been made regarding the strong association between relationship
problems (such as marital conflict and a lack of intimacy) and sexual dysfunction. In addition,
combining relationship and sex therapy has been found to produce greater improvements in sexual
functioning than sex therapy alone (Snyder, Castellani, & Whisman, 2006). There is likely to
be a bi-directional association between relationship and sexual difficulties, with each having a
negative impact on the other (McCabe et al., 2010). The extent to which this is the case varies for
men and women, with men generally being more likely to separate these two areas of difficulty.
Australian research has demonstrated that sexual problems in one partner may even lead to sexual
and relationship problems in the other partner (Hucker & McCabe, 2014; McCabe et al., 2010).
Given this association between sexual and relationship problems, any discussion of sexual problems
requires mention of relationship problems and vice versa. The remainder of the chapter will therefore
focus on relationship problems.
Historical and current approaches to understanding

relationship problems
Researchers have been interested in the factors related to marital problems for a long time. For example,
Terman, Buttenweiser, Ferguson, Johnson, and Wilson in 1938 published a book that was exclusively
focused on the psychological factors related to marital problems. The major focus of research in
the 1940s was on spouse personality characteristics that were associated with marital problems.
This research demonstrated that in unhappy marriages, spouses attribute negative long-lasting
characteristics to their partner (e.g., ‘My husband is selfish’), while in happy marriages the spouses
are generally viewed positively and any negative characteristics are attributed to temporary situational
factors (e.g., ‘My husband is unable to be supportive at the moment since he is busy at work’). These
early research findings demonstrated that it was the perception of the spouse’s personality (not their
personality per se) that was related to marital problems.
In the 1950s there was a substantial shift in the study of factors related to relationship problems.
There was a change from a focus on individual factors (e.g., personality characteristics) to a focus
on the interactional style of individuals in the relationship (Bateson, Jackson, Haley, & Weakland,
1956). These researchers suggested that it was dysfunctional interactional patterns that predicted
poor marital quality. Thus, the focus in research changed from individual questionnaire data to
the observation of the patterns of couple interaction (Bradbury, Fincham, & Beach, 2000). In the
standard relationship observation paradigm, couples are required to complete an inventory listing
their areas of conflict. The couple is then instructed to discuss a topic of conflict and attempt to
reach a resolution (typically for 10–15 minutes) in a manner that is as close as possible to their
style at home. The ensuing encounter is then videotaped and the encounters of couples who are
satisfied or dissatisfied with their relationship are compared. Thus there were shifts in both the
focus (interactional patterns) and methodology (behavioural observation) (Gottman, Markman, &
Notarius, 1977).
A new wave of research in the 1960s and 1970s increased the focus from behavioural observations
to also explore the internal states (i.e., cognitions and affect) of couples. Yet much of the observational
research conducted during this period failed to support the complex theoretical models that were
proposed at the time. Instead, research indicated that unhappy couples were simply more negative in
their behaviour, thoughts and feelings than happy couples (Gottman, 1979).
With the growth of feminism in the 1960s and 1970s, a new focus of investigation was how power,
and power imbalances, affected family dynamics (Broderick, 1993). The importance of gender roles
in the distribution of power was investigated, as well as the impact of family violence (Gelles, 1980).
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During the 1980s and 1990s the study of factors related to divorce became a new focus of marital
research. For instance, Gottman and Levenson (1992) found in a longitudinal study over a three-
year period that negative interaction patterns were highly predictive of later divorce. The research
in the 1990s also continued to focus on interaction patterns (Bradbury, Fincham, & Beach, 2000).
For example, the demand/withdraw pattern was investigated, where one spouse (typically the
wife) criticises the other spouse (typically the husband) who withdraws and disengages from the
confrontation. The end result of this process is a decline in the quality of the marital relationship.
More recent research has primarily focused on a more complex understanding of the factors that
may be related to relationship problems. Rather than factors being seen to directly predict relationship
satisfaction, more complex processes have been considered. An example of such a process is
that depression may lead to greater negativity in relationships (e.g., increased levels of anger and
discontent, particularly among wives), which may, in turn, lead to relationship problems (e.g., an
increase in conflict and a reduction in levels of intimacy) (McCabe & Gotlib, 1993). Thus depression
has an indirect rather than a direct impact on relationship quality through its role in triggering anger.
Also highlighting the interaction among multiple factors, violence has been shown to interact with
power in that men who perceive they have less power in a relationship tend to demonstrate higher
levels of violence. These men also offer less social support to their wives, which may be another factor
contributing to relationship problems (Pasch & Bradbury, 1998).
The aetiology of relationship problems

Factors that are theorised to be related to relationship problems have varied substantially depending
upon the focus of the researchers conducting the studies. Some studies have primarily focused on the
characteristics of the individuals involved in the relationship (e.g., the biological and psychological
characteristics of each partner) whereas others have focused on the dynamics of the relationships
(e.g., the communication, sexual satisfaction and conflict between the partners). Other research
has considered the broader context in which the relationship is situated (e.g., the role of children in
contributing to the relationship dynamics). This section evaluates research that has been conducted in
the past 20 years that has focused on factors related to relationship problems. In order to facilitate the
understanding and interpretation of these findings, they will be classified under the broad headings of
individual factors, relationship dynamics and contextual factors.
INDIVIDUAL FACTORS
Biological factors
Among the biological factors that have been investigated in terms of their possible association with
relationship problems are hormonal disturbances. One study assessed 90 couples at two time-points:
during the first year of marriage and 10 years later (Kiecolt-Glaser, Bane, Glaser, & Malarkey, 2003).
A variety of biological and psychological measures were taken at the first assessment including levels
of various stress-related hormones (e.g., adrenaline) and negative mood. These measures were taken
before and after the couple discussed with each other a topic of conflict in their relationship. It was
found that the levels of adrenaline were significantly higher in couples who had divorced by 10 years
compared to those couples who were still married. As shown in Figure 11.2(a), adrenaline levels
were significantly higher in couples who later divorced compared to those who remained married
both before and after the conflict discussion. In contrast, there was no significant difference between
the groups who later divorced and stayed married in terms of their depressed or hostile mood before
or after the conflict discussion (if anything, the married group had higher levels of depressed and
hostile mood). The results for depressed mood are shown in Figure 11.2(b). The researchers explained
the differences between the physiological and mood data by suggesting that disturbances in stress
hormone levels may be an early sign of distress among newlyweds that they have not yet consciously
acknowledged.
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(a) (b)
45 42
Divorced Divorced
Married Married
40
40
Depression scores
Adrenaline
35
38
30
25 36
Before conflict After conflict Before conflict After conflict
FIGURE 11.2 Levels of adrenaline (a) and depressed mood (b) before and after a conflict discussion in
couples who later divorced compared to those who remained married
Source: Kiecolt-Glaser, J. K., Bane, C., Glaser, R., & Malarkey, W. B. (2003). Love, marriage, and divorce: Newlyweds’ stress hormones
foreshadow relationship changes. Journal of Consulting and Clinical Psychology, 71, 176–188, © 2003 The American Psychological
Association. Used with permission.
Personality
Personality is another individual characteristic that has been investigated as a possible causal factor for personality
relationship problems. A longitudinal study conducted by Caughlin, Huston, and Houts (2000) found Habitual and
that high levels of neuroticism (i.e., being prone to negative affect) predicted the later development enduring ways of
thinking, feeling
of relationship problems over a 13-year period. Gattis, Berns, Simpson, and Christensen (2004)
and acting.
examined six personality dimensions of 132 distressed couples and 48 non-distressed couples. The
authors found that low levels of neuroticism and high levels of agreeableness (i.e., high desire to
please others), conscientiousness (i.e., being goal-directed) and positive forms of expression (i.e., an
open, pleasant demeanour) were related to relationship satisfaction.
Research has also sought to determine whether partners with complementary personalities (i.e., opposite
types of characteristics such as one partner being shy while the other is outgoing) or similar personalities
are more likely to experience satisfying relationships. Gattis and colleagues (2004) found no relationship
between the extent to which both partners were similar in personality traits such as conscientiousness and
agreeableness and their relationship satisfaction. In contrast, Zentner (2005) found that among couples
tracked over a nine-month period, the degree of similarity between partners in their levels of agreeableness
and openness to experience were associated with relationship satisfaction. However, it may simply be
that these two personality characteristics are directly associated with relationship satisfaction, and that
relationship satisfaction is even more likely to occur if both partners are high in these characteristics.
Cognitive factors
In addition to personality, cognitive factors have also been investigated as a possible contributor to
relationship problems. For example, in a study of couples who had been married in the past six months,
Neff and Karney (2005) found that it was the accuracy of the individual’s perceptions of his/her partner’s
qualities (i.e., the level of agreement between the individual’s and partner’s assessment of the partner)
that predicted the quality of the relationship. The results demonstrated that those couples with a realistic
evaluation of each other’s attributes were more likely to report being satisfied with their relationship.
This may well suggest that, rather than an optimistic view of the partner’s qualities being associated
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with relationship happiness, it is more important to accurately perceive the partner’s characteristics
(both strengths and weaknesses) and to nevertheless value the partner and the relationship.
One cognitive factor that has received considerable attention in the literature concerns the
attributions that an individual makes to explain the causes of his/her partner’s behaviour (Bradbury &
Fincham, 1990). Research has found that couples who are dissatisfied with their relationship are more
likely to use the following attributions to explain their partner’s negative behaviour (such as a husband
coming home late from work):
The cause is internal to the partner (e.g., ‘He came home late because work is more of a priority to
him than I am’).
The cause is stable over time (e.g., ‘He came home late because he always makes work his priority’).
The cause is global across situations (e.g., ‘He came home late because he makes work and other
situations such as his friends a priority over me’).
In contrast, couples who are satisfied with their relationship are more likely to use the following
attributions to explain their partner’s negative behaviour:
The cause is external to the partner (e.g., ‘He came home late because his boss has given him
extra work’).
The cause is unstable over time (e.g., ‘He came home late because for once he needed to make
work his priority given how busy he is at the moment’).
The cause is specific to this particular situation (e.g., ‘He came home late because he is busy at
work but otherwise he is usually on time’).
Bradbury and Fincham (1990) have proposed a model linking attributional style to each partner’s
behaviour and, ultimately, satisfaction with the relationship. As shown in Figure 11.3, the model
proposes that partner A’s behaviour (e.g., coming home late) triggers an attribution regarding this
behaviour by partner B (e.g., ‘He came home late because work is more of a priority to him than
I am’). This attribution in turn influences partner B’s behaviour (e.g., criticising partner A for not
being caring enough), which will in turn influence partner A’s behaviour (e.g., withdrawing). Partner
A’s behaviour then elicits further attributions by partner B (e.g., ‘Even when he is home he doesn’t
spend time with me because I’m not a priority to him’). These negative encounters not only influence
each partner’s satisfaction with the relationship in the short term at the time of the encounter, but may
also build up over time to reduce overall long-term satisfaction with the relationship.
Partner A’s
behaviour
(e.g., coming
home late)
Short-term
relationship satisfaction
Partner B’s
attribution
(e.g., ‘work is
more of a priority
than I am’) Long-term
relationship satisfaction
Partner B’s
behaviour
(e.g., criticise
partner A for
not caring)
FIGURE 11.3 A model of how attributions regarding a partner’s behaviour influence the subsequent
behaviour of both partners and both short- and long-term relationship satisfaction
Source: Bradbury, T. N., & Fincham, F. D. Attributions in marriage: Review and critique. Psychological Bulletin, 107, 3–33, 1990, the American
Psychological Association, reprinted with permission.
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RELATIONSHIP DYNAMICS
Communication
Much of the focus in research investigating the impact of relationship dynamics on satisfaction with
the relationship has been on communication. One aspect of communication is self-disclosure (i.e., the
extent to which a person discloses the type of person they are), which appears to be an important aspect
of relationship dynamics related to relationship problems. This factor may contribute to relationship
problems in that the partner may be unable to address the real needs and concerns of the other partner
if there are low levels of self-disclosure. Fitzpatrick and Sollie (1999) demonstrated that low levels of
self-disclosure were strongly predictive of relationship problems over time. However, the respondents
in this study had been in a relationship for only a mean of 15.3 months when levels of self-disclosure
were assessed and these early levels of self-disclosure may not have characterised the later stages of
the relationship (e.g., couples with initially low levels of self-disclosure may have become more open
with each other over time).
Nonetheless, lending further support to the notion that low levels of self-disclosure have a negative
effect on relationships are the results obtained by Finkenauer and Hazam (2000), who studied long-
term relationships. Specifically, their study included 73 men and women who had been married for a
mean of 42.5 years and found that both disclosure and secrecy were related to relationship problems.
The results demonstrated that participants who felt uncomfortable sharing their emotions and who
could not talk about difficult issues with their partner were less satisfied with their relationship.
Interestingly, the results also indicated that avoiding topics that are difficult to change (e.g., ‘you
shouldn’t have spent so much money’) was also associated with relationship satisfaction. Thus it
would appear that disclosure and communication are important elements of satisfying relationships,
but this does not imply that everything needs to be discussed. In fact, it may be that communication
should focus on those issues that can be changed and resolved.
In support of this proposal, Mackey, Diemer, and O’Brien (2004) found that, for relationships that
had lasted for an average of 30 years, good communication was an essential ingredient in predicting
relationship satisfaction. However, avoidance of issues that are perceived to lead to conflict (especially
by men) was also associated with relationship satisfaction. What seemed to be important in the
relationship was that both partners understood and accepted the difficulty in discussing differences
and so any potential anger at the partner for withdrawing from such conversations was reduced.
Conflict
Conflict is another important aspect of relationship dynamics that has been found to be negatively
associated with relationship satisfaction. Clements, Stanley, and Markman (2004) conducted a
longitudinal study of 100 couples over a period of 13 years. The results demonstrated that pre-marital
interaction styles and levels of conflict were important predictors of marital outcomes, with initially
higher levels of conflict predicting later marital problems. It would appear that early interactions
influence both partners to view the relationship in either a predominantly positive or negative
manner. These perceptions of the relationship then create filters through which the partner and the
relationship are viewed. Positive filters further enhance the relationship whereas negative filters may
create a negative spiral. Specifically, positive interactions lead to a positive view of the relationship.
This predisposes both partners to approach each other in a positive manner, which creates another
positive relationship experience that in turn strengthens the overall positive view of the relationship.
High levels of conflict, in contrast, lead to negative perceptions of the relationship. This perception
predisposes both partners to respond to one another in a destructive and negative manner (e.g., being
critical of one another or withdrawing), which creates further negative experiences and solidifies the
overall negative view of the relationship.
However, it may be the way in which conflict is managed, rather than the actual presence of
conflict, that is important in predicting relationship satisfaction. Mackey, Diemer, and O’Brien (2000)
found among 216 partners who had been in a relationship for an average of 30 years that it was not
actually the presence or absence of conflict that predicted relationship satisfaction. Instead, it was
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the resolution of conflict that predicted the success of relationships. It would seem that the way in
which couples are able to discuss difficulties in a positive and solution-focused manner contributes to
relationship satisfaction. In contrast, the tendency to engage in negative behaviours (e.g., criticising
or interrupting the partner) when discussing conflict topics has been found to predict relationship
dissatisfaction 10 years later (Kielcolt-Glaser, Bane, Glaser, & Malarkey, 2003).
Extreme levels of conflict may entail violence and aggression. Alarmingly, Halford, Farrugia,
Lizzio, and Wilson (2010) found that more than 20 per cent of newlywed Australian couples reported
at least one incident of relationship violence in the past year. The authors suggest that strategies which
enhance relationship self-regulation (i.e., strategies which ensure that both partners have a voice in the
relationship and that they are satisfied with the way in which the relationship is progressing) may help
reduce the prevalence of aggression.
Sexual functioning
As previously stated, an association has also been found between sexual functioning and relationship
problems. Christopher and Sprecher (2000) conducted a review of papers completed in the 1990s that
examined sexuality in marital and committed relationships. This review demonstrated that research
has found an association between sexual satisfaction and relationship satisfaction, although sexual
intimacy may not be as strong a predictor of relationship quality as other forms of factors (such as the
quality of communication). Christopher and Sprecher (2000) suggest that both sexual satisfaction and
relationship satisfaction are likely to be reciprocal associations, with a problem in one area leading to
a high level of difficulty in the other area.
Yet there is some data to
suggest that this reciprocal
interaction between sexual
and relationship satisfaction
is stronger for women than
for men. That is, McCabe
and Cobain (1998) found
that sexual dysfunction was
likely to be associated with
problems in most aspects of

a woman’s relationship (e.g.,
intimacy, anger and conflict)
but was relatively independent
of relationship functioning
for men. These findings
DAL
Relationship problems stem from a range of factors such as personality

suggest that a woman’s sexual
traits, poor communication and contextual features (e.g., having children).
response, and her satisfaction
Treatments aim to increase positive couple behaviours, improve with that sexual response, is
communication and use problem solving as an alternative to arguing. closely related to her level
of relationship satisfaction:
if one of these aspects of her
life is functioning well, it is likely to spill over into the other area of her functioning. In contrast,
men are more likely to separate these different dimensions of their lives, with sexual and relationship
satisfaction tending to operate more independently of one another. More recent findings support these
results. Giles and McCabe (2009) found that relationship factors predicted most aspects of sexual
dysfunction among women, but McCabe and Connaughton (2014) found that relationship problems
did not predict any aspect of male sexual dysfunction.
CONTEXTUAL FACTORS
The wider context in which a relationship is embedded is also likely to influence the development of
problems within that relationship.
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Becoming a parent
The literature indicates that becoming a parent may be associated with high levels of relationship
problems as reported by Twenge, Campbell, and Foster (2003) who conducted a meta-analysis of meta-analysis
studies that have investigated this association. The negative association between parenthood and Statistical
relationship satisfaction appears to be further exacerbated with increasing numbers of children, and is technique for
summarising
most prominent for women when their children are young.
results across
There have been a number of reasons suggested for the increase in relationship problems with the several studies.
advent of children. One of these is that the arrival of a child presents additional stressors on the mother
in terms of fatigue, possible feelings of inadequacy as a mother, changing roles and confinement
to the home. In fathers, the stressors traditionally relate to economic pressures, the wife’s sexual
unresponsiveness, and a general disenchantment with the parental role.
Twenge and colleagues (2003) suggest that, rather than discouraging people from having children,
the results of their meta-analysis should help potential parents to be aware of the possible challenges
of having children and put in place strategies to protect their relationship satisfaction. Strategies
to consider are a more equitable sharing of responsibilities between spouses to reduce the burden
on women as caregivers. Parents may also consider the use of reliable day care in order to provide
mothers with a break from their childcare role.
Employment
Related to the role of parenthood is the issue of employment and how this might impact on relationship
satisfaction. Many more married women are now in the workplace compared to previous generations
(Saginak & Saginak, 2005). The typical family profile now is of both mothers and fathers working,
with figures from the United States indicating that 75 per cent of mothers who have school-aged
children work, many of them full time (United States Bureau of the Census, 1998). As a result, men
are now more likely to be involved in the care of children, with some estimates suggesting that fathers
contribute about one-third of childcare responsibilities in the home. There has been limited research
that has examined the impact of both partners working on marital problems. Early research suggested
that the wife’s employment detracted from the time she had available to spend with her partner,
and, particularly for wives who were employed full time, this detracted from her husband’s health
(Stolzenberg, 2001). This is primarily because the wife generally still completes most of the household
tasks, despite her employment outside of the home (Shelton & John, 1993). In fact, research suggests
that work for the male partner enhances both his own wellbeing as well as that of the relationship,
whereas employment for the female partner (in the context of a high workload in the home) appears to
detract from marital quality and fails to improve her own wellbeing (Stolzenberg, 2001).
There is little doubt that the role of work is more complex than these preliminary studies would
suggest, and future research needs to focus not only on work outside the home but work within the
home and how this level of work is negotiated between the partners. For instance, a factor that is likely
to predict marital problems is the perception of equality held by both the husband and wife in the way
in which labour is divided. Zimmerman, Haddock, Current, and Ziemba (2003) found that, for couples
with children where both partners were working, an important predictor of relationship satisfaction
was if they believed there was shared responsibility for both household tasks and parenting. This was
despite the fact that wives were likely to complete more of the work. The important factors were that
the decision-making process was shared, that there was respect and recognition of the contribution of
both partners, and that there was equal access to financial resources. Consistent with these findings,
Stevens, Kiger, and Riley (2001) also found that negotiation over household tasks and a sense of
equity in the way in which these tasks were shared were both important factors that contributed to
relationship satisfaction.
These changing roles in the division of labour are likely to benefit both men and women.
Negotiations of a balance between work and family not only enhance relationship satisfaction, but
also increase each partner’s feelings of success. There is an increased opportunity for men to interact
with their children and obtain a greater appreciation of the joys of parenthood. There is also a greater
opportunity for women to obtain satisfaction from the development of their skills through working
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outside the home. More research is needed regarding the impact on the relationship that stems from
these changing gender roles.
Negative social attitudes towards homosexual couples

Homosexuality includes people who identify as homosexual, who engage in same-sex sexual
behaviour and/or who experience sexual or erotic attraction to members of the same sex (Herek &
Garnets, 2007). Thus, homosexuality comprises a cognitive, behavioural and emotional component,
and people may experience all or only some of these aspects within their homosexual orientation. In
a study that looked at the sexual orientation of 34 653 adults, 6 per cent of the participants reported
a same-sex sexual attraction and 4 per cent reported at least one same-sex sexual partner during their
lifetime, yet only 2 per cent of the participants actually identified as lesbian, gay or bisexual (McCabe,
Hughes, Bostwick, West, & Boyd, 2009).
A contextual factor that specifically places homosexual couples at risk of developing relationship
problems is that of negative social attitudes towards gay and lesbian relationships (Bepko &
Johnson, 2000). Given the association between relationship and sexual problems outlined earlier
in this chapter, these relationship problems are likely to also be associated with sexual difficulties
for homosexual men and women. There is evidence indicating that living in a culture that expresses
varying degrees of homophobic attitudes places considerable strain on lesbian and gay couples.
For example, any public display of affection between the couple may trigger verbal or physical
aggression from others. These attitudes and behaviours can be understood within the context of
a minority stress model (Meyer, 2003). Put simply, minority stress is believed to be a form of
psychological stress derived from membership of a low-status minority group: it is unique, chronic
and socially based. Not only the wider society but family and friends may also find it difficult to
support an individual’s homosexuality, which may in turn have a negative impact on the relationship
as the following scenario describes:
Josh was invited as a single guest to his cousin’s wedding. Although many of his extended relatives
knew of his 10-year relationship with Sean, the wedding hosts knew how embarrassed and anxious
Josh’s parents would be if the couple attended together. Sean endorsed confrontation with Josh’s
family. He was irritated with Josh’s divided loyalty which led to conflict between them.
Bepko & Johnson, 2000, p. 412
The pervasiveness of these negative social attitudes may result in homosexual individuals
internalising such attitudes themselves, which in turn has a negative impact on their relationships, as
illustrated in the following case:
John had struggled for most of his life with shame about his perception that he was effeminate.
Given that he also wanted to ‘pass’ as straight, he was very vigilant about his ability to act in a
masculine manner and to hide his femininity. When he developed a relationship with Paul, his
concern about being ‘butch’ created multiple problems for the couple. John became anxious at the
prospect of appearing dependent or conciliatory towards Paul when outside their home. He also
became irritated with the playful effeminacy and mockery of gender stereotypes by Paul’s friends.
Bepko & Johnson, 2000, p. 410
Successful couple therapy for homosexual couples would need to address the unique strains to
which they are exposed. Of course, therapists are also part of the broader society and so may be
affected by the homophobic views of this society. It is therefore important that therapists are aware of
the extent to which they hold these views and hence how they may affect their therapeutic intervention.
INTEGRATIVE MODELS
One model that attempts to integrate the various individual, relational and contextual factors that
contribute to relationship satisfaction has been put forward by Karney and Bradbury (1995) and
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is depicted in Figure 11.4. According to this model, stressful events (e.g., becoming a parent or
employment demands) may trigger a range of negative relationship dynamics on the part of the
couple (e.g., increased conflict and reduced partner support). These negative dynamics may in turn
worsen the stressful event (e.g., increased couple conflict making parenting more difficult). As such,
the couple becomes locked into a vicious cycle characterised by increasing stress and deteriorating
relationship dynamics. The model also proposes that each partner may have certain longstanding
vulnerabilities (e.g., high levels of the personality trait neuroticism) that increase their likelihood of
experiencing negative couple dynamics and may also result in greater exposure to stressful events
(e.g., individuals high in neuroticism are known to experience higher stress in response to negative
life events). Over time, negative relationship dynamics (e.g., poor conflict resolution) contribute to
decreasing relationship satisfaction and eventual instability (possibly culminating in relationship
termination). Finally, low levels of satisfaction with the relationship are hypothesised to exacerbate
negative relationship dynamics (e.g., an individual who is dissatisfied with the relationship may be
less likely to provide his/her partner with support).
Individual vulnerabilities Stressful events

(e.g., neuroticism) (e.g., parenting)
Relationship dynamics
(e.g., conflict)
Relationship dissatisfaction
and instability
FIGURE 11.4 A model regarding the development of relationship dissatisfaction and instability that
integrates stressful events, relationship dynamics and individual vulnerabilities
Source: From Karney, B. R., & Bradbury, T. N., The longitudinal course of marital quality and stability: A review of theory, method and
research. Psychological Bulletin, 118, 3–34., 1995, the American Psychological Association, reprinted with permission.
A developmental perspective on relationship problems

With life expectancy increasing over the past century, the number of years people will remain married
has also increased. In previous generations, men and women did not survive long after the rearing of
their children. However, partners in relationships now need to negotiate a number of different stages:
early years before children; child-rearing years; children leaving home; retirement for one or both
partners; and sharing old age, with the possibility of health problems for one or both partners. Each
of these stages brings positive and negative experiences to relationships. The stresses on relationships
among older people are demonstrated by the finding that about one-fifth of all terminated marriages
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are those of middle-aged or older adults (Weishaus & Field, 1988). Despite the increased number
of older people in the community, there has been limited investigation of their relationships and the
factors that contribute to relationship satisfaction.
Cross-sectional studies conducted in the 1970s and 1980s suggested that relationship problems
were low in the early years of marriage, increased in the child-rearing years and then decreased again
when children left home (Anderson, Russell, & Schumm, 1983; Gilford & Bengtson, 1979; Rollins &
Cannon, 1974; Weishaus & Field, 1988). The researchers claimed that this was partly due to increased
positive interactions later in life: the couple now had increased time to spend together and increased
time for leisure activities (as opposed to parenting and work) so that there was more opportunity to
develop greater intimacy.
However, this view of increased marital happiness in older age is contaminated by methodological
cross-sectional problems in the research studies that gathered the data. The studies were primarily of cross-sectional
design design, and so the older people who formed part of the study were those whose relationships had not
Type of research ended in divorce. In contrast, the samples for the younger groups may have consisted of a more
examining diverse group in terms of relationship satisfaction (including those who would later divorce). There
participants at
were also problems in how the samples of older married couples were recruited. That is, they were
one point in
time but not frequently recruited through senior citizen centres and churches (Sporakouski & Axelson, 1984),
following them retirement communities (Lauer, Lauer, & Kerr, 1990) and advertisements (Roberts, 1979). These
over time (as in strategies are likely to attract participants who are in better health, more socially active and happier
a longitudinal with their marriage. Thus the sample of older participants may not have been representative of
design). older adults in general in terms of their relationship satisfaction. These studies highlight the need
for further research (ideally longitudinal in design) to clarify the changing nature of relationship
problems across the lifespan.
The treatment of relationship problems

BEHAVIOURAL AND COGNITIVE-BEHAVIOURAL COUPLE THERAPY
Behavioural and cognitive-behavioural treatments (CBT) have been the most widely evaluated
interventions for couples experiencing relationship problems (Baucom & Epstein, 1990; Baucom,
Shoham, Mueser, Daiuto, & Stickle, 1998; Halford, Sanders, & Behrens, 1993). Behavioural
treatment for relationship difficulties was initially developed approximately 30 years ago (Schmaling,
Fruzzetti, & Jacobson, 1989). Since this time it has evolved extensively, most notably in the addition
of cognitive techniques to supplement the behavioural techniques. Typical techniques utilised in
behavioural approaches to relationship problems include behaviour exchange, communication training
and problem solving. CBT also incorporates challenging dysfunctional cognitions in addition to these
behavioural strategies (Epstein, Baucom, & Daiuto, 1997; Schmaling, Fruzzetti, & Jacobson, 1989).
Behaviour exchange seeks to engage both partners in activities designed to enhance each other’s
relationship satisfaction. Each partner is asked what behaviours s/he could perform to improve his/
her partner’s satisfaction with the relationship. Typically these behaviours are low-effort behaviours
that can be incorporated into the couple’s daily routine (e.g., bringing the partner a coffee in bed in
the morning). Behaviour exchange is a technique utilised in the initial stages of therapy as a means of
inducing immediate positive change that can help to foster a new sense of collaboration between the
partners and thus lay the foundations for working on other major issues.
In communication training, each partner is taught skills to improve their roles as both the speaker
(expressive skills) and the listener (receptive skills). Expressive skills entail having the speaker express
his/her thoughts and feelings using ‘I’ statements and attempting to minimise the impact of expressing
negative feelings by including relevant positive feelings (e.g., ‘It really makes me happy when you
come home and ask me how my day went’ rather than ‘When you come home from work, all you can
think about is yourself’). It is also important that thoughts and feelings are expressed in specific rather
than vague terms so as to enhance clear communication (e.g., ‘I felt rejected and hurt when you left
early last night’ rather than ‘I felt weird when you left early last night’). Receptive skills include using
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appropriate non-verbal cues while the speaker is talking (e.g., making eye contact and head-nodding)
and to summarise the speaker’s most important thoughts and feelings when the speaker has finished
talking to ensure correct understanding (e.g., ‘So it really makes a difference to you when I come
home and show some interest in how your day has been’ rather than ‘Nothing I do is ever enough
for you’). Key among effective listener skills is being an empathic listener, which entails showing
understanding and acceptance of the speaker. The main expressive and receptive skills are outlined
in Table 11.6.
TABLE 11.6 Expressive and receptive skills that are taught in CBT as part of communication training
Expressive (speaking) skills
1. State your views as your own feelings and thoughts (using ‘I statements’) rather than as absolute
truths.
2. Express your emotions or feelings.
3. When expressing negative emotions or criticisms also include any positive feelings you have about
the person or situation.
4. Make your statements as specific as possible.
5. Express your feelings and thoughts in a way that shows you are aware of the impact your statement
may have on your partner and that you understand and care about your partner’s feelings.
Receptive (listening) skills
1. Show that you understand your partner’s statement and accept his/her right to have those thoughts
and feelings. Demonstrate this acceptance through your tone of voice, facial expression and posture.
2. After your partner finishes speaking, summarise your partner’s most important feelings, desires,
conflicts and thoughts.
3. Try to put yourself in your partner’s place and look at the situation from his/her perspective in order
to determine how your partner feels and thinks about the issue.
4. While in the listener role, do not:
• ask questions
• express your own viewpoint
• interpret or change the meaning of your partner’s statement

• offer solutions or attempt to solve the problem
• make judgments about what your partner has said.
Source: Baucom, D. H., & Epstein, N. (1990). Cognitive-behavioral marital therapy. Levittown: Brunner/Mazel.
Problem solving provides a set of skills that couples can utilise to reach a solution to areas of
conflict within the relationship. Thus, rather than arguing about conflict topics, couples are taught the
skills of constructively resolving problems. The steps of problem solving involve:
1. stating clearly what the problem is
2. discussing a range of possible solutions
3. deciding upon a specific solution that is acceptable to both partners
4. implementing and evaluating the selected solution.
Another key aspect of CBT for relationship problems is to challenge dysfunctional cognitions that
are having a negative impact on relationship satisfaction. For example, a woman who reports the belief
‘my husband doesn’t care about me’ might be asked to look for any evidence of caring behaviour from
her husband (e.g., ‘He went to the chemist to get pain medication for my headache’) and to evaluate
possible reasons for his seemingly non-caring behaviour (e.g., ‘He’s been diagnosed with depression,
which is making him tired and withdrawn’).
Numerous well-controlled studies support the effectiveness of behavioural and CBT approaches in
helping couples who are dissatisfied and distressed regarding their relationship (Baucom et al., 1998;
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Halford et al., 2010; Shadish & Baldwin, 2005). Couples receiving these approaches have consistently
been found to experience significantly greater improvements compared to couples who do not receive
treatment. For example, a meta-analysis of 30 studies comparing behavioural couple therapy with
a no-treatment control group found that the average individual who received behavioural treatment
improved to a greater degree than an estimated 72 per cent of those in the control group (Shadish &
Baldwin, 2005).
However, behavioural and CBT approaches have not always been found to be more effective than
other types of treatment for distressed couples. In fact, one study found that emotion-focused therapy
(which focuses on helping couples to more effectively express their emotions regarding themes
such as intimacy and control) was more effective than behavioural therapy, at least in the short term
(Johnson & Greenberg, 1985). While this study has been criticised for a number of reasons (e.g., the
behavioural therapy may not have been adequately implemented), it highlights the need for ongoing
investigation of innovative approaches for couple therapy (Markman, 1991).
DAL
Improving communication is a key component of CBT approaches for relationship difficulties.
LIMITATIONS OF CURRENT COUPLE THERAPY

A limitation of behavioural and other treatment approaches for distressed couples is that a substantial
proportion of individuals (an estimated one-third) do not significantly benefit from treatment (Shadish
& Baldwin, 2005). This is of particular concern since it is the more distressed couples who are likely
to experience a poorer response to treatment (Snyder, Castellani, & Whisman, 2006). In addition,
improvements obtained through treatment may not necessarily be maintained in the long term, with
approximately 30–60 per cent of treated couples experiencing significant deterioration when followed
up two or more years after treatment (Shadish & Baldwin, 2005). In the case of behavioural treatment,
for instance, one study found that approximately 30 per cent of couples relapsed over a two-year
period (Jacobson, Schmaling, & Hotzworth-Munroe, 1987), while another study found that 38 per cent
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of couples divorced in the four-year period following behavioural therapy (Snyder, Wills, & Grady-
Fletcher, 1991). Therefore, a key challenge for future research is to identify treatment approaches that
will be beneficial for a greater proportion of distressed couples and will more effectively help couples
to maintain their improvements once treatment ends.
One response in the field to this challenge has been to develop other approaches to the treatment of
distressed couples. An example is the development of integrative behavioural couple therapy (IBCT),
which aims to extend traditional behavioural approaches by focusing on enhancing partners’ acceptance
of each other rather than solely focusing on change (Wheeler, Christensen, & Jacobson, 2001). As
such, IBCT includes both behavioural change strategies (e.g., communication training) and acceptance
strategies. A range of techniques are employed for building a sense of mutual acceptance between the
partners. For instance, in the technique of ‘tolerance building’, individuals are assisted to minimise
their distress at some aspect of their partner’s behaviour by exploring its more positive aspects (e.g., a
husband’s tendency to make light of his wife’s concerns may be part of his generally optimistic attitude
to life). In a large study, 134 couples with chronic and serious relationship problems were allocated
to IBCT or traditional behaviour therapy (Christensen et al., 2004). Both treatments were successful,
with 71 per cent of IBCT couples and 59 per cent of behaviour therapy couples having improved
by the end of treatment. However, in a follow-up study assessing relationship satisfaction two years
after treatment ended, the findings suggested that IBCT had some advantages over behaviour therapy
(Christensen, Atkins, Yi, Baucom, & George, 2006). First, couples who received IBCT experienced
increased relationship satisfaction sooner than those who received behaviour therapy during this two-
year period. In addition, of the couples who stayed together rather than divorcing, the results tended
to favour IBCT over behaviour therapy. The findings from this study thus suggest that IBCT may be a
promising approach for enhancing the long-term outcomes of severely distressed couples.
Not only do novel approaches continue to be explored in assisting distressed couples, but the
focus of couple therapy has also expanded considerably in the past decade. Specifically, couple
therapy has been found to successfully help individuals experiencing psychological difficulties
(e.g., substance use disorders, mood disorders and anxiety disorders) and medical problems
(e.g., coping with chronic pain and terminal illness) (Snyder, Castellani, & Whisman, 2006). For
instance, in the case of substance use disorders, behavioural couple therapy has been found to result in
higher rates of abstinence, fewer substance-related problems and greater relationship satisfaction than
individual therapy (O’Farrell & Fals-Stewart, 2000). As applied to the treatment of substance misuse,
behavioural couple therapy includes standard techniques (such as communication training) as well as
substance-specific techniques (such as increasing both partners’ awareness of the positive aspects of
abstinence). The ongoing development and evaluation of couple therapy for specific psychological
and medical conditions is likely to be a priority for future research.
SUMMARY
The DSM-5 categories of sexual dysfunction are largely based on a linear model of the sexual response consisting of problems
in the desire, arousal or orgasm phases. However, this linear model has been recently challenged as providing an inaccurate
conceptualisation of women’s sexuality and an alternative, circular model has been proposed (Basson, 2000). In terms of
aetiology, McCabe’s (1991) model suggests that a complex interplay between developmental experiences, the individual’s current
functioning, the quality of the relationship, and the individual’s cognitive interpretation of sexual and relationship events results in
the development of sexual dysfunction. Since medical approaches do not address such factors, they are likely to have a limited role
in the treatment of sexual dysfunctions, especially for women. There is some evidence to support the use of CBT in treating sexual
dysfunctions, which incorporates a variety of behavioural techniques (e.g., sensate focus exercises) and cognitive techniques (e.g.,
challenging dysfunctional cognitions). However, research on the treatment of sexual dysfunctions is limited in both quantity and
quality, and much work remains to be done here in terms of developing more effective interventions.
The paraphilias refer to deviant types of sexual behaviours that lead to sexual gratification through sexual activity with inanimate
objects (e.g., fetishistic disorder) or behaviours that do not involve consent and are often harmful to others (e.g., exhibitionistic
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disorder). Research on the paraphilias is very limited: obtaining large samples for research is difficult due to the private nature of the
behaviours. As a result, there are no reliable data regarding the prevalence of these conditions and understanding their aetiology
and best treatment approaches is underdeveloped. Learning accounts have been a dominant approach in theories regarding the
aetiology of paraphilias and have informed treatment approaches such as aversion therapy and systematic desensitisation.
With continuing high divorce rates in the Australian population, identifying the factors that contribute to problems in relationships
and developing effective treatments is a priority. Research suggests that a wide array of factors is involved in the development of
dissatisfaction, and even divorce, in relationships. These include a range of individual factors (e.g., personality traits), relational
factors (e.g., poor communication between the couple) and contextual features (e.g., having children). Behavioural and cognitive-
behavioural approaches have been the most extensively researched treatments for relationship problems and aim to improve
the quality of the relationship through increasing positive couple behaviours, improving communication, using problem solving as
an alternative to arguing, and challenging any dysfunctional beliefs that are having a negative impact on the relationship. These
approaches have been found to be effective in the short term, but a considerable proportion of couples are not able to maintain
these changes over time. As with sexual problems, then, there is certainly a need for innovative treatments to improve the outcomes
for couples in distress.
KEY TERMS
androgen. . . . . . . . . . . . . . . . . . . . . . . . 341 female sexual arousal disorder. . . . . 331 performance anxiety. . . . . . . . . . . . . . 336
anxiety. . . . . . . . . . . . . . . . . . . . . . . . . . 336 fetishistic disorder. . . . . . . . . . . . . . . . 345 personality. . . . . . . . . . . . . . . . . . . . . . . 351
arousal phase. . . . . . . . . . . . . . . . . . . . 329 frotteuristic disorder. . . . . . . . . . . . . . . 345 premature ejaculation. . . . . . . . . . . . . 332
behaviour therapy. . . . . . . . . . . . . . . . 337 gender identity disorder. . . . . . . . . . . 347 sensate focus exercises. . . . . . . . . . . 337
cognitive behaviour therapy (CBT). . 338 hypertension. . . . . . . . . . . . . . . . . . . . . 331 sexual dysfunction. . . . . . . . . . . . . . . . 329
cross-sectional design. . . . . . . . . . . . . 358 hypoactive sexual desire disorder . . 330 sexual masochistic disorder. . . . . . . . 347
delayed ejaculation. . . . . . . . . . . . . . . 332 meta-analysis . . . . . . . . . . . . . . . . . . . . 355 sexual sadistic disorder. . . . . . . . . . . . 347
desire phase. . . . . . . . . . . . . . . . . . . . . 329 oestrogen . . . . . . . . . . . . . . . . . . . . . . . 341 social skills training . . . . . . . . . . . . . . . 348
erectile disorder. . . . . . . . . . . . . . . . . . 331 orgasm. . . . . . . . . . . . . . . . . . . . . . . . . . 329 transvestic disorder. . . . . . . . . . . . . . . 347
exhibitionistic disorder . . . . . . . . . . . . 344 paedophilic disorder. . . . . . . . . . . . . . 346 voyeuristic disorder. . . . . . . . . . . . . . . 347
female orgasmic disorder. . . . . . . . . . 332 paraphilias. . . . . . . . . . . . . . . . . . . . . . . 343
REVIEW QUESTIONS
LO 11.1
11.1 What are some of the factors contributing to differences found across studies in the prevalence of sexual
dysfunction?
11.2 Traditionally male and female sexual dysfunction was classified according to the desire, arousal and orgasm
phases of the response cycles. How has the DSM-5 changed this classification?
11.3 What are the main psychological treatments for sexual dysfunction and how effective are they?
11.4 What are the aims of sensate focus exercises?
LO 11.2
11.5 Describe the paraphilic disorders that involve sexual activities not involving contact with a living person.
11.6 What are the treatments for the paraphilias, and how effective are they?
11.7 Why is there such concern about paedophilic disorders?
LO 11.3
11.8 What are the main factors that contribute to relationship dissatisfaction?
11.9 Marriage is for life . . . Or is it? What are the developmental stages that need to be negotiated in a relationship?
11.10 What are the essential ingredients of the treatment of relationship problems?
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REFERENCES
Ahlers, C. J., Schaefer, G. A., Mundt, I. A., Roll, S., Englert, H., Baucom, D. H., Shoham, V., Mueser, K., Daiuto, A. D., & Stickle, T. R.
Willich, S. N., & Beier, K. M. (2011). How unusual are the (1998). Empirically supported couple and family interventions
contents of paraphilias? Paraphilia-associated sexual arousal for marital distress and adult mental health problems. Journal of
patterns in a community-based sample of men. Journal of Sexual Consulting and Clinical Psychology, 66, 53–58.
Medicine, 8, 1362–1370. Beaber, T. E., & Werner, P. D. (2009). The relationship between
Allgeier, E. R., & Allgeier, A. R. (2000). Sexual interactions anxiety and sexual functioning in lesbians and heterosexual
(5th ed.). New York: Houghton Mifflin Company. women. Journal of Homosexuality, 56, 639–654.
Althof, S. E. (2002). When an erection alone is not enough: Beitchman, J. H., Zucker, K. J., Hood, J. E., Da Copsta, G. A.,
Biopsychosocial obstacles to lovemaking. International Journal Akman, D., & Cassaria, E. (1992). A review of the long-term
of Impotence Research, 14, 99–104. effects of child sexual abuse. Child Abuse and Neglect, 16,
Althof, S. E., Leiblum, S. R., Chevret-Measson, M., Hartmann, U., 101–118.
Levine, S. B., McCabe, M., . . . Wylie, K. (2005). Psychological Bepko, C., & Johnson, T. (2000). Gay and lesbian couples in therapy:
and interpersonal dimensions of sexual function and dysfunction. Perspectives for the contemporary family therapist. Journal of
Journal of Sexual Medicine, 2, 793–800. Marital and Family Therapy, 26, 409–419.
Althof, S. E., McMahon, C. G., Waldinger, M. D., Serefoglu, E.-C., Bhugra, D., Popelyuk, D., & McMullen, I. (2010). Paraphilias across
Shindel S. W., Adaikan, P. G., . . . Torres L. O. (2014). An update cultures: Contexts and controversies. Journal of Sex Research, 47,
of the International Society of Sexual Medicine’s Guidelines for 242–256.
the diagnosis and treatment of premature ejaculation (PE). Sexual Blanchard, R., Lykins, A. D., Wherrett, D., Kuban, M. E., Cantor, J.
Medicine, 2, 60–90. M., Blak, T., . . . Klassen, P. E. (2008). Pedophilia, hebephilia, and
American Psychiatric Association (2013). Diagnostic and statistical the DSM-V. Archives of Sexual Behavior, 38, 335–350.
manual of mental disorders (5th ed.). Arlington: Author. Bradbury, T. N., & Fincham, F. D. (1990). Attributions in marriage:
Anderson, S. A., Russell, C. S., & Schumm, W. R. (1983). Perceived Review and critique. Psychological Bulletin, 107, 3–33.
marital quality and family life-cycle categories: A further analysis. Bradbury, T. N., Fincham, F. D., & Beach, S. R. H. (2000). Research
Journal of Marriage and the Family, 45, 127–139. on the nature and determinants of relationship satisfaction: A
Aubin, S., Heiman, J. R., Berger, R. E., Murallo, A. V., & Yung- decade in review. Journal of Marriage and the Family, 62, 964–980.
Wen, L. (2009). Comparing sildenafil alone vs. sildenafil plus Broderick, C. B. (1993). Understanding family process: Basics of
brief couple sex therapy on erectile dysfunction and couples’ family systems theory. Newbury Park: Sage Publications.
sexual and marital quality of life: A pilot study. Journal of Sex and Carpiano, R. M. (2001). Passive medicalisation: The case of Viagra
Marital Therapy, 35, 122–143. and erectile dysfunction. Sociological Spectrum, 21, 441–450.
Balon, R. (2013). Controversies in the diagnosis and treatment of Caruso, S., Intelisano, G., Lupo, L., & Agnello, C. (2001).
paraphilias. Journal of Sex & Marital Therapy, 39, 7–20. Premenopausal women affected by sexual arousal disorder treated
Bancroft, J. (1970). Disorders of sexual potency. In O.W. Hill (Ed.), with sildenafil: A double-blind, cross-over, placebo-controlled
Modern trends in psychosomatic medicine-2 (pp. 246–261). study. British Journal of Obstetrics & Gynaecology, 108, 623–
London: Butterworths. 638.
Basson, R. (2000). The female sexual response: A difference model. Caughlin, J. P., Huston, T. L., & Houts, R. M. (2000). How does
Journal of Sex and Marital Therapy, 26, 51–65. personality matter in marriage? An examination of trait anxiety,
Basson, R. (2003). Biopsychosocial models of women’s sexual interpersonal negativity, and relationship satisfaction. Journal of
response: Application to management of ‘desire disorders’. Sexual Personality and Social Psychology, 78, 326–336.
and Relationship Therapy, 18, 108–115. Charlton, R. S. (1997). Evaluation of sexual disorders. In R. S.
Basson, R., Leiblum, S., Brotto, L., Derogatis, L., Fourcroy, J., Charlton (Ed.), Treating sexual disorders (pp. 59–95). New York:
Fugl-Meyer, K., Graziottin, A., . . . Weijmar, S. W. (2003). Definitions Jossey-Bass Publishers.
of women’s sexual dysfunction reconsidered: Advocating expansion Charlton, R. S., & Quatman, T. (1997). A therapist’s guide to the
and revision. Psychosomatic Obstetrics and Gynecology, 24, physiology of sexual response. In R. S. Charlton (Ed.), Treating
221–249. sexual disorders (pp. 29–58). New York: Jossey-Bass Publishers.
Basson, R., McInnes, R., Smith, M. D., Hodgson, L., Spain, T., & Christensen, A., Atkins, D. C., Berns, S., Wheeler, J., Baucom, D. H.,
Koppiker, N. (2002). Efficacy and safety of sildenafil in women & Simpson, L. E. (2004). Traditional versus integrative behavioural
with sexual dysfunction associated with female sexual arousal couple therapy for significantly and chronically distressed married
disorder. Journal of Women’s Health Gender Based Medicine, 11, couples. Journal of Consulting and Clinical Psychology, 72,
339–349. 176–191.
Bateson, G., Jackson, D. D., Haley, J., & Weakland, J. (1956). Christensen, A., Atkins, D. C., Yi, J., Baucom, D. H., & George, W.
Toward a theory of schizophrenia. Behavioural Science, 1, H. (2006). Couple and individual adjustment for 2 years following
251–264. a randomised clinical trial comparing traditional versus integrative
Baucom, D. H., & Epstein, N. (1990). Cognitive-behavioral marital behavioural couple therapy. Journal of Consulting and Clinical
therapy. Levittown: Brunner/Mazel. Psychology, 74, 1180–1191.
rie66620_ch11_327-368.indd 363 07/29/17 02:01 PM

Christensen, B. S., Gønbæk, M., Osler, M., Pedersen B. V., Graugaard, Goldhammer, D., & McCabe, M. P. (2011). Development and
C., & Frisch, M. (2011). Sexual dysfunctions and difficulties in psychometric properties of the Female Sexual Desire Questionnaire
Denmark: Prevalence and associated sociodemographic factors. (FSDQ). Journal of Sexual Medicine, 8, 2512– 2521.
Archives of Sexual Behavior, 40, 121–132. Gottman, J. M. (1979). Marital interaction: Experimental
Christopher, F. S., & Sprecher, S. (2000). Sexuality in marriage, investigations. San Diego: Academic Press.
dating, and other relationships: A decade review. Journal of Gottman, J. M., & Levenson, R. W. (1992). Marital processes
Marriage and the Family, 62, 999–1017. predictive of later dissolution: Behavior, physiology, and health.
Clayton, A. H. (2003). Sexual function and dysfunction in women. Journal of Personality and Social Psychology, 63, 221–233.
Psychiatric Clinics of North America, 26, 673–682. Gottman, J. M., Markman, H., & Notarius, C. (1977). The topography
Clements, M. L., Stanley, S. M., & Markman, H. J. (2004). Before of marital conflict: A sequential analysis of verbal and nonverbal
they said ‘I do’: Discriminating among marital outcomes over 13 behaviour. Journal of Marriage and the Family, 39, 461–477.
years. Journal of Marriage and the Family, 66, 613–626. Graber, B. (1993). Medical aspects of sexual arousal disorders.
Conaglen, H. M., Williamson, A. R., & Conaglen J. V. (2009). In W. O’Donohue & J. H. Geer (Eds.), Handbook of sexual
Effect of erectile dysfunction medications on coexisting sexual dysfunctions: Assessment and treatment (pp. 103–156). Needham
dysfunctions in couples: Partners’ Preference Study. Sexual and Height: Allyn & Bacon.
Relationship Therapy, 24, 316–332. Halford, K. W., Farrugia, C., Lizzio, A., & Wilson, K. (2010).
De Block, A., & Adriaens, P. R. (2013). Pathologizing sexual Relationship aggression, violence and self-regulation in Australian
deviance: A history. Journal of Sex Research, 50, 276–298. newlywed couples. Australian Journal of Psychology, 62, 82–92.
Delizonna, L. L., Wincze, J. P., Litz, B. T., Brown, T. A., & Barlow, Halford, K. W., Wilson, K., Watson, B., Verner, T., Larson, J., Busby,
D. H. (2001). A comparison of subjective and physiological D., & Holman, T. (2010). Couple relationship education at home:
measures of mechanically produced and erotically produced Does skill training enhance relationship assessment and feedback?
erections. Journal of Sex and Marital Therapy, 27, 21–31. Journal of Family Psychology, 24, 188–196.
Halford, W. K., Sanders, M. R., & Behrens, B. C. (1993). A
Dunn, K. M., Croft, P. R., & Hackett, G. I. (1999). Association of
comparison of the generalisation of behavioural marital therapy
sexual problems with social, psychological, and physical problems
and enhanced behavioural marital therapy. Journal of Consulting
in men and women: A cross sectional population survey. Journal of
and Clinical Psychology, 61, 51–60.
Epidemiological Community Health, 53, 144–148.
Hawton, K., Catalan, J., Martin, P., & Fagg, J. (1986). Long-term outcome
Epstein, N. B., Baucom, D. H., & Daiuto, A. (1997). Cognitive-
of sex therapy. Behavioural Research and Therapy, 24, 665–675.
behavioural couples therapy. In W. K. Halford & H. J. Markman
Heiman, J. R. (2002). Sexual dysfunction: Overview of prevalence,
(Eds.), Clinical handbook of marriage and couple interventions
etiological factors and treatments. Journal of Sex Research, 39, 73–78.
(pp. 415–449). Brisbane: John Wiley & Sons.
Herek, G. M., & Garnets, L. (2007). Sexual orientation and mental
Feldman, H. A., Goldstein, I., Hatzichristou, G., Krane, R. J.,
health. Annual Review of Clinical Psychology, 3, 353– 375.
& McKinlay, J. B. (1994). Impotence and its medical and
Higgins, D. J., McCabe, M. P., & Ricciardelli, L. A. (2003). Child
psychosocial correlates: Results of the Massachusetts Male Aging
maltreatment, family characteristics and adult adjustment:
Study. Journal of Urology, 151, 54–61.

Mediating and moderating processes. Journal of Aggression,
Finkelhor, D. (1984). Child sex abuse. New York: Free Press. Maltreatment and Trauma, 6, 61–86.
Finkenauer, C., & Hazam, H. (2000). Disclosure and secrecy in Hucker, A., & McCabe, M. P. (2014). A qualitative evaluation
marriage: Do both contribute to relationship satisfaction? Journal of online chat groups for women completing a psychological
of Social and Personal Relationships, 17, 245–263. intervention for female sexual dysfunction. Journal of Sex and
Fitzpatrick, J., & Sollie, D. L. (1999). Influence of individual and Marital Therapy, 40, 58–68.
interpersonal factors on satisfaction and stability in romantic Jacobson, N. S., Schmaling, K. B., & Hotzworth-Munroe, A. (1987).
relationships. Personal Relationships, 6, 337–350. Component analysis of behavioural marital therapy: 2-year follow-
Frank, E., Anderson, A., & Rubenstein, D. (1978). Frequency of up and prediction of relapse. Journal of Marital and Family
sexual dysfunction in ‘normal’ couples. New England Journal of Therapy, 13, 187–195.
Medicine, 299, 111–115. Johnson, S. M., & Greenberg, L. S. (1985). Differential effects of
Gattis, K. S., Berns, S., Simpson, L. E., & Christensen, A. (2004). experiential and problem-solving interventions in resolving marital
Birds of a feather or strange birds? Ties among personality conflict. Journal of Consulting and Clinical Psychology, 53, 175–184.
dimensions, similarity, and marital quality. Journal of Family Jones, L., & McCabe, M. P. (2011). The effectiveness of an
Psychology, 18, 564–574. internet-based psychological treatment program for female sexual
Gelles, R. J. (1980). Violence in the family: A review of research in dysfunction. Journal of Sexual Medicine, 8, 2781–2792.
the seventies. Journal of Marriage and the Family, 42, 873–885. Kaplan, H. S. (1974). The new sex therapy. New York: Brunner/
Giles, K., & McCabe, M. P. (2009). Conceptualising women’s sexual Mazel.
function: Linear vs. circular models of sexual response. Journal of Kaplan, H. S. (1979). Disorders of sexual desire and other new
Sexual Medicine, 6, 2761–2771. concepts and techniques in sex therapy. New York: Brunner/Mazel.
Gilford, R., & Bengtson, V. (1979). Measuring relationship Karney, B. R., & Bradbury, T. N. (1995). The longitudinal course
satisfaction in three generations: Positive and negative dimensions. of marital quality and stability: A review of theory, method, and
Journal of Marriage and the Family, 39, 387–398. research. Psychological Bulletin, 118, 3–34.
rie66620_ch11_327-368.indd 364 07/29/17 02:01 PM

Kelley, K., & Byrne, D. (1992). Human sexuality. Englewood Cliffs: Matic, H., & McCabe, M. P. (2007). The impact of the use of PDE5
Prentice Hall. inhibitors for erectile dysfunction on the lives of Australian men.
Kelly, M. P., Strassberg, D. S., & Turner, C. M. (2006). Behavioural International Journal of Impotence Research, 19, 418–423.
assessment of couples’ communication in female orgasmic Matic, H., & McCabe, M. P. (2008). Duration of erectile dysfunction
disorder. Journal of Sex and Marital Therapy, 32, 81–95. and its relationship to treatment seeking and satisfaction with
Kennedy, S. H., Eisfeld, B. S., Dickens, S. E., Bacchiochi, J. R., & treatment using PDE5 inhibitors. International Journal of Urology,
Bagby, R. M. (2000). Antidepressant-induced sexual dysfunction 15, 346–349.
during treatment with moclobemide, paroxetine, sertraline, and Masters, W. H., & Johnson, V. G. (1970). Human sexual inadequacy.
venlafaxine. Journal of Clinical Psychiatry, 61, 276–281. London: J & A Churchill.
Kiecolt-Glaser, J. K., Bane, C., Glaser, R., & Malarkey, W. B. McCabe, M. P. (1991). The development and maintenance of sexual
(2003). Love, marriage, and divorce: Newlyweds’ stress hormones dysfunction: An explanation based on cognitive theory. Sexual and
foreshadow relationship changes. Journal of Consulting and Marital Therapy, 6, 245–260.
Clinical Psychology, 71, 176–188. McCabe, M. P. (1997). Intimacy and quality of life among sexually
Kleinplatz, P. J. (2003). What’s new in sex therapy? From stagnation dysfunctional men and women. Journal of Sex and Marital
to fragmentation. Sexual and Relationship Therapy, 18, 95–106. Therapy, 23, 276–290.
Kontula, O., & Haavio-Mannila, E. (2009). The impact of aging on human McCabe, M. P. (2001). Evaluation of a cognitive behavior therapy
sexual activity and sexual desire. Journal of Sex Research, 46, 46–56. program for people with sexual dysfunction. Journal of Sex and
Kruger, T. H. C., & Schiffer, B. (2011). Neurocognitive and Marital Therapy, 27, 259–271.
personality factors in homo- and heterosexual pedophiles and McCabe, M. P. (2007). Effect of sexual dysfunction and its treatment on
controls. Journal of Sexual Medicine, 8, 1650–1659. quality of life of affected men. In F. R. Kandeel, R. S. Severdloff, &
Lauer, R. H., Lauer, J. C., & Kerr, S. T. (1990). The long-term J. L. Pryor (Eds.), Pathophysiology and treatment of male sexual and
marriage: Perceptions of stability and satisfaction. International reproductive dysfunction (pp. 519–525). New York: Marcel Dekker.
Journal of Aging and Human Development, 31, 189–195. McCabe, M. P. (2009). Anorgasmia in women. Journal of Family
Laumann, E., Paik, A., & Rosen, P. (1999). Sexual dysfunction in the Psychotherapy, 20, 177–197.
United States: Prevalence and predictors. Journal of the American McCabe, M. P., Althof, S. E., Assalian, P., Chevret-Measson, M.,
Medical Association, 281, 537–544. Leiblum, S. R., Simonelli, C., & Wylie, K. (2010). Psychological
Lee, G., McMahon, C. G., McCabe, M. P., Jiang, H., Lee, S. W., Lim, P., and interpersonal dimensions of sexual function and dysfunction.
& Jiann B.-P. (2016). Initiators and barriers to discussion and treatment Journal of Sexual Medicine, 7, 327–336.
of premature ejaculation among men and their partners in Asia Pacific: McCabe, M. P., & Cobain, M. J. (1998). The impact of individual
Results from a web-based survey. Sexual Medicine, 4, e233–e241. and relationship factors on sexual dysfunction among males and
Leiblum, S. R. (2001). Critical overview of the new consensus-based females. Sexual and Marital Therapy, 13, 131–143.
definitions and classification of female sexual dysfunction. Journal McCabe, M. P., Conaglen, H., Conaglen, J., & O’Connor, E. (2010).
of Sex and Marital Therapy, 27, 159–168. Motivation for seeking treatment for ED: The women’s perspective.
Letourneau, E., & O’Donohue, W. (1993). Sexual desire disorders. International Journal of Impotence Research, 22, 152–158.
In W. O’Donohue & J. H. Geer (Eds.), Handbook of sexual McCabe, M. P., & Connaughton, C. (2014). Psychosocial factors associated
dysfunctions: Assessment and treatment (pp. 53–81). Boston: with male sexual difficulties. Journal of Sex Research, 51, 31–42.
Allyn & Bacon. McCabe, M. P., & Goldhammer, D. (2013). Prevalence of women’s
Levine, S. B. (2003). Erectile dysfunction: Why drug therapy isn’t sexual desire problems: What criteria do we use? Archives of
always enough. Cleveland Clinic Journal of Medicine, 70, 241–246. Sexual Behavior, 2, 1073–1078.
Li, P., Zhu, G. S., Xu, P., Sun, L. H., & Wang, P. (2006). Interventional McCabe, M. P., & Matic, H. (2007). Severity of ED: Relationship
effect of behaviour psychotherapy on patients with premature to treatment-seeking and satisfaction with treatment using PDE5
ejaculation. Zhonghua Nan Ke Xue, 12, 717–719. inhibitors. Journal of Sexual Medicine, 4, 145–151.
Mackey, R. A., Diemer, M. A., & O’Brien, B. A. (2000). McCabe, M. P., Price, E., Piterman, L., & Lording, D. (2008).
Psychological intimacy in the lasting relationships of heterosexual Evaluation of an internet-based psychological intervention for
and same-gender couples. Sex Roles, 43, 201–227. the treatment of erectile dysfunction. International Journal of
Mackey, R. A., Diemer, M. A., & O’Brien, B. A. (2004). Relational Impotence Research, 20, 324–330.
factors in understanding satisfaction in the lasting relationships of same- McCabe, M. P., Sharlip, I. D., Atalla, E., Balon, R., Fisher, A.,
sex and heterosexual couples. Journal of Homosexuality, 47, 111–136. Laumann, E., Lee, S.-W., Lewis, R., & Segraves, R. T. (2016a).
Mannino, D. M., Klevens, R. M., & Flanders, W. D. (1994). Cigarette Definitions of sexual dysfunctions in women and men: A
smoking: An independent risk factor for impotence? American consensus statement for the fourth International Consultation on
Journal of Epidemiology, 140, 1003–1008. Sexual Medicine 2015. Journal of Sexual Medicine, 13, 135–143.
Markman, H. J. (1991). Backwards into the future of couples therapy McCabe, M. P., Sharlip, I. R., Lewis, R., Atalla, E., Balon, R.,
and couples therapy research: A comment on Jacobson. Journal of Fisher, A., Laumann, E., Lee S.-W., and Segraves, R. T. (2016b).
Family Psychology, 4, 416–425. Risk factors for sexual dysfunction among women and men:
Marshall, W. L., & Marshall, L. E. (2015). Psychological treatment A consensus statement for the fourth International Consultation
of paraphilias: A review and an appraisal of effectiveness. Current on Sexual Medicine 2015. Journal of Sexual Medicine, 13,
Psychiatry Reports, 17, 47–52. 144–152.
rie66620_ch11_327-368.indd 365 07/29/17 02:01 PM

McCabe, S. B., & Gotlib, I. H. (1993). Interactions of couples with Pasch, L. A., & Bradbury, T. N. (1998). Social support, conflict, and
and without a depressed spouse: Self-report and observations development of marital dysfunction. Journal of Consulting and
of problem-solving situations. Journal of Social and Personal Clinical Psychology, 66, 219–230.
Relationships, 10, 589–599. Patterson, D. G., & O’Gorman, E. C. (1989). Sexual anxiety in sexual
McCabe, S, E., Hughes, T. L., Bostwick, W. B., West, B. T., & Boyd, C. dysfunction. British Journal of Psychiatry, 155, 374–378.
J. (2009). Sexual orientation, substance use behaviors and substance Pinnock, C. B., Stapleton, A. M. F., & Marshall, V. R. (1999). Erectile
dependence in the United States. Addiction, 104, 1333–1345. dysfunction in the community: A prevalence study. Medical
McCarthy, B. W. (2004). An integrative cognitive-behavioral Journal of Australia, 171, 353–357.
approach to understanding, assessing and treating female sexual Rhoden, E. L., Teloken, C., Sogari, P. R., & Souto, C. A. V. (2002).
dysfunctions. Journal of Family Psychotherapy, 15, 19–35. The relationship of serum testosterone to erectile function in
McConaghy, N. (1993). Sexual behavior: Problems and management. normal aging men. Journal of Urology, 167, 1745–1748.
New York: Plenum Press. Riley, A. (2002). The role of the partner in erectile dysfunction and its
McVary, K. T., Carrier, S., & Wessells, H. (2001). Smoking and treatment. International Journal of Impotence Research, 14, 105–109.
erectile dysfunction: Evidence based analysis. Journal of Urology, Roberts, W. L. (1979). Significant elements in the relationship of long-
166, 1624–1632. married couples. Aging and Human Development, 10, 265–272.
Meana, M. (2009). Painful intercourse: Dyspareunia and vaginismus. Rollins, B., & Cannon, K. (1974). Relationship satisfaction over the
Journal of Family Psychotherapy, 20, 198–220. family life cycle: A reevaluation. Journal of Marriage and the
Metz, M. E., & Epstein, N. (2002). Assessing the role of relationship Family, 36, 271–282.
conflict in sexual dysfunction. Journal of Sex and Marital Therapy, Rosen, R. C. (1996). Erectile dysfunction: The medicalisation of
28, 139–164. male sexuality. Clinical Psychology Review, 16, 497–519.
Meyer, I. H. (2003). Minority stress and mental health in gay men. In Rosen, R. C., Taylor, J. F., Leiblum, S. R., & Bachmann, G. A.
L. D. Garnets & D. C. Kimmel (Eds.), Psychosocial perspectives (1993). Prevalence of sexual dysfunction in women: Results of a
on lesbian, gay and bisexual experiences, (pp. 699– 731). New survey study of 329 women in an outpatient gynaecological clinic.
York: Columbia University Press. Journal of Sex and Marital Therapy, 19, 171–187.
Mirin, S. M., Meyer, R. E., Mendelson, J. H., & Ellingboe, J. (1980). Royal Commission into Institutional Responses to Child Sexual
Opiate use and sexual function. American Journal of Psychiatry, Abuse (2015). Redress and civil litigation report. Canberra:
137, 909–915. Commonwealth of Australia. Retrieved from http://www.
Monga, M., & Rajasekaran, M. (2003). Erectile dysfunction: Current childabuseroyalcommission.gov.au/about-us/our-reports.
concepts and future directions. Archives of Andrology, 49, 7–17. Saginak, K. A., & Saginak, M. A. (2005). Balancing work and family:
Morokoff, P. J., Baum, A., McKinnon, W. R., & Gilliland, R. (1987). Equity, gender, and relationship satisfaction. Family Journal:
Effects of chronic unemployment and acute psychological stress on Counseling and Therapy for Couples and Families, 13, 162–166.
sexual arousal in men. Health Psychology, 6, 545–560. Sand, M., & Fisher, W. (2007). Women’s endorsement of models
Morokoff, P. J., & Gilliland, R. (1993). Stress, sexual functioning, of female sexual response: The nurses sexuality study. Journal of
and marital satisfaction. Journal of Sex Research, 30, 44–54. Sexual Medicine, 4, 708–719.
Mulligan, T., Retchin, S. M., Chinchilli, V. M., & Bettinger, C. B. Sarwer, D. B., & Durlak, J. A. (1997). A field trial of the effectiveness
(1988). The role of aging and chronic disease in sexual dysfunction. of behavioral treatment for sexual dysfunction. Journal of Sex and
Journal of the American Geriatric Society, 36, 520–524. Marital Therapy, 23, 87–97.
Neff, L. A., & Karney, B. R. (2005). To know you is to love you: The Schiavi, R. C. (1981). Psychological determinants of erectile
implications of global adoration and specific accuracy for marital disorders. Sexuality and Disability, 4, 86–92.
relationships. Journal of Personality and Social Psychology, 88, Schiavi, R. C., Stimmel, B. B., Mendeli, J., & White, D. (1995).
480–497. Chronic alcoholism and male sexual function. American Journal of
Nobre, P. J. (2009). Determinants of sexual desire problems in Psychiatry, 152, 1045–1051.
women: Testing a cognitive-emotional model. Journal of Sex and Schmaling, K. B., Fruzzetti, A. E., & Jacobson, N. S. (1989). Marital
Marital Therapy, 35, 360–377. problems. In K. Hawton, P. M. Salkovskis, J. Kirk, & D. M. Clark
O’Donohue, W., Dopke, C. A., & Swingen, D. N. (1997). (Eds.), Cognitive behaviour therapy for psychiatric problems (pp.
Psychotherapy for female sexual dysfunction: A review. Clinical 339–369). Oxford: Oxford University Press.
Psychology Review, 17, 537–566. Segraves, R. T. (1988). Drugs and desire. In S. R. Leiblum & R. C.
O’Farrell, T. J., & Fals-Stewart, W. (2000). Behavioural couples Rosen (Eds.), Sexual desire disorders (pp. 313–347). New York:
therapy for alcoholism and drug abuse. Journal of Substance Abuse Guilford Press.
Treatment, 18, 51–54. Segraves, R. T. (2006). Female sexual disorders: Psychiatric aspects.
Panser, L. A., Rhodes, T., Girman, C. J., Guess, H. A., Chute, C. Canadian Journal of Psychiatry, 47, 419–425.
G., Oesterling, J. E, . . . Jacobsen, S. J. (1995). Sexual function in Segraves, R. T., & Balon, R. (2005). Treatment of sexual disorders in
men ages 40 to 79 years: The Olmsted County Study of Urinary the 21st century. In R. Balon & R. T. Segraves (Eds.), Handbook of
Symptoms and Health Status Among Men. Journal of the American sexual dysfunction (pp. 1–12). New York: Taylor & Francis Group.
Geriatric Society, 43, 1107–1111. Seibel, S. L., Rosser, S. B. R., Horvath, K. J., & Evans, C. D. (2009).
Parish, S. J., & Hahn S. R. (2016). Hypoactive sexual desire Sexual dysfunction, paraphilias and their relationship to childhood
disorders: A review of epidemiology, biopsychology, diagnosis, abuse in men who have sex with men. International Journal of
and treatment. Sexual Medicine Reviews, 4, 103–120. Sexual Health, 21, 79–86.
rie66620_ch11_327-368.indd 366 07/29/17 02:01 PM

Seto, M. C. (2009). Pedophilia. Annual Review of Clinical Stoller, R. J. (1977). Sexual deviations. In F. Beach (Ed.), Human
Psychology, 5, 391–407. sexuality in four perspectives (pp. 190–214). Baltimore: Johns
Shadish, W. R., & Baldwin, S. A. (2005). Effects of behavioural Hopkins University Press.
marital therapy: A meta-analysis of randomised controlled trials. Stolzenberg, R. M. (2001). It’s about time and gender: Spousal
Journal of Consulting and Clinical Psychology, 73, 6–14. employment and health. American Journal of Sociology, 107, 61–100.
Shelton, B. A., & John, D. (1993). Does marital status make a Swaby, A. N., & Morgan, A. D. (2009). The relationship between
difference? Housework among married and cohabiting men and childhood sexual abuse and sexual dysfunction in Jamaican adults.
women. Journal of Family Issues, 14, 401–420. Journal of Child Sexual Abuse, 18, 247–266.
Silverstein, C. (2009). The implications of removing homosexuality Terman, L. M., Buttenweiser, P., Ferguson, L. W., Johnson, W. B., &
from the DSM as a mental disorder. Archives of Sexual Behavior, Wilson, D. P. (1938). Psychological factors in marital happiness.
38, 161–163. New York: McGraw-Hill.
Snyder, D. K., & Berg, P. (1983). Determinants of sexual Tiefer, L. (2002). Beyond the medical model of women’s sexual
dissatisfaction in sexually distressed couples. Archives of Sexual problems: A campaign to resist the promotion of ‘female sexual
Behavior, 12, 237–246. dysfunction’. Sexual and Relationship Therapy, 17, 127–135.
Snyder, D. K., Castellani, A. M., & Whisman, M. A. (2006). Current Tiefer, L., Hall. M., & Travis, C. (2002). Beyond dysfunction: A new
status and future directions in couple therapy. Annual Review of view of women’s sexual problems. Journal of Sex and Marital
Psychology, 57, 317–344. Therapy, 28, 255–232.
Snyder, D. K., Wills, R. M., & Grady-Fletcher, A. (1991). Long- Twenge, J. M., Campbell, W. K., & Foster, C. A. (2003). Parenthood
term effectiveness of behavioural versus insight-oriented marital and relationship satisfaction: A meta-analytic review. Journal of
therapy: A 4-year follow-up study. Journal of Consulting and Marriage and the Family, 65, 574–583.
Clinical Psychology, 59, 138–141. United States Bureau of the Census (1998). Marital status and living
Speckens, A. E., Hengeveld, M. W., Lycklama à Nijeholt, G., van arrangements (update). Current Population Reports (Series P20-514).
Hemert, A. M., & Hawton K. E. (1995). Psychosexual functioning Ventegodt, S. (1998). Sex and quality of life in Denmark. Archives of
of partners of men with presumed non-organic erectile dysfunction: Sexual Behavior, 27, 295–307.
Cause or consequence of the disorder? Archives of Sexual Behavior, Weishaus, S., & Field, D. (1988). A half century of marriage: Continuity
24, 157–172. or change? Journal of Marriage and the Family, 50, 763–774.
Spector, I., & Carey, M. (1990). Incidence and prevalence of the Wheeler, J. G., Christensen, A., & Jacobson, N. S. (2001). Couple
sexual dysfunctions: A critical review of the empirical literature. distress. In D. H. Barlow (Ed.), Clinical handbook of psychological
Archives of Sexual Behavior, 19, 389–408. disorders (pp. 609–630). New York: Guilford Press.
Spector, K. R., & Boyle, M. (1986). The prevalence and perceived Wiederman, M. W. (1998). The state of theory in sex therapy. The
aetiology of male sexual problems in a non-clinical sample. British Journal of Sex Research, 35, 88–99.
Journal of Medical Psychology, 59, 351–358. Wincze, J. P., & Carey, M. P. (2001). Sexual dysfunction. A guide
Spence, S. H. (1991). Psychosexual therapy: A cognitive-behavioural for assessment and treatment (2nd ed.). New York: Guilford Press.
approach. Melbourne: Chapman & Hall. Zentner, M. R. (2005). Ideal mate personality concepts and
Sporakouski, M., & Axelson, L. (1984). Long-term marriages: A compatibility in close relationships: A longitudinal analysis.
critical review. Lifestyles: A Journal of Changing Patterns, 7, 76–93. Journal of Personality and Social Psychology, 89, 242–256.
Stevens, D., Kiger, G., & Riley, P. J. (2001). Working hard and hardly Zimmerman, T. S., Haddock, S. A., Current, L. R., & Ziemba, S.
working: Domestic labour and relationship satisfaction among dual- (2003). Intimate partnership: Foundation to the successful balance
earner couples. Journal of Marriage and Family, 63, 514–527. of family and work. American Journal of Family Therapy, 31,
Stinson, R. D. (2009). The behavioral and cognitive-behavioral 107–124.
treatment of female sexual dysfunction: How far we have come and
the path left to go. Sexual and Relationship Therapy, 24, 271–285.
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GRADUATE SPOTLIGHT
NAME: DR KRISTEN MURRAY
Degree studied: Bachelor of Arts/Bachelor of Science

(Psychology) with First Class Honours; Doctor of
Philosophy (Clinical Psychology)
University: Australian National University
Current position: Assistant Professor in Clinical

Psychology
Employer: University of Canberra

I am fascinated by human behaviour, so psychology is a constant source of curiosity and fulfilment for me.
I have always been interested in the complexity of people and how we live healthy and meaningful lives.
I also enjoy conducting research and interpersonal engagement, both of which are core aspects of my
training and work in psychology.

After completing my undergraduate training and a PhD in Clinical Psychology, I became a Registered
Psychologist and worked in public and private clinical settings. I gained specialist endorsement in Clinical
Psychology from the Psychology Board of Australia and also continued to work in research and teaching.
I now have an academic appointment as Assistant Professor in Clinical Psychology at the University of
Canberra.

My current position allows me to conduct research, teaching and clinical practice in one role. I teach
undergraduate and postgraduate clinical psychology, supervise research projects and students gaining
clinical experience by undertaking placements in various health settings, and continue my own research
and clinical practice.

My work allows me to discuss psychological theory and its applications every day! I enjoy conceptualising
issues and identifying strategies to address these. The diversity of my role also means my work is always
dynamic and interesting.

Psychology students receive a strong grounding in theory, critical thinking and research. These are valuable
skills that allow graduates to apply their knowledge to complex social issues. Psychology can take you in
many directions—my advice is to use these skills to enact change in the areas most important to you.
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CHAPTER 12
Gender dysphoria
Ken Pang
Riki Lane
Harjit Bagga
CHAPTER OUTLINE
● Definition of terms and the diagnosis of gender dysphoria
● The epidemiology of gender dysphoria
● The aetiology of gender dysphoria
● Treatment options for gender dysphoria
● Summary

12.1 Describe the diagnostic features of gender dysphoria in children, adolescents and adults.
12.2 Describe current understandings of the epidemiology of gender dysphoria and associated mental health concerns.
12.3 Describe current understandings of the aetiology of gender dysphoria.
12.4 Describe current understandings of the treatment options available for individuals experiencing gender dysphoria.
GENDER VARIANCE: AN AUSTRALASIAN FOCUS

Health care for trans and gender diverse (TGD) people is in a period of rapid change. For decades, the model of care was
for that of a psychiatric disorder, with treatment dominated by mental health professionals. This has consequences in
relation to stigma and discrimination. In recent years, the number of people attending specialist gender clinics has grown
exponentially, and the approach has shifted to that of dealing with a natural variation, with clients and multidisciplinary
teams working together to achieve positive outcomes.
Media coverage of TGD issues has increased greatly, both in Australia and internationally, which has helped to
promote more accepting societal attitudes towards TGD individuals. Similarly, changes in the law and in relation to
changing one’s gender on official government-issued documents are removing some of the barriers to social inclusion.
However, significant obstacles continue to exist. One example is the requirement in some Australian States and
Territories for married TGD people to divorce in order to enable them to change the gender on their birth certificate.
There also continue to be difficulties in accessing public toilets appropriate to their affirmed gender. Concerningly, studies
report that most TGD people experience harassment and discrimination in their daily lives. This includes high rates of
social exclusion, stigma, discrimination, verbal abuse and physical threats or violence, with 87.4 per cent experiencing at
least one form of stigma or discrimination based on gender identity (Couch, 2007).
Unfortunately, this discrimination extends to healthcare settings, which is a significant barrier for TGD people
accessing health care. Discrimination, humiliation or misunderstanding from medical providers—including the use of
an incongruent name or gender—can lead not only to a lower standard of care but also to avoidance of necessary care
(Riggs, Coleman, & Due, 2014). TGD people often feel they have to educate their doctors (Hyde et al., 2014). Related
continued
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to this, a lack of trained health professionals creates long

wait lists for access to specialist treatment, which can also
be expensive. Faced with these challenges, some TGD
people seek hormones via the internet, which carries risks.
However, where care is delivered that affirms an individual’s
gender identity, there are generally good outcomes.
Andreja Pejić’s story exemplifies some of the issues
facing TGD people, and the rapid changes in medical care,
social acceptance and media coverage. The following
description of Andreja’s experiences has been drawn from
People magazine (Zuckerman, 2014), the Evening Standard
magazine (Godwin, 2016) and personal communication
between Andreja and the authors.
In 2011, Andrej Pejić had a spectacular emergence
as an androgynous male model, wearing both men’s and
women’s wear at haute couture design shows. However, in
2014 she underwent gender affirmation surgery and said, ‘I
want to share my story with the world because I think I have
a social responsibility. I hope that by being open about this,
it becomes less of an issue.’
Andreja spoke about her early life: ‘I always dreamt
MAKE UP FOR EVER

of being a girl. One of my earliest memories is spinning
around in my mum’s skirt trying to look like a ballerina.’ She
said, ‘My traditional Balkan family’s understanding of the
gender binary was pretty rigid and conventional. I showed
signs of “cross-gender” behaviour early on, but mostly got
away with it. My mum and grandma thought I would grow Australian Andreja Pejić was the world’s first
out of it and the neighbours perceived my expression as transgender supermodel.
adorable childish antics. My brother looked down on my
feminine behaviour.’
However, after moving to Australia from Bosnia in 1991 with her mother and younger brother as war refugees, Andreja
had, by the age of 9, received ‘a social message, from my brother and friends at school’ that it was time to put away the
dolls and skirts. She said, ‘I wanted to please my parents’, by trying to hang out with the boys and participating in team
sports, but with little success. ‘I kept my dreams and my imagination to myself and became pretty good at acting as a
boy. But I was hiding who I was.’
‘I loved learning and taking classes, but recess and lunchtime represented pure torture. The social landscape at
school was very polarised on the basis of gender. I didn’t fit in with the boys, as much as I tried, and playing with girls
would get me teased, so I mainly kept to myself or went to the library. My main concern was learning and staying clear
of bullies.’
In 2004, at the age of 13, Andreja accessed information about gender affirmation surgery online: ‘The internet gave
me the sense that there were words to describe my feelings and medical terms,’ and she realised that ‘this is what I need
to do’. She added, ‘It also connected me to people all around the world who were going through the same thing, which
was powerful and made me feel less insane.’
Soon after, Andreja ‘found the Monash Gender Clinic and saw Dr Kennedy, who was compassionate and
understanding. She was convinced that I required transition. However, the clinic dealt with older patients and legally
her hands were tied.’ At that time, accessing puberty-blocking hormones required Australian Family Court approval,
which was a lengthy process, costing up to $30 000. Male hormones were beginning to affect her body, so, lacking the
time and necessary money for legal action, Andreja ordered medication online. While not recommending this course of
action, she said, ‘It helped me to be a much happier person today by starting early . . . I knew that if I went through a full
male puberty, it would have been a lot more difficult for me to be comfortable in my own skin later in life.’ She also said,
‘At 16, an endocrinologist prescribed a stronger anti-androgen that previously I couldn’t afford. This helped my anxiety
by further lowering my testosterone levels and eased my mother’s anxiety about self-medication.’
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Chapter 12 Gender dysphoria 371
Looking back at her experience of the healthcare system, Andreja said, ‘the care that I was given was better than
nothing but pretty inadequate. As a patient in the late 2000s, I felt let down. Australia is a modern country, with modern
medical care, and it is more than capable of providing transgender youth with the life-saving treatment they need at the
time they need it.’
Fortunately, since that time, the Royal Children’s Hospital in Melbourne has developed an extensive, world-class
gender service for young TGD people, with over 220 referrals in 2016 alone, compared with the period 2003–2007 when
they had only three referrals. Moreover, another young trans woman and her family took up a legal appeal, resulting in
the 2013 Re Jamie decision that overturned the need for court approval for use of puberty-blocking hormones (Williams,
Chesterman, & Grano, 2014). However, in 2017, TGD people under 18 with the relevant medical diagnosis still need court
approval for gender affirming hormones. Australia is the only jurisdiction in the world where this is the case. Andreja
agreed that ‘Re Jamie was a step forward. Puberty for a transgender individual can be incredibly difficult. Imagine being
a girl and growing hair everywhere and your voice deepening. Or being a boy and growing boobs and going through
periods. Now times that by a million because reality is that much stronger than imagination.’
Andreja had planned ‘to finish high school as Andrej, transition, and forget about my male past’. However, on being
recruited as a model at age 17, these plans changed as it allowed her to see the world and gain the necessary finances
for gender affirmation surgery. While working as an androgynous model, Andreja felt like ‘an in-between alien’—
highlighting the social difficulties faced by people with a non-binary gender presentation.
‘My dream was: start young, take hormones, live as a woman, try and become as passable as possible, bury your
past, change your friends. Now I’ve realised that I don’t have to be ashamed of my past. I can still own my story and it
doesn’t make me any less of a woman. I was born a girl, it just took me a little while to become one fully.’
Since her transition, Andreja has become a campaigner for trans acceptance. Commenting on recent debates in
Australia around the Safe Schools Coalition, she said, ‘I am a fan of this organisation. LGBT youth experience enormous
levels of bullying and discrimination as a result of ignorance on the part of their peers, teachers and school administration.
Transgender children are particularly vulnerable at school because there is still a widespread lack of understanding
about what we go through. We need to protect trans kids; it doesn’t take much.’
In supporting access to hormones or surgery by individuals under the age of 18 without Family Court approval,
Andreja said, ‘Early intervention preserved me from experiencing enormous amounts of anxiety and suicidal thoughts. It
greatly contributed to my sanity today, to my overall happiness with my body and the ease with which I transitioned into
womanhood. I have many friends who transitioned later in life and who wish they had had the chance to do it earlier. I
don’t believe that access to life-saving treatment or even treatment that greatly improves the quality of a child’s life is a
matter that should be decided in a courtroom.’

This chapter focuses on gender variance and gender dysphoria, and will cover: terms and definitions; diagnosis,
including a historical perspective, current practices and differential diagnoses; epidemiology, including prevalence, age
of onset, course and associated psychological and medical problems; aetiology, exploring biopsychosocial factors; and
treatment, detailing the various psychological, pharmacological and surgical options.
sex
Biological
characteristics
described as
LO 12.1 Definition of terms and the diagnosis female/male,
including genes,
of gender dysphoria chromosomes,
gonads, internal/
external genitalia,
What is meant by trans and gender diverse (TGD)? hormones
and hormone
Language and terms around gender variance have changed rapidly and continue to change. People receptors.
have varying understanding of the meaning of terms such as ‘trans’, ‘transgender’, ‘gender diverse’
gender
and ‘gender non-conforming’. Social categories
Sex, gender, sexual orientation and gender identity need to be clearly distinguished to help of woman/man,
understand the field of gender variance. Sex refers to the biological characteristics of male/female girl/boy, feminine/
reproductive differences, while gender refers to the social categories of male/female that are culturally masculine/
associated with sexual difference. Sexual orientation refers to people’s sexual and romantic attraction: androgynous.
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sexual for example, to men, women, both or neither. Gender identity refers to how individuals identify with
orientation the social categories of gender: for example, as men, women, both or neither. These terms are shown
How people in Figure 12.1.
identify physical
and emotional
attraction to
others, unrelated
to gender
identity. TGD
people can
have any sexual
orientation (gay,
lesbian, bisexual,
heterosexual,
asexual,
pansexual, no
label or another
self-description).
gender identity
A person’s
internal sense
of being a man,
woman, both or
neither. Gender
identity usually
develops at a
young age.
gender
expression
The way a FIGURE 12.1 The Genderbread Person: differences between gender identity, sex, gender expression and
person acts, sexuality
dresses, speaks
Source: http://bit.ly/2h8Ccqw.
and behaves in
order to show
his/her gender Currently, ‘trans and gender diverse’ (TGD) is a widely used umbrella term for people whose
as feminine, gender expression or gender identity varies from that generally expected for someone assigned to their
masculine, both sex at birth. Just like cisgender people (whose gender identity aligns with that usually associated with
or neither. the sex assigned at birth), TGD people have a wide range of sexual orientations and feel and express
trans man their gender in many varied ways. For example, some people born with the physical characteristics of
A person a female strongly feel that they are male, while others feel they are both female and male, or neither
assigned female male nor female, or somewhere between male and female. These feelings begin very early in life for
at birth who feels some people, but can occur later for others.
they are male and Most TGD people will express their inner sense of gender through their clothing, appearance and
lives as a man.
behaviour. For example, people assigned female at birth who identify as male may cut their hair short,
Some just use the
term male.
begin wearing trousers and shirts, and bind their breasts. A person who feels they are neither male
nor female may adopt clothing and hairstyles that are not traditionally male or female. TGD people
trans woman often change their name to match their affirmed gender. Most TGD people also prefer the use of
A person pronouns aligned with their affirmed gender (e.g., he/him or she/her), while some prefer non-specific
assigned male at pronouns (e.g., they/them). Some, but not all, change their bodies to more closely align with their
birth who feels
sense of gender through obtaining hormonal and surgical treatments. As is true for all people, it is very
they are female
and lives as a important for TGD people’s mental health and wellbeing for them to be able to live in a way that is
woman. Some consistent with how they feel about their gender, and to be accepted for who they are.
just use the term TGD people use many terms to describe themselves and their communities. Both these self-
female. descriptions and the terminology used by health professionals have changed over time. However, as
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each TGD person may use particular terms or definitions, it is best to ask each person which terms they transsexual
prefer. Some of the relevant terms include: trans man or trans woman; transsexual and gender variance/ An older term
non-conformity; disorder of sexual development or intersex; sex or gender assigned at birth (birth- for those TGD
people who
assigned male or birth-assigned female; also referred to as natal sex); trans/transgender; cis/cisgender;
identify as a
trans and gender diverse; transition/gender affirmation process. The following terms are considered member of the
offensive by most and should not be used: she-male, he-she, it, tranny, ‘real’ woman and ‘real’ man. ‘opposite’ sex,
i.e., other than
The diagnosis of gender dysphoria their birth sex.
Transsexuals
HISTORICAL PERSPECTIVE usually seek
In Australia, the Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American hormone therapy
Psychiatric Association (APA) is a commonly taught and used diagnostic system. The first two and often surgery
to bring their
versions of the DSM (I and II) made no reference to gender variance or gender dysphoria and
body into line
instead acknowledged cross-dressing behaviour. The DSM-I (APA, 1952) included transvestism as with their gender
an example of ‘sexual deviation’, which was listed under the diagnosis of sociopathic personality identity.
disturbance. The DSM-II (APA, 1968) continued the notion that practices such as transvestism were
gender variance/
part of a severe personality disturbance.
non-conformity
The DSM-III (APA, 1980) introduced significant changes in diagnosis driven by research from
Identity,
prominent figures in the TGD healthcare field (Drescher, 2010). Provocative terms such as ‘sexual behaviours or
deviation’ were removed and clearer criteria for the phenomenon of gender dysphoria were specified. interests that
Three diagnostic categories were included: gender identity disorder of childhood, transsexualism (for differ from
both adolescents and adults) and psychosexual disorder not elsewhere classified. These diagnostic those culturally
categories specifically referred to the dissonance between an individual’s experienced and birth- expected for
assigned gender, which continued in all further editions of the DSM (Cohen-Kettenis & Pfafflin, 2010). people of their
sex assigned at
The inclusion of gender identity disorder of childhood in the DSM-III for the first time acknowledged
birth. A gender
childhood experiences of gender dysphoria, which assisted with access to treatment and support for non-conforming
children (Zucker, 2010). The revised DSM-III-R (APA, 1987) retained gender identity disorder of person is not
childhood and transsexualism, and included the additional diagnoses of gender identity disorder of necessarily TGD
adolescence and adulthood, nontranssexual type (to describe individuals who did not wish to pursue (for example,
sex reassignment) and gender identity disorder not otherwise specified (for people who did not fulfil a woman who
the full criteria for gender identity disorder). dresses in a

The DSM-IV (APA, 1994) and DSM-IV-TR (APA, 2000) included a chapter entitled ‘Sexual and masculine style,
but identifies as
Gender Identity Disorders’, which covered gender identity disorder. This shift was significant and female; a boy
reflected changes in the way gender variance was being perceived in the healthcare community. who likes to play
This single diagnostic category encompassed diagnoses for children, adolescents and adults. A new with girl dolls, but
diagnostic category was also included—transvestic fetishism (with gender dysphoria)—which identifies as a
recognised the potential emergence of gender dysphoria that some people with a fetishist aspect to boy, etc.).
cross-dressing may experience. sex or gender
CURRENT CLASSIFICATION assigned at birth
The sex (male or
With much anticipation and debate, the current DSM-5 was released in 2013 and significant changes
female) assigned
to the diagnosis of gender dysphoria were evident. First, the word ‘disorder’—often seen as a a child at birth,
pejorative term that increased stigma—was removed and ‘gender dysphoria’ as a diagnostic category usually based
was created. This change in terminology was made in order to emphasise the distress associated with a on a child’s
discordance between an individual’s experienced and assigned gender. This element of distress as well genitalia—
as the associated impacts upon an individual’s occupational and social functioning were some of the individuals are
reasons why gender dysphoria has stayed in the DSM (i.e., as a mental disorder). described as
birth-assigned
A second change with the DSM-5 was that gender dysphoria had an independent chapter, no longer
male or birth-
connected with sexual disorders. Third, there was a notable shift from a binary concept of gender assigned female.
(e.g., ‘male’ or ‘female’) to fluidity in gender experience. Finally, a new specifier for gender dysphoria Other terms
was included for individuals in ‘post-transition’, that is, those individuals who were living full time include natal or
in their desired gender and who had had or were planning to undergo a medical treatment to facilitate birth sex.
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trans/ gender change. This was included to assist individuals to continue receiving support through insurance
transgender predominantly in the United States (given that access to insurance is dependent on having a diagnosed
People whose condition) even after they had transitioned and their dysphoria had dissipated.
gender identity While the shift from gender identity disorder to gender dysphoria has been welcomed by many
differs from
that usually
TGD people, some continue to critique the existence of any mental health diagnosis for gender
associated with variance (Inch, 2016; Starcevic, Monti, D’Agostino, & Berle, 2013).
the sex assigned The specific DSM-5 diagnostic criteria are outlined in Tables 12.1 and 12.2. As with the
at birth. DSM-III, there are separate diagnoses for gender dysphoria in children (Table 12.1) and gender
dysphoria in adolescents and adults (Table 12.2), reflecting differences in developmental stages and
cis/cisgender
symptom manifestations (Elaut, Heylens, De Cuypere, Van Hoorde, & Baetens, 2016).
People whose
gender identity
TABLE 12.1 Summary of DSM-5 gender dysphoria diagnostic features for children
aligns with
that usually
associated with Desire to be another gender
the sex assigned
at birth.
Desire for cross gender play
trans and gender

diverse (TGD) Preference for toys and clothing typically associated with
An umbrella term preferred gender
for all whose Experience of gender
incongruence with
gender identity is
associated distress or Resistance or rejection to toys and clothing typically
not aligned with impairment in life associated with assigned gender
their birth sex. functioning can occur
with the following:
Preference for playmates of the preferred gender
transition/gender
affirmation
process Dislike of primary and/or secondary sex characteristics
The process of
a TGD person
coming to Desire for primary and/or secondary sex characteristics of

the preferred gender
recognise, accept
and express their Source: Adapted from Diagnostic and Statistical Manual of Mental Disorders (5th ed,), copyright 2013, American Psychiatric Association.
gender identity.
This usually
refers to the TABLE 12.2 Summary of DSM-5 gender dysphoria diagnostic features for adolescents and adults
period when they
make social, legal
and/or medical Desire to be another gender
changes, such
as their clothing,
Desire to be free of assigned primary and/or
name, sex
secondary sex characteristics
designation and Experience of gender
body via medical incongruence with
interventions. associated distress or Desire to have the primary and/or secondary sex
This process, impairment in life characteristics of preferred gender
often called functioning can occur
gender with the following:
Desire to be treated as another gender
affirmation, can
greatly improve
a TGD person’s Firmly held belief that one has the common feelings
mental health or reactions as an individual of another gender
and general
wellbeing. Source: Adapted from Diagnostic and Statistical Manual of Mental Disorders (5th ed,), copyright 2013, American Psychiatric Association.
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The other main classification system is the World Health Organization’s (WHO) International gender
Classification of Diseases (ICD), which included mental health disorders in its sixth edition in dysphoria
1948. However, it was only in the ICD-9 (WHO, 1978) that transsexualism as a diagnosis first ‘The discomfort
appeared. The ICD-11 is due for publication in late 2017 or 2018. Similar to the debate with the or distress that
is caused by
DSM, there is dissent regarding the inclusion of a gender-related diagnosis. A 2015 draft of the a discrepancy
ICD-11 listed ‘gender incongruence’ under ‘Conditions Related to Sexual Health’, thus removing between a
it from the mental health diagnoses entirely (Robles et al., 2016). Nevertheless, much controversy person’s gender
exists regarding the potential stigma for individuals, particularly children who receive a diagnosis, identity and
and their accessibility to appropriate health care (Drescher, Cohen-Kettenis, & Reed, 2016; that person’s
Drescher, Cohen-Kettenis, & Winter, 2012). For example, children who wish to seek information sex assignment
or better understand their gender identity without undergoing medical treatment will still be given at birth, and
the associated
a diagnosis that is likely to remain highly stigmatising under the proposed system (Winter, 2016).
gender role
As an alternative, it has been proposed to use the ICD’s so-called Z codes, which relate to ‘factors and/or primary
influencing health status and contact with health services’ rather than mental disorders, as a way to secondary sex
support TGD individuals without stigma. characteristics’
While such debate is currently ongoing, both the DSM and ICD have seen changes over time (i.e., (Coleman et al.,
moving away from models of pathology for TGD individuals), a trend that seems likely to continue in 2012). This is the
the future. Many TGD advocacy groups and healthcare providers have advocated for the removal of basis for a clinical
psychiatric
gender dysphoria in the latest diagnostic classification systems, just as homosexuality was removed
diagnosis in
from the DSM in 1973. For example, the World Professional Association for Transgender Health the DSM-5
(2010)—an international interdisciplinary professional and education organisation that aims to that describes
develop evidence-based, high-quality TGD health care—strongly advocates to depathologise gender an intense,
variance. From an Australasian perspective, this stance has been supported by the Australian and New continuous
Zealand Professional Association for Transgender Health (2016). distress
The shift to remove gender dysphoria from diagnostic systems has recently been enacted overseas. resulting from
On New Year’s Day, 2017, the Danish government formally announced a move to depathologise an individual’s
sense of the
gender dysphoria. A decision was made, following significant lobbying from TGD organisations, to inappropriateness
declassify gender dysphoria as a mental disorder and remove the diagnostic label (Russo, 2017). The of their assigned
implications around the world of this landmark decision are yet to be seen, but it is regarded by many sex at birth.
as a move forward in terms of supporting the rights and liberties of TGD individuals. Previously known
as ‘gender
identity disorder’.
Differential diagnosis
Differential diagnosis refers to the process of correctly diagnosing someone with a disorder by
distinguishing their disorder from others with which it shares similar features. This practice of
diagnostic clarification is particularly important in the context of gender dysphoria as some of the
medical treatments for the condition can have irreversible effects. At times, this can be challenging,
especially for those individuals who experience gender dysphoria in the context of another mental
health condition that may have gender-associated symptoms. The other main diagnostic categories that
warrant consideration when an individual requests assessment for gender variance include transvestic
disorder, schizophrenia and other psychotic disorders, body dysmorphic disorder, personality disorder,
dissociative identity disorder and autism spectrum disorder.
Transvestic desires were described early in the DSM and over time were distinguished from the
phenomenon of TGD. Individuals who have a transvestic fetish experience sexual excitement when
engaging in cross-dressing behaviour but do not question their gender identity. It is possible for
individuals to have both a transvestic fetish and gender dysphoria. A common clinical presentation
would be a birth-assigned male presenting later in life for support for their gender dysphoria that
developed subsequent to a history of transvestic fetishism commencing in their youth.
Certain individuals may experience symptoms of gender dysphoria as part of a disorder on the
schizophrenia spectrum. For example, individuals may have delusions, sometimes of a bizarre nature,
that are gender related (as described in the case study of Jarc that follows). The distress associated
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with an individual’s gender identity may reduce once the psychosis is treated, which helps to clarify
the diagnosis as one of schizophrenia or another psychotic disorder, rather than gender dysphoria.
Some people may experience a perceived defect or flaw in the appearance of parts of their body that
are stereotypically related to their gender (e.g., genitals, chest or breasts) as part of body dysmorphic
disorder. If the individual also experiences discomfort in their gender identity they may also have
gender dysphoria.
The concept of gender may be considered to be a fundamental part of an individual’s identity and
sense of self. For example, it is common and developmentally appropriate for many adolescents to
explore their identity and question their sense of self. However, for some, gender identity concerns
may arise as part of a broader identity disturbance, and for others this may be part of a personality
disorder. For instance, identity disturbance can be a diagnostic feature of borderline personality
disorder, and part of this broader identity disturbance may be distress associated with one’s gender
or sexual orientation. In these instances, establishing the persistence of gender incongruence over
time and determining whether there are broader aspects of identity disturbance beyond concerns
regarding one’s gender can help to determine if the individual meets criteria for gender dysphoria
and/or borderline personality disorder.
It is possible that an individual with dissociative identity disorder may have an ‘alter’ or distinct
personality state that experiences gender dysphoria. This can lead to clinical and ethical concerns in
supporting the conflicting needs of the primary individual and their alters.
Awareness has been growing among healthcare professionals that an increasing number of
individuals presenting for support have both gender dysphoria and autism spectrum disorder. The
reason for this co-occurrence is unknown, but it could be due to factors such as functional brain
differences, different levels of foetal sex hormones and challenges with attachment bonds (Glidden,
Bouman, Jones, & Arcelus, 2016).
Other aspects for clinical consideration include the presence of gender dysphoria in the context of
internalised homophobia. In this situation, individuals may reject their experience of homosexuality,
finding the experience of same sex attraction to be unacceptable, and this in turn can sometimes lead
to confusion about their gender identity. Anecdotally, this phenomenon appears to be reducing in
frequency, with increasing societal acceptance of a variety of sexual orientations in Australia. However,
in other countries, such as Iran, where at the time of writing homosexual acts performed between
men is punishable by death, some men in this position may choose to undergo gender-reassignment
surgery to overcome the legal implications of their sexual orientation (Aghabikloo, Bahrami,
Saberi, & Emamhadi, 2013). Finally, some individuals who have a congenital condition resulting in
atypical anatomical, chromosomal or gonadal variation or a disorder of sex development may also
experience gender dysphoria.
CASE STUDY: JARC

Life had been isolated for 30-year-old Jarc. He grew up in a rural town with not much to do. He remembered that he
always felt different from the other kids in the area—although he had a couple of friends at school, he often felt lonely.
He found academic schoolwork difficult but enjoyed hands-on subjects such as woodwork. At home his parents often
argued and his father left the family home when Jarc was 14. Jarc got on well with his mother but always felt his father did
not understand him. He rarely saw his father after his parents separated, but his father told him during one visit that he
had cancer. His father died a year later when Jarc was 15.
Jarc got his first job as a labourer working after school and on the weekends when he was 16. He described himself
as ‘a legend at it’ and said that he ‘loved it’. A mate at the work site introduced Jarc to marijuana and then speed. Jarc
recalled smoking a ‘bad batch’ of marijuana when he was 17. Looking back on this time he described the experience as,
‘smoke and fire were coming out of my head and lungs! My lungs became all black! That fire made me a woman! I knew
I was a girl!’.
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Over time Jarc began to believe his workmates and teachers from school were watching him day and night. He
became increasingly fearful and refused to go to school or work. He withdrew from school and was eventually fired from
his job. He would spend days hiding in his bedroom with the blinds drawn and would not shower or change his clothes.
His mother tried to coax him to eat but Jarc believed his meals had been poisoned. Jarc’s mother was very worried
about him, and eventually, when he was 18, Jarc was admitted to hospital, where he was diagnosed with schizophrenia.
His mother was told that Jarc had grandiose and persecutory delusions. Since his first hospital admission he had trialled
several antipsychotic medications and had varying degrees of medication adherence. He had several relapses and
required hospitalisation three more times over the years.
Jarc had been living alone for the past three years. He liked being on his own, had a good routine established and
saw his mother often. He had developed a good relationship with his case manager and agreed to try an injectable
antipsychotic medication. He told his case manager that he ‘always wanted to be female’ as he had ovaries, a uterus
and a vagina in his abdomen. To test this belief, Jarc had a medical scan that revealed no female reproductive organs in
his pelvic cavity. When Jarc received his test results he did not believe them and requested a second opinion. A second
scan was completed and the same results were found. Jarc was disappointed that the machines were wrong. He and his
case manager decided a referral to a specialist gender dysphoria clinic for assessment and support would be helpful.
Jarc was keen to start feminising hormones. He told clinicians that after commencing hormone therapy he wanted to
be a female FBI officer. After completing a comprehensive assessment, the team spoke with Jarc and his case manager.
Jarc was reporting symptoms of gender variance but this appeared to be occurring in the context of schizophrenia.
He continued to experience symptoms of psychosis, including paranoid and grandiose delusions. His bizarre delusion
about having female reproductive organs persisted. His case manager had noticed that over time, when Jarc’s psychosis
was not managed well, he had increasing thoughts about being female. Since he had started his new antipsychotic
medication only two months prior to the assessment in the gender dysphoria clinic, a period of stability in his mental
health was recommended before he was re-assessed. Jarc was disappointed but keen to come back to the clinic.
Three years later, in consultation with Jarc, his case manager re-referred him to the specialist gender dysphoria clinic.
In the past three years Jarc had not had any psychiatric hospitalisations. His psychotic symptoms were being managed
well with the injectable antipsychotic medication, he attended the majority of his appointments with his case manager,
and he had been attending training courses to help him enter the workforce over the past 12 months. He said he was
keen to work at a local recycling factory and was short listed for a job there. He still enjoyed living alone and had two pet
cats. Although he said he still wanted feminising hormones, he now expressed doubt that he had female reproductive
organs. He had spoken more with his mother about being female and, while she was not fully accepting, she was slowly
becoming used to the idea that this was something Jarc wanted. He had purchased some female clothing, such as
T-shirts and track-suit pants, which he would wear at home, and he had some online contact with transgender support
groups. Another comprehensive assessment at the gender dysphoria clinic indicated that Jarc had stability in his mental
health and met the criteria for hormone therapy. He was therefore referred to his GP to start hormone treatment.
It took some time for Jarc to get used to the feminising hormones. He worked closely with his GP and the specialist
gender dysphoria clinic, and felt nervous but excited when he started this treatment, though he initially experienced
some nausea. After several months Jarc was pleased with some of the physical changes he experienced. He was happy
to continue to occasionally wear feminine clothing at home but decided he was not ready to come out more publicly
and that he may never do that. He continued to see his mother, who was still not sure if this was the right thing for Jarc.
They did not speak much about it but were happy in each other’s company. He was not sure if he would continue with
feminising hormones but together Jarc and his support network decided to take things one day at a time.
LO 12.2 The epidemiology of gender dysphoria

Prevalence
The available data regarding the prevalence of people who experience gender incongruence, gender
dysphoria or identify as being TGD both in Australia and overseas is limited. In a growing clinical
field, this information is necessary to contribute to governmental and non-governmental health
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program and policy development as well as resource allocation, planning and evaluation. This is
important since better access to healthcare services for TGD communities not surprisingly improves
healthcare outcomes and reduces overall costs to the health system (Meier & Labuski, 2013; Reed,
Rhodes, Schofield, & Wylie, 2009; Youth Coalition of the ACT, 2010).
One of the greatest challenges in prevalence research in the field of gender dysphoria is defining the
population of interest. As noted in the DSM-5, ‘the area of sex and gender is highly controversial and
has led to a proliferation of terms whose meanings vary over time and within and between disciplines’
(APA, 2013, p. 451). Given this lack of uniformity in definitions, those individuals who identify as
being TGD are not a homogeneous group. For example, ‘a transgender person may dress, behave or
self-identify anywhere along a culturally defined gender spectrum’ (Meier & Labuski, 2013, p. 291).
An additional challenge to collecting accurate prevalence data is the variable degree to which
TGD individuals seek treatment. For instance, a TGD person may not want hormonal or surgical
interventions or be able to afford them, or may not experience distress associated with their gender
incongruence, so treatment is not sought.
Difficulties in ascertaining the prevalence of different manifestations of gender variance are even
greater when comparing prevalence data across different countries. While it is widely accepted that
people from all cultures may experience gender variance (Harte, 2012), obtaining prevalence data will
be more difficult in those countries where there are strong cultural sanctions against gender variance.
These cultural differences in acceptability can be vast, from limited acceptance in Iran to relative
tolerance in Thailand, where TGD individuals are referred to as ‘Kathoey’ or the ‘third gender’.
Another factor that can make it difficult to compare prevalence data from different regions of the
world is the fact that treatment options and their availability differ from country to country, resulting
in differences in observed rates of clinical referrals. In the United Kingdom, for instance, most TGD
medical procedures are government funded through the National Health Service, but in most parts of
the world treatment either requires self-funding or is simply not available.
Adding to the confusion, past epidemiological research has failed to use consistent data-collection
methods. In theory, national data-collection surveys, such as the Australian Census, could provide
a strong platform for collecting information about gender identity, but efforts have been limited up
to this point. For example, in 2013 the AIDS Council of NSW made a submission to the Australian
Bureau of Statistics for the inclusion of indicators of sexual orientation, gender identity and intersex
status for the 2016 Australian Census (ACON, 2013). Subsequently, the 2016 Census was the first to
give people the opportunity to specify their gender as ‘other’ if they did not identify with the binary
‘male’ or ‘female’ options. However, this option was not available on the default online forms. As a
result, individuals needed to contact the Australian Bureau of Statistics to obtain a code to access a
special online form or else request a paper form in order to be able to record ‘other’ for their gender,
which present obvious impediments for accurate data collection.
Given each of these factors, it is not surprising that there are major differences in the prevalence
rates of gender dysphoria within the published literature. For example, De Cuypere and colleagues
(2007) reviewed 10 studies across 8 countries over a 39-year span, and reported that the prevalence
ranged from 1 in 11 900 to 1 in 45 000 for birth-assigned males, and from 1 in 30 400 to 1 in
200 000 for birth-assigned females. Locally, Ross, Wålinder, Lundströ, & Thuwe (1981) contacted all
psychiatrists who were registered to practise in Australia and inquired about the number of individuals
seen with gender variance. They reported that the prevalence was 1 in 24 000 for birth-assigned males
and 1 in 150 000 for birth-assigned females. More recently, Bagga and Erasmus (2014) found that
1 in 22 145 Australian passport holders had modified the gender marker on their passport, while 1 in
14 244 Victorians had modified the gender on their birth certificates. Given the barriers involved with
changing one’s gender identity on these government documents (e.g., in Victoria it is necessary to
have had sex-reassignment surgery in order to change one’s gender on a birth certificate), even these
recent estimates are likely to significantly underestimate the true prevalence rates of TGD individuals.
Consistent with the likely underestimation of prevalence rates in the aforementioned studies, a
representative household survey of American adults reported that 0.5 per cent identified as transgender
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(Conron, Scott, Stowell, & Landers, 2012), while 1.2 per cent of a population-based sample of
New Zealand high school students identified as transgender (Clark et al., 2014). A recent meta-
analysis indicated an increased prevalence of TGD individuals over the past 10 years and estimated
the current rate of TGD individuals in the United States to be 1 in every 250 adults (Meerwijk &
Sevelius, 2017). These rates are much higher than previously reported and may at least in part reflect
the methodological differences across studies. It would be expected that different prevalence rates
would be obtained from prevalence data based on whether individuals (1) identify as TGD, (2) have
sought treatment and been formally diagnosed with gender dysphoria or (3) elected to change their
identity markers (e.g., in their passports and birth certificates). Nevertheless, it also seems likely that
the rise in prevalence—together with the increased number of referrals to specialist gender clinics
worldwide—reflects changing societal attitudes and awareness as well as the improved availability
of safe and effective treatments (Telfer, Tollit, & Feldman, 2015). Whether the true prevalence has
actually increased is therefore difficult to know.
Age of onset and course

The age of onset for gender dysphoria varies alongside developmental changes in an individual’s
gender expression. In general, there are two pathways for the onset of gender dysphoria for both birth-
assigned males and birth-assigned females (APA, 2013).
The first, ‘early-onset’ pathway commences in childhood and persists into adolescence and
adulthood (as described in the case study on Aubrey that follows). For example, cross-gender behaviour
may be seen in children from 2–4 years of age; parents may report that their child displays cross-
gender behaviour, such as a preference for play with stereotypically male or female toys, or that their
child describes themselves as being of a gender opposite to their sex. According to the APA (2013),
the estimated rates of persistence of gender dysphoria from childhood to
adulthood vary widely, from 2.2–50 per cent.
The second, ‘late-onset’ pathway typically commences in puberty or
much later in life. Puberty can typically be a time of distress for adolescents,
and when an individual’s body changes do not match a young person’s
experienced or felt gender, this distress can escalate. This may also be a
time for young people and their families to seek specialist support. Many of
those individuals who experience an onset of gender dysphoria later in life
do not recall any gender variance in their formative years.
The course of gender dysphoria is difficult to trace, with the data limited
to those who have sought professional support or attended specialist clinics.
It is expected that, with the increasing acceptance of gender variance within
Australian society, the course of gender dysphoria will alter over time in
terms of reductions in the distress associated with gender variance.
Associated psychological and medical

problems
Many studies have identified the discrimination and stigma that TGD
individuals experience, with these experiences of social rejection, stigma
and violence being strong predictors of distress and dysfunction—more
so than the experience of gender variance itself (Robles et al., 2016).
DAL
Australian population surveys reflect poorer markers of mental health in

TGD individuals, such as higher rates of psychological distress, suicidality, Cross-gender behaviour, such as a preference
depression and anxiety (Leonard et al., 2012; Smith et al., 2014). It is for stereotypically male or female toys, may be
therefore not surprising that many TGD individuals may seek support for observed in children between the ages of
depressive disorders, anxiety disorders, substance-related and addictive 2 and 4 years of age.
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disorders, self-harm and suicidality (Dhejne, Van Vlerken, Heylens, & Arcelus, 2016; Eden, Wylie, &
Watson, 2012; Heylens et al., 2014; Marshall et al., 2016). One study reported that up to 41 per cent
of TGD individuals will have made a suicide attempt (Grant, Mottet, & Tanis, 2011). Although there
are no known medical problems associated with gender dysphoria per se, for TGD individuals who
pursue medical treatments to affirm their gender identity, side effects need to be considered (as will be
discussed in the section on Treatment).
CASE STUDY: AUBREY

From a young age, Otto was different from his male peers. Otto avoided rough and tumble play, showed a preference for
female playmates, enjoyed playing with dolls and liked to dress up in his older sister’s fairy dresses and his mother’s high
heels at home. At the start of primary school, Otto told his parents that he wanted to grow his hair long and be a girl. At
this point, his parents took a wait-and-see approach, thinking that he might be going through ‘a phase’.
However, Otto’s wish to be a girl only intensified over the next two years, as he began to insist that he actually was
a girl and became increasingly distressed by the presence of his penis, which he wanted to have cut off. Concerned by
this, Otto’s parents were referred to a psychologist who specialised in seeing gender diverse children and adults. Over a
series of sessions spanning several months, the psychologist explored Otto’s sense of gender identity and came to the
view that Otto strongly identified as female and was experiencing significant gender dysphoria.
Subsequently, with the help of the psychologist, Otto’s parents began to learn about gender diverse children and how
they can be supported to explore their gender identity. They joined a local support group, through which Otto met other
gender diverse children, and they talked to parents who had been through similar experiences. With Otto continuing to
identify as a girl, and asking to be called Aubrey instead and referred to using female pronouns, Otto’s parents decided
to have a trial over the summer holidays, when they were holidaying on the Gold Coast. During this time, they started
using the name Aubrey and allowed her to wear dresses in public and to begin to grow her hair long. Almost immediately,
they noticed a change in Aubrey. Having been prone to staying in her bedroom and appearing withdrawn at times, she
now appeared happier and more outgoing.
Upon beginning Grade 3, Aubrey’s parents spoke to her school to inform them of Aubrey’s desire to live full time as a
girl, including at school. Not having faced this situation before, the school principal contacted the Safe Schools Coalition,
who provided education to the staff on how best to offer a safe and supportive environment for gender diverse students
as well as developing a plan to facilitate Aubrey’s transition to attending school as a girl. Subsequently, at the start of
term two, the school celebrated Aubrey’s Coming Out Day, during which she was presented to her fellow students as
Aubrey and wore the female uniform for the first time.
Over the next few years, Aubrey continued to live as a female full time, and successfully moved to secondary school
at the age of 13. Around this time, she became increasingly worried about the onset of puberty and the associated
physical changes that would occur, especially changes to her voice, the development of facial hair and genital growth.
Shortly thereafter, Aubrey met with a paediatrician who agreed that Aubrey had gender dysphoria and identified that
early pubertal changes had already occurred. Aubrey was subsequently started on a course of regular, three-monthly
injections of puberty blockers, which successfully stopped the further masculinisation of her body, much to Aubrey’s
relief.
LO 12.3 The aetiology of gender dysphoria

What causes people to be TGD is a much-debated topic and, in recent years, ideas of a neurological
basis have become dominant. However, the converse question is just as fundamental: what causes
gender identity formation in cisgendered people? In this regard, many biomedical researchers maintain
that biological differences (through genetic or hormonal effects) directly produce sexed brains that
create an innate mental sense of maleness or femaleness. Consistent with this, they argue that most
societies have two distinct identity categories—namely, male and female—with associated distinct
roles around child-raising and other activities (Brizendine, 2006; 2010).
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This biological determinist viewpoint of ‘hard-wired’ male and female brains is strongly
contested by feminist writers, who instead highlight recent research indicating a complex process
of neurological development in which psychological, social and cultural influences impact not only
on gendered behaviours, but on sex differences in brain structures and hormone levels (Fine, 2010;
2017). A related view from social science—including gender studies and queer theory—highlights
the enormous variability across cultures and time in gender expression, that is, the culturally accepted
markers of being male or female. In this conception, a binary gender identity structure where only
male or female are liveable options is seen as a social construct that is maintained through tradition
and social coercion (Connell & Pearse, 2014).
However, gender identity is the most sexually dimorphic psychological trait in humans (Lane, sexual
2011), with only a small proportion of people having a gender identity different from that usually dimorphism
associated with their biological sex. Gender identity is much more dimorphic than sexual orientation, An observable
which is itself much more dimorphic than gender expression and gendered social roles (e.g., traits difference in
form (external
such as aggression, which are seen as typically male but are commonly seen in both sexes). As such,
or internal)
the argument for a biological basis for gender identity in the general population seems fairly strong, or behaviour
although much less so for gender expression and gendered social roles. This raises the question: why between males
do some people develop a gender identity which differs from that culturally associated with their and females in a
biological sex? Perhaps even more importantly: how can TGD people be best helped to live happily given species.
and productively? The first ‘why’ question will be addressed in this section, while the second ‘how’
question will be addressed in the Treatment section.
Gender identity formation: nature versus nurture

Debates over a biological versus a psychosocial basis for gender identity formation have waxed and
waned for more than 150 years. Empirically, it has been observed that gender identity usually forms
and becomes fixed quite early, with children having a sense of their gender before 3 years old and
developing gender constancy between 2 and 7 years (Slaby & Frey, 1975). But what factors influence gender
this process? constancy
From the 1950s to 1980s, psychosocial theories for gender identity formation were dominant. The typical
Consistent with this, a large body of literature documented the psychological and social processes development
in childhood
that shape gender expression and role development and how these vary across cultures and time. An
of a sense that
influential case study from the New Zealand-born psychologist Dr John Money acted as a famous gender is fixed
rallying point for those proponents of a nurture-based causation. In 1965, David Reimer lost his penis and does not
as an infant in a circumcision accident and his parents were subsequently advised by Dr Money to change over time.
raise him as a girl, in contrast to his genetically identical twin brother. As recounted by Dr Money,
David happily adapted to his female gender role throughout his childhood and adolescence, lending
significant credence to the importance of nurture over nature in gender identity formation (Money,
1975; Money & Ehrhardt, 1972). However, during the 1990s, it emerged that David Reimer had
never been happy in the assigned female role and had reverted to a male gender identity during his
adolescence (Diamond & Sigmundson, 1997). Tragically, he later committed suicide, after suffering
from depression for many years.
Since the 1990s, biologically-based ‘brain sex theories’ have become dominant, in part because
they have received significantly greater empirical support. In this case, biological differences such as
hormones, genes and brain structures are believed to strongly influence gender identity.
Today, the more sophisticated view is that of a spectrum of gendered identities and behaviours, with
interactions between biological, psychological and social forces. Specifically, while an individual’s
biology may establish particular predispositions in relation to gender identity, psychological and
social factors are likely to affect the trajectory that arises from these predispositions. For example,
anatomical differences between children, such as their genitalia, might lead parents to alter their
child-rearing practices and hold different expectations, while children might modify their behaviours
through modelling same-sex parents or other carers. Parents are also likely to impact on gender identity
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through reinforcing or undermining different social norms. In the same way, social institutions (e.g.,
religion and the media) and ideologies (e.g., laws against cross-dressing and restrictions on women’s
activities) will enforce, modify and/or maintain particular gender roles and expressions (Butler, 1990).
In this case, the question of which gender positions are culturally viable varies greatly across societies
and across time: from those where two quite separate gender positions with sharply delineated roles
are the only ones accepted, to others where a range of gender positions other than only male and
female are acknowledged.
Biological influences on gender variance

The most prominent theories on the aetiology of gender variance are biologically based and consistent
with a neurological model (Reed, 2006). These theories tend to be formulated around ‘transsexuals’
(i.e., people who transition completely across the gender binary) and involve the concept of a gender
identity centre or network in the brain that is sex reversed. In general, these theories principally focus
on three different aetiological aspects: in utero hormones, brain structure differences and genetics.
IN UTERO HORMONES
The main theoretical postulate of brain sex theories is that hormonal events in utero form a gender
identity brain centre or network that is sexually differentiated. Based originally on rodent studies
from the 1950s (Phoenix, Goy, Gerall, & Young, 1959), this is known as the organisation/activation
theory and involves hormonal (usually testosterone) exposure organising early brain structures that
are later activated by additional hormones at puberty. In this schema, a transgender identity results
from hormonal influences that affect only the brain and not the body. Although attractive in theory,
there is little empirical evidence on how prenatal hormones impact on TGD brain formation or to
show TGD individuals have differences in hormonal exposure. For example, using finger digit length
as a proxy for in utero testosterone exposure, studies have failed to show any consistent differences
between TGD people and others assigned the same sex at birth (Schneider, Pickel, & Stalla, 2006;
Vujovic et al., 2014). Studies in adults of hormone levels, androgen receptor response and oestrogen
feedback have also failed to show differences (Gooren, 2006).
The strongest evidence to date of a role for hormones in TGD identity development is from people
with a disorder of sexual development that disrupts normal hormonal signalling. This includes both
genetically female (XX) individuals with greatly increased androgen production due to congenital
adrenal hypoplasia and genetically male (XY) individuals whose androgen receptors are non-
functional (either complete or partial androgen insensitivity syndrome). Specifically, it has been
observed that XX individuals with congenital adrenal hypoplasia show elevated rates of same-sex
attraction, atypical gender expression and a male gender identity, while XY individuals with partial
androgen insensitivity syndrome have a female body appearance and almost always develop a female
gender expression and identity (Cohen-Bendahan, van de Beek, & Berenbaum, 2005). These findings
point to a significant role for in utero hormonal exposure in gender identity formation. However,
critics of this research point out that it is difficult to separate confounding psychological influences
such as altered parental expectations, based on their children’s atypical genital appearance, as well as
the children’s experience of repeated medical investigations and procedures (Fausto-Sterling, 2000).
NEUROANATOMICAL DIFFERENCES
The best evidence of neuroanatomical differences in TGD individuals comes from a series of studies
that analysed a particular region of the hypothalamus known as the central bed stria terminalis (BSTc).
Researchers compared a small number of deceased TGD people with a larger number of cisgendered
people. Across three separate studies, sexual dimorphism in this region in cisgender adults was found,
with a sex-reversed pattern for TGD individuals (Chung, De Vries, & Swaab, 2002; Kruijver et al.,
2000; Zhou, Hofman, Gooren, & Swaab, 1995). Specifically, men showed a larger BSTc than women
on average, while TGD subjects displayed a BSTc whose size was more consistent with their gender
identity than their sex at birth.
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However, later research by this same group suggested that the changes in BSTc may actually be
a consequence rather than a cause of TGD. Specifically, when these researchers examined BSTc
size throughout development, they found that the overall difference between female and males did
not appear until early adulthood, prompting them to note that ‘changes in BSTc volume in male-to-
female transsexuals may be the result of a failure to develop a male-like gender identity’ (Chung et al.,
2002, p. 1032).
More recently, a number of fMRI studies have examined differences in grey and white matter brain
structures between cisgender and TGD participants. Sex differences in these studies were smaller on
average (and with greater overlap) than in the studies on the BSTc region, and results for TGD people
tended to be intermediate between male and female (Saraswat, Weinand, & Safer, 2015).
Overall, such neuroanatomical findings suggest that these brain structures do differ on average
for TGD people than for others assigned the same sex at birth. However, there is significant overlap
between males and females in these brain structures, and the direction of causality is not certain.
Nevertheless, they support the concept that differences in brain structures are connected to the
development of gender identity.
GENETIC INFLUENCES
Twin studies are a common method used to suggest whether there is a genetic contribution to
a particular trait or disorder. In a review of published studies looking at gender identity, Heylens
and colleagues (2012) reported that 39.1 per cent of 23 monozygotic (identical) female and male twins
were concordant for the DSM-IV diagnosis of gender identity disorder, while none of the 21 dizygotic
(non-identical) twin pairs were concordant, suggesting that genetic influences are important in the
development of a TGD identity. These findings need to be replicated using larger sample sizes to
increase confidence in their validity.
To further explore possible genetic influences, multiple studies have examined whether TGD
individuals exhibit differences in sex steroid-related genes (including oestrogen receptor, androgen
receptor and aromatase). This research focus arises from the proposed role in the organisation/
activation theory of hormonal pathways in gender identity formation. Although some researchers have
reported genetic variants that increase the likelihood of being TGD (Bentz et al., 2010; Fernandez
et al., 2014b; Hare et al., 2009; Henningsson et al., 2005), others have failed to replicate their findings
(Fernandez et al., 2014a; Lombardo et al., 2013; Ujike et al., 2009), suggesting that there is no simple
genetic causation for gender variance involving sex steroid-related genes. It is more likely to be the
case that gender variance is influenced by a complex set of interactions between multiple genetic
variations and environmental factors.
Psychosexual theories on gender variance

Psychological theories of TGD aetiology were put forward in the 1960s and 70s, but have not yielded
significant empirical support. In one of these theories, Stoller (1967) proposed that male-to-female
transsexualism was caused by a ‘mother who maintains physical contact with the child so intense as
to inhibit development of concepts of separate body boundaries between mother and child, and an
absent or disinterested father’ (p. 431). However, he later considered that biological factors could be of
greater importance (Stoller, 1971).
There is also some evidence that TGD people have higher rates of abuse as children, but this
does not imply causality. After all, even though some have postulated that abuse contributes to the
development of gender variance, it is also quite feasible that TGD children are more likely to be
abused due to prejudice (Bandini et al., 2011).
The main psychological theory competing with the biological aetiological approach comes from
Blanchard, who argued that there are only two types of trans women: ‘homosexual transsexuals’
(attracted to men) and ‘autogynephilic transsexuals’ (sexually excited at the idea of being a woman)
(Bailey, 2003; Blanchard, 1985; 1989). The latter were strongly associated with transvestic fetishism.
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This is not an explicit aetiological theory, but uses a framework in which TGD people’s gender identity
can be seen as a by-product of sexuality and implies that there are potentially different aetiologies:
neurological for ‘homosexual transsexuals’ and psychological for ‘autogynephilic transssexuals’
(Blanchard, 2008).
Blanchard’s approach is in keeping with the existence of two fairly distinct clusters of trans women
in Western societies and is endorsed by some influential clinicians and researchers. However, it is
strongly rejected by many clinicians and TGD people, who see it as using offensive language and
lacking empirical evidence. For instance, most TGD people say this does not correspond well with
their lived experience. Where Blanchard creates a false dichotomy of two exclusive categories, they see
a complex array of combinations of sexual orientation and gender identity among TGD individuals.
Consistent with this, some studies have observed that Blanchard’s ‘two types of transsexuals’ do not
occur in many non-Western contexts such as South-East Asia (Winter, 2006), where TGD people have
traditionally made an early social transition. Other studies in more recent cohorts in Western contexts
indicate a complex pattern of variation (Nuttbrock et al., 2011; Veale, 2014), with interactions between
sexual orientation, age, ethnicity and transvestic fetishism. This suggests that in Western societies,
due to delays into late adulthood, ‘expression of a gender-variant identity in older and White people
tends to be more secretive and therefore experienced as exotic and associated with physiological and
emotional arousal, leading to the sexual arousal component’ (Veale, 2014, p. 1183).
Sociocultural influences on gender variance

There is considerable variation in the social acceptance of gender variance. In some cultures, there is a
relatively high level of acceptance. For example, varied forms of gender expression have traditionally
occurred in different countries, including Kathoey in Thailand, Mak Nyah in Malaysia, Fa’afafine in
Polynesia and Hijra in South Asia, each of which differs from one another and from Western ideas
of TGD.
In other cultures, gender variance has been sharply repressed, although this can evolve over time.
For instance, increasing tolerance in Western countries and changes in treatment modalities have seen
a growing acceptance of social gender transition in childhood, adolescence and later life. Similarly,
a shift away from strong social enforcement of a normative gender binary makes it more possible for
people to express positions in between male and female.

The expression of gender identity is constrained by the individual’s social and cultural setting.
For example, people assigned male at birth, but feeling female, faced very different possibilities in
the 1950s (and even today) for expressing their gender identity in Australia, Thailand and India. In
Australia they may have lived as homosexual males and participated in drag queen subcultures, or
repressed their gender identity and presented as cisgendered heterosexual males. In Thailand they
would likely have lived in a female role from adolescence as Kathoeys, while in India they may have
had an operation to become a eunuch and lived in a Hijra community.
Concluding remarks
The aetiology of gender variance remains poorly understood. Evidence for the various theories is
limited, but is stronger for biological rather than psychological and/or social influences. Moreover,
many TGD people and their families find reassurance in a biological aetiology, which can be mobilised
by advocates to assist with de-pathologisation and increased rights for TGD people. A useful reading
of the available literature is that biopsychosocial interactions in gender identity development create
diversity, which is then expressed within the culturally available options for gender expression.
Looking ahead, efforts to better understand aetiology will continue, but it seems unlikely that the
existing debates will be resolved any time soon. Regardless of aetiology, accepting that TGD people
exist and examining how TGD people relate to existing social institutions (Namaste, 2000) will be
critical in working towards a society that welcomes gender diversity (Devor, 1997).
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LO 12.4 Treatment options for gender dysphoria

Current treatment guidelines for gender dysphoria are based on expert consensus opinion, and are
summarised in the World Professional Association for Transgender Health’s (WPATH) Standards
of Care for the Health of Transsexual, Transgender, and Gender-Nonconforming People (Version 7)
(Coleman, 2012). Within the Standards of Care, treatment options encompass multiple domains,
including changes in gender expression and role, psychotherapy, pharmacological interventions,
surgery, voice and communication therapy and the management of reproductive health. Each
of these domains is described in the following sections, with a particular emphasis on the role of
psychotherapy. Relevant to each of these interventions are a number of principles that guide treatment
in this continually evolving field.
Guiding principles
Although medical interventions for those with gender dysphoria date back to the 1930s when
gender reassignment surgery was first performed in Germany (Stryker, 2008), strong evidence for
the efficacy of current treatment options remains lacking. For example, although retrospective and
prospective observational studies suggest that both hormonal and surgical interventions are beneficial
for individuals with gender dysphoria, no controlled clinical trials have been performed to evaluate
their effectiveness. Further research to rigorously evaluate the utility of current treatment options
therefore remains a priority. Given the lack of strong evidence to justify current treatment options,
the clinical management of individuals with gender dysphoria can be quite divergent. Nevertheless,
several principles are helpful in guiding treatment.
INDIVIDUALISE TREATMENT
Individuals with gender dysphoria demonstrate a spectrum of clinical presentations and needs, and
the treatment options that are appropriate for one individual might not be helpful for another. For
example, while many TGD patients benefit from both hormonal intervention and surgery, others may
choose only one of these options, and some may decide to have neither (Bockting, 2008; Bockting &
Goldberg, 2006; Lev, 2004). The importance of tailoring treatment in this way is especially true for
individuals with a non-binary gender identity, but also applies to those with more conventional trans non-binary
male and trans female presentations. gender
Any gender
AVOID HARM identity that does
In the past, psychological therapies have attempted to realign an individual’s gender identity in such not fit within a
a way that it becomes congruent with their sex assigned at birth (Gelder & Marks, 1969). Similar to binary of male
and female.
conversion therapies for homosexuality, such practices lacked efficacy (Cohen-Kettenis & Kuiper,
For example,
1984; Pauly, 1965) and are now considered both unethical and harmful. Avoiding harm is also an a person may
important ethical consideration for health professionals when weighing up different treatment options. identify as neither
For example, some clinicians might resist offering surgery to individuals with gender dysphoria or both male or
on the basis that such intervention damages anatomically normal tissues. However, in such cases, female. Many
withholding surgery can itself cause harm by failing to provide relief from the dysphoria and its other terms are
attendant psychological comorbidities, such as self-harm and suicide. used, such as
genderqueer,
USE APPROPRIATE LANGUAGE gender neutral,
gender fluid,
The terminology used to describe gender identity is rapidly evolving, and can cause confusion and
agender.
misunderstanding, not only among lay people but also among health professionals. For example, while
some individuals may identify as trans male or trans female, others prefer not to use the ‘trans’ prefix
and instead refer to themselves simply as male or female. With this in mind, it is important not to be
presumptuous and to instead ask individuals their preferred terminology, which includes pronouns, so
as to avoid misgendering.
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BE RESPECTFUL
Australian research reveals a positive association between mental health and services that are
perceived by TGD individuals to be comfortable and respectful. Conversely, experience of healthcare
environments that are perceived as discriminatory are negatively correlated with mental health
outcomes (Riggs, Coleman, & Due, 2014). Recommendations regarding the language to use in order
to create a respectful environment are shown in Table 12.3.
TABLE 12.3 Best practices for a trans and gender diverse-affirming environment
BEST PRACTICES EXAMPLES
When addressing clients, avoid using gender terms ‘Your client is here in the waiting room.’
such as Mr or Mrs. ‘How may I help you today?’
Politely ask if you are unsure about a client’s preferred name. ‘What name would you like us to use?’
‘I would like to be respectful—how would you like to be
addressed?’
Ask respectfully about names if they do not match ‘Could your details be under another name?’
in your records. ‘What is your name on Medicare?’
Record preferred name, gender marker and pronouns ‘What pronoun would you prefer us to use? How do you want
on all records. your name and gender recorded?’
Did you make a mistake? Politely apologise. ‘I apologise for using the wrong pronoun. I did not mean to
disrespect you.’
Use their preferred name and pronoun even when the client This maintains respect for the client and helps other staff
is not present. learn the client’s preferences.
Politely correct colleagues if they use wrong names ‘This client is transitioning their gender, so we need to
and pronouns. remember to call her Claire and use female pronouns.’
Ask only for information that is required: avoid asking Ask yourself:
unnecessary questions. What do I need to know?

How can I ask this in a sensitive way?
Discuss their gender identity only when necessary ‘I see that you have moved out of your parents’ home. Is that
for appropriate care. connected to your gender transition?’
Politely correct colleagues if they make insensitive comments. ‘Jamie, that is a bit rough—this person is having a difficult time
with their family while transitioning.’
SOCIOCULTURAL CONSIDERATIONS
Various social, cultural and legal influences heavily impact upon the provision of TGD health care
around the globe. For example, in many countries, it remains illegal to be TGD, which represents
an obvious barrier to accessing treatment. Even in countries where being TGD is not illegal, social
acceptance and tolerance are often lacking—not only among the general public but also among health
professionals—which drives many TGD individuals into the shadows and presents a further barrier to
health care. Research indicates that Indigenous TGD Australians experience the additional problems
of racism in the broader Australian context and transphobia within traditional community groups
(Kerry, 2014). Finally, it is worth noting that Australia is unique among other Western countries
insofar as legal impediments exist for certain treatments. As mentioned earlier, adolescents below the
age of 18 must apply to the Family Court for approval to access cross-sex hormones, even when the
young person, their family and the treating health professionals all agree that it is the best course of
action (as described in the case study of Kelsey that follows).
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CASE STUDY: KELSEY

Kelsey had long been regarded as a tomboy. As a young child, Kelsey enjoyed being outdoors, was a keen sportsperson
and socialised mostly with male classmates. Despite this, Kelsey was quite content to wear dresses and have long hair,
and never expressed a desire to be male.
At the age of 11, Kelsey noted the first signs of puberty and felt increasingly uncomfortable with the onset of breast
development and menstruation. Over the next few years, Kelsey largely ignored these feelings, believing that it was a
relatively common aspect of adolescence. However, during this time, Kelsey began to feel increasingly depressed and
received some cognitive behaviour therapy, which helped somewhat.
At the age of 15, Kelsey watched a TV show featuring a TGD child, which was the first time Kelsey had come across
someone who identified as transgender. Subsequently, Kelsey began to research TGD issues online, and came to
identify as a trans male, which prompted him to cut his hair short. With great apprehension, he came out to his parents as
transgender a few months later. They were initially shocked, but gradually came to accept and support him. Afterwards,
Kelsey came out to his friends, classmates and teachers, and started living as a male full time, using he/him pronouns and
wearing masculine clothing. He was happy to retain his birth-assigned name, Kelsey, which he felt was suitable for both
boys and girls, but eventually changed his gender on official documents, such as his Medicare card.
Having transitioned, Kelsey’s mood further improved, but he still felt significant distress in relation to his body. He
therefore saw his GP, who prescribed him medication to stop his menstrual periods and referred him to a specialist
gender clinic. A comprehensive assessment was undertaken at this clinic over several months with both a psychiatrist
and paediatrician, during which time Kelsey was insistent and consistent in his desire to commence testosterone to
masculinise his body. As a result, Kelsey, his parents and his treating clinicians all agreed that it was in Kelsey’s best
interests to commence testosterone. However, before Kelsey could do so, his parents engaged the services of a pro
bono lawyer, who assisted them with applying to the Family Court for approval of testosterone therapy. Six months
later, the Family Court granted its approval, and Kelsey, who was by this time almost 17, started receiving testosterone
injections every few weeks. Over the course of the next few months, Kelsey noticed increased body and facial hair
growth, more muscle bulk and a slight deepening of his voice, all of which helped him to feel increasingly comfortable
with his body. However, his breasts provided an ongoing source of distress, so he was keen to have chest surgery once
he was older and had saved enough money to cover the surgical costs.
Changes in gender expression and role

Living in a gender role and expressing one’s gender in a manner that is congruent with one’s gender
identity is critical for most TGD individuals, and frequently helps to alleviate symptoms of gender
dysphoria quite separate from other forms of more formal intervention. Indeed, many individuals
make this social transition—either partially or completely—prior to accessing healthcare services.
Making the social transition to a different gender role can encompass various aspects. Changing
one’s name is often an important milestone in affirming one’s true gender identity, and can be made
official by altering legal identity documents with relative ease. Changing one’s gender on identity
documents can be more difficult. For example, in Australia, changing one’s gender on a birth
certificate requires the completion of sex-reassignment surgery in some states and territories but not
in others. However, in recent years it has become considerably easier to change the gender marker on
everyday identity documents such as one’s Medicare card, driver’s licence and passport, with only a
doctor’s letter required.
For many individuals, changing their physical appearance is a key component in helping to
minimise gender dysphoria and aspects of this can be done as part of the social transition without any
need for medication or surgery. This might include changing hairstyles, wearing different clothing
and accessories, wearing make-up, removing unwanted hair (e.g., via electrolysis, laser treatment
or waxing), breast binding, genital tucking, enhancing cleavage (e.g., via padded bras), using penile
prostheses and inserting hip and buttock padding.
Obtaining support to change one’s gender expression and role can occur via in-person and online
peer support groups and various community organisations. These resources can assist both the
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individual and their wider networks of friends and family in providing information and support, and
can also play an important advocacy role. Support for changing one’s gender expression and role is
also an important aspect of psychotherapy.
Psychological therapies
The aim of psychological therapy for TGD individuals is not to ‘cure’ clients of their gender variance
but instead to work towards goals that are client-centred. The WPATH Standards of Care recommend
supportive and affirming therapies in individual, couple, family or group formats (Coleman, 2012).
Preliminary studies indicate that psychological therapy is helpful for individuals with gender
dysphoria in terms of the distress associated with a dissonance between the individual’s birth-assigned
and experienced gender (Bockting, 2008; Hakeem, 2012; Lev, 2009; Wylie, Eden, & Watson, 2012).
However, the literature regarding psychological therapies for TGD individuals is limited and more
research is needed in the area.
The body of research that relates to practices that are gender affirmative is even smaller but
developing. As a professional organisation committed to evidence-based psychological practice, the
Australian Psychological Society (2016) has developed guidelines that echo these sentiments and
recommends the practice of affirmative therapy. Gender-affirming therapy refers to an eclectic range
of practices and may draw from psychological therapies such as cognitive behaviour therapy (CBT),
self-psychology, psychodynamic therapy, interpersonal psychotherapy (IPT), schema therapy and
motivational interviewing. Depending on the individual client’s needs, it may involve exploration of an
individual’s gender identity, roles and expression, and strategies to alleviate dysphoria. For example,
creating an environment that is non-judgmental, safe and supportive can give individuals ‘permission’ to
talk about and explore their gender identity. Psycho-education can help individuals understand they are
not alone in their experiences and can provide a terminology to describe their experiences. Affirmative
therapy allows for acceptance and understanding of gender fluidity or ambiguity (as described in the
case study of Surajek that follows), and moves away from the traditional concept of binary gender,
which can be limiting or restrictive for many.
For some people, support in ‘coming out’ or transitioning may be needed. For example, motivational
interviewing techniques can help an individual work through a decision to ‘come out’ (e.g., by
evaluating the pros and cons of doing so). In addition, behavioural exposure techniques can be used
for those who are particularly anxious about dressing in public for the first time, perhaps beginning
with safer contexts before progressing to more challenging public dressing situations. Facilitating
the development of an individual’s resilience and coping strategies can also be helpful through the
transition process, given that the experience of having one’s gender identity misidentified (e.g., using
the individual’s pre-transition name), misperceived or negatively judged can be distressing.
Some individuals may wish to pursue medical gender-affirming treatments. For these individuals,
the role of therapy involves discussing issues around readiness to pursue treatment, expectations and
managing side effects. Often, long waiting periods to access services can be a source of stress and
tension, in addition to the financial burden associated with these services. Here, developing stress
management strategies may be helpful in a therapy context. For TGD individuals seeking feminising
hormones, smoking is often contraindicated with these hormones. Thus a client’s engagement in a
smoking cessation program may become a focus of therapy. Once medical gender-affirming treatment
has commenced, there may be a number of areas where individuals require support. This includes
support with managing mood changes and issues related to the medical transition. Sometimes, after
surgical intervention, pain or other somatic issues may arise, and strategies to manage and adjust to
these can also be a focus of psychological therapies.
In addition to practices related to the process of gender affirmation, specific psychological therapies
such as CBT can be used to support individuals who experience discrimination, social exclusion,
victimisation and bullying (GLBTI Health and Wellbeing Ministerial Advisory Committee, 2014) and
co-occurring depression, anxiety and stress.
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Finally, loss and adjustment is a consideration for individuals, family members and significant
others. For example, family members of adults often report ‘losing’ their child/sibling and may need
time to readjust to using a new name or pronouns. The partners of TGD individuals also undergo
their own adjustment in terms of being with a partner who may prefer a different gender identity.
Some partners may question their own identity, for example, their sexual orientation, and this can be
a source of distress and stress in the relationship. In such instances, relationship and family therapy
may be useful.
CASE STUDY: SURAJEK

Surajek was born female and migrated to Australia with the family at the age of 5. Surajek always felt a little different. It
was not just the different language spoken at home, the food the family ate, or the colour of their skin. It was something
more. Surajek had only a couple of friends at primary school, girls who were also on the outer edges socially, but being
tall Surajek managed to avoid bullying.
Puberty came early for Surajek, with menstruation starting at the end of Grade 5. That was tough. Surajek found these
bodily changes difficult. High school was an even greater struggle. Wearing a dress as dictated by school policy was
awful and this distress was relieved only in winter, when wearing pants and a shirt was acceptable. Physical education
classes were also a torment: in particular, Surajek found that changing into sports clothing with a tight-fitting T-shirt in
an open changing room with female classmates was humiliating and was sure that peers were staring at Surajek’s large
breasts, attempting to disguise them by either slouching or wearing multiple crop tops in an effort to flatten them. Also
loathsome were the thick hairs growing on Surajek’s arms and legs and the short upper lip hairs that were sprouting.
This, combined with family expectations for Surajek to cook, clean and one day marry within their own culture, led
Surajek to begin to feel increasingly stuck at this time.
These were the memories that Surajek disclosed to a clinical psychologist at a specialist gender clinic at the age
of 21. With the support of this psychologist, Surajek identified not wanting to be male, just less female. Given Surajek’s
distress regarding menstruation, the psychologist referred Surajek to a TGD-friendly GP who commenced Surajek on a
medication known as Primolut that effectively suppressed the periods and significantly reduced the associated distress.
In turn, this gave Surajek an opportunity to focus on elements of identity in subsequent sessions with the psychologist.
Over time, Surajek came to identify as androgynous and was aware that there were times of feeling more masculine,
other times of feeling more feminine, and sometimes no sense of any gender.
Nevertheless, Surajek’s ongoing process of self-discovery and ability to express gender identity was complicated.
Surajek came to understand and appreciate their own gender diversity, but was afraid to tell anyone other than some
online friends. With health professionals and when online, Surajek preferred the pronoun ‘they’ and ideally would have
liked to use the title ‘Mx’. One day, in a large shopping centre, Surajek experimented with wearing a wig with short hair
and a bulky jumper to disguise their shape. However, when they tried using the male toilets—a big step for Surajek—two
older men yelled, ‘You’re in the wrong toilet, young lady!’ Moreover, Surajek’s family had strong cultural beliefs around
gender. ‘God gave you this body, Surajek. It is his gift to you,’ Surajek’s mother would say. Surajek knew the family did not
understand or accept people who had sexual orientations different from their own and would certainly not understand an
androgynous or non-binary gender. Coming out would therefore risk losing family and friends. Consequently, Surajek felt
there was nothing to be done and, amid growing parental pressure to marry, Surajek eventually complied.
After getting married, Surajek had a child. Surajek loved the child dearly and tried breastfeeding but felt detached
from their breasts and switched to using formula instead and to wearing multiple crop tops to once again flatten the
breasts. Surajek’s husband believed in traditional values and roles within the relationship. He would often berate Surajek
for looking like a ‘lesbian’ and repeatedly told Surajek to be ‘more like a lady’. Not wanting the child to see its parents
fighting, Surajek tried to be more feminine—which was extremely difficult—but desired to be a good parent and to put
the child’s needs first. And so Surajek continued to tolerate their partner despite the marriage having become a sham.
Even after Surajek’s child had completed high school and gone on to live independently, Surajek was still unable to
live alone, remaining financially dependent on their husband and feeling that divorce would shame their parents. Having
lived with a secret gender identity for so long, Surajek could not really see any practical way forward. Instead, Surajek
would dream of having no breasts, a flat chest, and no nipples to mark their gender, and loved to picture themselves
free of body hair, with prominent biceps and a short hairstyle. In this way, the only safe place for Surajek to be free and
authentic was in their imagination.
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Pharmacological interventions
Pharmacological treatments for gender dysphoria involve a range of different hormonal therapies. The
main types of medications used are puberty blockers and gender-affirming hormones.
For many TGD individuals who are children or adolescents, the physical changes that accompany
puberty are a significant source of distress. To ease this distress and to avoid their bodies becoming
masculinised or feminised, these individuals can be offered a type of hormone known as a
gonadotrophin-releasing hormone (GnRH) analogue, which mimics a natural hormone produced
by the brain’s hypothalamus that regulates pubertal development. Long-term injection of GnRH
analogues blocks puberty (hence why they are commonly referred to as puberty blockers) in an
almost fully reversible manner. Ideally, to avoid the unwanted physical changes of puberty (such as
breast development and menstrual periods in a trans male, or facial hair, voice deepening and the
development of an Adam’s apple in a trans female), GnRH analogues are commenced shortly after the
onset of puberty and are typically ceased after gender-affirming hormones have been well established.
The use of gender-affirming hormone therapies to achieve feminine or masculine physical
characteristics can help improve the quality of life of individuals with gender dysphoria (Erasmus,
Harte, Bagga, Davies, & Cowling, 2014), by not only inducing physical changes consistent with an
individual’s identified gender (as shown in Table 12.4) but by also reducing their endogenous sex
hormone levels. For individuals seeking to feminise their appearance through hormonal intervention,
there are two main options—oestrogen and anti-androgens—and the two are often used in combination.
Oestrogen is usually administered orally, and is available on the Australian Pharmaceutical Benefits
Scheme, giving individuals access to subsided medication. Oestrogen binds to its target receptors
to induce feminising effects and suppress endogenous testosterone production. Similar to the oral
contraceptive pill, potential adverse effects of oestrogen include mood changes, weight gain and deep
vein thrombosis. Anti-androgens, such as spironolactone and cyproterone acetate, are often prescribed
alongside oestrogen to help minimise the effects of an individual’s endogenous testosterone, and can
be particularly helpful in reducing body or facial hair and minimising erections.
For individuals seeking to masculinise their appearance through hormonal intervention,
testosterone therapy is the mainstay. Like oestrogen, testosterone is available on the Australian
Pharmaceutical Benefits Scheme, giving individuals access to subsided medication. However, in
2015, restrictions were placed on GPs prescribing testosterone under the Pharmaceutical Benefits
Scheme. This change arose due to concerns over the over-prescribing of testosterone therapy by GPs
TABLE 12.4 Effects of masculinising and feminising hormones
EFFECTS OF TESTOSTERONE EFFECTS OF OESTROGEN
Skin oiliness/acne Body fat redistribution
Facial/body hair growth Decreased muscle mass/strength
Scalp hair loss Softening of skin/decreased oiliness
Increased muscle mass/strength Decreased libido
Body fat redistribution Decreased spontaneous erections
Cessation of menses Male sexual dysfunction
Clitoral enlargement Breast growth
Vaginal atrophy Decreased testicular volume
Deepened voice Decreased sperm production
Thinning and slowed growth of body and facial hair
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within the general population. Testosterone can therefore now be prescribed by a GP only if the
individual has been referred to an endocrinologist (Andrology Australia, 2015). TGD individuals can
also be prescribed testosterone by a sexual health physician or urologist, but accessing specialists in
this area may be costly and difficult. This introduces another complexity in the health care of TGD
individuals, and the impact of these changes on TGD individuals seeking masculinising hormones is,
at this stage, unknown.
Testosterone binds to its target receptors to induce masculinising effects and suppress endogenous
oestrogen production. Usually, testosterone is administered as either a short- or long-acting injection
or implant, although topical formulations (e.g., gels, patches and creams) are also used. Potential
adverse effects of testosterone include acne, baldness and mood changes. Although testosterone will
usually abolish menstrual bleeding—a common source of distress and dysphoria—some trans males
suppress their menses through the use of a continuous progesterone. This is especially common in the
adolescent TGD population prior to the commencement of testosterone treatment.
Current practices to access gender-affirming medical

interventions
The Australian and New Zealand Professional Association for Transgender Healthcare (ANZPATH)
endorses the WPATH Standards of Care guidelines (Coleman, 2012), which indicate that prior to
an individual commencing hormone therapy it is recommended they undertake a comprehensive
psychosocial assessment. This assessment should be completed by a suitably qualified and experienced
mental health professional, for example, a clinical psychologist or psychiatrist. ANZPATH also
recognises that members of the medical community, such as GPs or sexual health physicians, may also
be suitably qualified and have relevant experience in TGD health care to undertake these assessments.
The main reason that a comprehensive psychosocial assessment is recommended for hormone
therapy is to ensure the safety, health and wellbeing of the individual. Feminising and masculinsing
hormone therapy or gender-affirming surgeries can lead to irreversible physical changes and it is
necessary that individuals are legally able to provide informed consent prior to treatment. This is true
for any medical treatment or procedure. The other role of mental health clinicians in these assessments
is to minimise the chance of regret associated with these procedures. This is done by working with the
individual to ensure that the treatment is suitable, that the potential benefits outweigh the risks or that
any risks are able to be managed, that the individual has realistic expectations of the potential outcome
of treatment, and that they have adequate psychosocial supports available to manage the side effects
associated with the treatment.
After completing an assessment, if both the mental health clinician and client agree that hormone
therapy is a suitable option, the mental health clinician can refer the client to a hormone prescriber,
such as an endocrinologist or GP who has a special interest in gender dysphoria. It is recommended
that the mental health clinician follow up with the client after hormone therapy as this is often a period
of significant adjustment.
However, there is some dispute about the need for individuals to have a specialist assessment
prior to accessing medical interventions. For example, members of the general community who wish
to access plastic surgery are not required to undergo such an extensive assessment process. As an
alternative approach, several specialist gender services in North America have developed guidelines
that follow an informed consent model of care. This model is thought to better support an individual’s
autonomy in making decisions about their health care without the need for the involvement of mental
health professionals. Practitioners working within this model believe that removing the need for
mental health clinicians in the decision-making process leads to a better understanding by the treating
medical practitioner of TGD clients and contributes to improved delivery of patient care (Cavanaugh,
Hopwood, & Lambert, 2016). As of early 2017, ANZPATH has supported the introduction of an
informed consent model to be used in a gender diverse general practice in Melbourne. This is the
beginning of an approach that is likely to be increasingly adopted in the future.
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Informed consent is an agreement an individual has with their healthcare provider to provide
treatment. This treatment can include medical interventions, therapy, tests or other procedures, such
as hormone therapy or gender-affirmation surgery. In seeking consent, a healthcare practitioner needs
to be satisfied that:
∙ they have explained the proposed treatment and options available and that these are understood
∙ any risk or the chance of risk is explained and understood
∙ the benefits of treatment are understood
∙ the patient is free from coercion.
REPRODUCTIVE HEALTH
Just like cisgender individuals, many TGD people wish to have children. However, certain forms of
hormonal therapy and surgery commonly used in TGD health care limit fertility. For instance, puberty
blockers prevent sperm production and stop ovulation reversibly. Similarly, testosterone impairs
fertility in birth-assigned females, but this is also likely to be reversible, given that a number of
trans men have successfully become pregnant and given birth after discontinuing testosterone. More
permanent effects follow oestrogen therapy (which inhibits sperm production in birth-assigned males
long term) as well as gender-affirming surgery involving the removal of either the testes or ovaries.
It is therefore important that individuals considering hormonal and surgical interventions that affect
fertility be counselled about options for preserving their reproductive potential. For birth-assigned
males, this may include the collection and cryopreservation of sperm prior to hormonal or surgical
intervention, which can be done with relative ease and cost-effectiveness. For birth-assigned females,
oocyte and embryo freezing are also being performed, but both of these options are expensive, invasive
and complex. Oocyte freezing in particular remains a relatively new procedure, with only a modest
chance of success, and, while embryo freezing is associated with higher pregnancy rates, it requires
an individual to identify a suitable sperm donor potentially years in advance of the actual pregnancy.
VOICE AND COMMUNICATION THERAPY

Many TGD people experience significant gender dysphoria due to the differences in vocal
characteristics that tend to exist between birth-assigned males and females. To address this, speech
and language therapists can offer assistance to safely adapt a person’s voice not only in terms of
pitch—which is perhaps the most obvious gender-based difference—but also other qualities, such as
intonation, loudness, stress patterns, resonance, articulation, speech rate and phrasing. Since attempts
to feminise and masculinise one’s voice can be associated with vocal strain and damage, an important
component of clinical voice training is to prevent vocal misuse and ensure ongoing vocal health.
In addition to voice therapy, there are various aspects of both verbal and non-verbal
communication—including choice of language, gestures, posture and facial expressions—that show
gender-based variation and which can also be modulated to enable greater consistency between an
individual’s gender identity and their gender expression.
SURGERY
TGD individuals are able to access a range of gender-affirming surgeries (as described in the case study
of Naya below), although many choose not to for a range of reasons, including personal preference
and the fact that such surgery is often a major undertaking in terms of cost, practicality and physical
health. Such surgeries include not only the removal of undesired internal and external genitalia (i.e.,
penis and testicles for trans women, and breasts, ovaries, Fallopian tube and uterus for trans men), but
also the modification of existing structures and the creation of new tissues (i.e., breast and buttock
augmentation and facial feminisation as well as the formation of a vagina, clitoris and vulva for trans
women, and the creation of a male chest, penis and scrotum and implantation of erection/testicular
prostheses for trans men).
In Australia at the present time most surgery is available only in the private sector, requiring
individuals to have private health insurance to subsidise costs. Surgical outcomes are generally very
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good, although some forms of masculinising genital surgery can be technically complex. Some
Australian residents choose to have gender-affirming surgery overseas, such as in Asia or Europe,
given that not all gender-affirming surgeries are available in Australia and other places are perceived
as offering more affordable surgical care.
Research indicates generally favourable outcomes for individuals who choose to have surgery
(Coleman et al., 2012). Very few individuals choose to revert back to their birth-assigned gender. This
‘regret rate’ is estimated to occur in 2–3 per cent of people (Dhejne, Oberg, Arver, & Landen, 2014).
A decision to revert may be attributed to a number of factors including dissatisfaction with surgical
outcomes such as the function or physical appearance of anatomical changes (Lawrence, 2003).
Resources
∙ The World Professional Association for Transgender Health (WPATH) (www.wpath.org) is an
international interdisciplinary body that aims to promote evidence-based health care for TGD
individuals.
∙ The Standards of Care for the Health of Transsexual, Transgender, and Gender Nonconforming
People (SOC) provides clinical guidance for health professionals and is free to download from the
WPATH website (http://www.wpath.org/site_page.cfm?pk_association_webpage_menu=1351&
pk_association_webpage=3926).
∙ The Australian and New Zealand Professional Association for Transgender Health (ANZPATH)
is a body that actively promotes collaboration among healthcare professionals involved in the care
of individuals who experience differences in sexual formation and/or gender expression. (www.
anzpath.org).
∙ There are now clinics or clinicians in all states in Australia and the ACT that have a special interest
in gender dysphoria. These resources are listed on the ANZPATH website.
CASE STUDY: NAYA

Naya was 51 and had lived a full life but had never felt she was being true to herself. She was one of five sisters but she
was born male. She remembered that she had loved playing ‘dress-ups’ with her sisters when they were younger. Naya
did not mind the toy cars or building blocks she had, but she loved dressing her sisters’ dolls and she would admire her
older sister’s make-up when her sister would get dressed up to go out. Her father would reprimand her when he saw her
playing with her sisters’ toys, so she began to do it when he was at work. Her older sister would sometimes let Naya wear
her lipstick or eye shadow if Naya did the dishes for her sister. The make-up felt wonderful for Naya, but she would hide
it from her parents. One evening, when the family were out, 12-year-old Naya snuck into her older sister’s room and put
on a summer dress and heels. Her father came home and caught her. He was horrified. He slapped and punched Naya,
calling her a ‘sissy’ and a ‘faggot’. Naya was shocked. She did not know what to do. It had felt comfortable and good in a
dress, so it was hard for her to understand that it was wrong. Her father never spoke about it again.
Naya went to a Technical School and then on to an apprenticeship as a fitter and turner. This was what her father
wanted and, being good with her hands, it suited her. It was hard, physical work but Naya liked it. It also helped her to feel
like a ‘normal’ man. She was able to move out and into a shared house. She was lucky that she had her own room, but she
resisted any urges to keep any female clothing in her room, fearful that her housemates would find it. She would go to the
pub after work and match her male mates beer for beer. She tried hard to talk about women in the same way as her mates.
While she was attracted to women, she wanted to be one. She had never had a romantic relationship and sometimes got
teased for that. Finally, when Naya was 20, she moved out to a small apartment on her own. She loved it! She had her own
space. She had a few of her older sister’s clothes that her sister thought had been thrown out. Naya felt conflicted wearing
these clothes, though. It made her feel both good and bad. She felt at ease and secure but then reminders of her father’s
vitriolic attack would enter her mind and she would tear the clothes from her body and savagely throw them in the bin.
She met a woman through friends and had her first romantic relationship when she was 21. She loved her partner,
who was fun to be with and they got along well. She pushed any thoughts about being female out of her mind and
continued
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thought that she was ‘fixed’. Naya proposed to her girlfriend, but the relationship ended a year after she had proposed
as her girlfriend was not ready to settle down. Looking back, Naya was relieved, but at the time she was heartbroken.
Over the years Naya continued to live by herself. She dated women occasionally and this was interspersed with time
dressing in stereotypically female clothing covertly at home. A cycle of self-loathing and guilt ensued for many years.
She would throw out her female clothes, feeling guilty and ashamed. Then the urge to dress as a woman again would
be intense. It was so hard and she felt depressed. Trying to push the thoughts out of her mind was not helping and she
decided to see her doctor. She told her doctor that she was not sleeping well and felt depressed and was prescribed
some antidepressants. They helped give her a bit more energy but she still did not feel right.
One of her closest female friends knew something was wrong and decided to speak to Naya. During this conversation,
Naya decided to tell her friend how horrible she felt. It was hard but a relief. With the help of her friend, Naya joined a
support group but did not know if she was a cross-dresser, a freak like her father told her or something else. It was
helpful, though, to meet others who were feeling confused and in turmoil too. She got tips and ideas about make-up
and dressing and decided to dress up at the next meeting. Naya was incredibly nervous, feeling her make-up run as she
was sweating from worry. But her friends at the group were supportive and caring. She kept on going like this for a few
months, and each time it got easier and easier. To help along the way she started getting electrolysis on her face and
tried taking the oral contraceptive pill, which her friend gave her. She was not sure if taking oestrogen in this form did
much, but she liked the idea that she was doing something to make a change.
Naya still went to work as a male. She had been at the same job for almost 30 years but the company was no longer
doing well and she was eventually made redundant. She started doing some odd jobs for people and decided to run her
own business. Working on her own gave her time to think and on her 49th birthday Naya called a specialist gender clinic
to make an appointment. This was a turning point for Naya. She was tired to being ‘fake’ and she knew what she wanted
to do. It was difficult to talk to the psychiatrist about personal things—how do you describe your gender? She was worried
about what the psychiatrist would think of her. She decided she just needed to be honest. She told the psychiatrist about
taking the Pill and about her secret desire to be female. The psychiatrist was very reassuring and kind. Several months
later, Naya started her own hormone treatment. She felt good. She regularly saw her psychiatrist and was doing well. She
had changed her name and driver’s licence. She felt comfortable in her ‘new’ but same skin. While looking in the mirror
she knew she was not perfect but she was content. Finally, at 51, Naya had gender-affirmation surgery. It was painful but
she was glad she had it done. It did not dramatically change her life but it helped to make her feel more at peace within
herself. Naya was the same person she had always been but a more content version of herself inside.
SUMMARY
Awareness of gender variance has increased greatly in recent years, which has helped to promote more accepting societal attitudes
towards TGD individuals and driven significant increases in referrals for gender-affirming health care. Diagnostic approaches in
this area have similarly changed significantly over time and continue to evolve. The introduction of the DSM-5 saw the re-naming
of gender identity disorder as gender dysphoria in an effort to remove the stigma associated with the term ‘disorder’, while at
the same time acknowledging the distress that can arise when there is incongruence between an individual’s experienced and
assigned gender. Looking ahead, efforts to completely remove gender variance from diagnostic systems are highly likely, as was
the case for homosexuality in the 1970s.
The true prevalence rate of TGD individuals has been difficult to establish, but recent studies within the general population
estimate around 1 per cent of people identify as transgender. Onset can occur not only in early childhood but also in adolescence
and adulthood.
Despite more accepting societal attitudes, many TGD individuals continue to experience significant harassment, discrimination
and rejection. Not surprisingly, rates of depression, anxiety, self-harm and suicide are much higher in TGD individuals than in the
general population.
What causes people to be TGD is much debated. The perceived importance of nature versus nurture in gender identity formation
has waxed and waned over many years. Empirically, it has been observed that gender identity usually forms and becomes fixed
quite early in childhood, and nowadays the argument for a biological basis for gender identity appears fairly strong. However,
psychosocial influences powerfully shape how an individual expresses an underlying TGD predisposition.
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A variety of gender-affirming therapies and medical interventions are available for TGD people. Treatment options include
support to change gender expression and role, psychotherapy, pharmacological interventions, surgery, voice and communication
therapy, and the management of reproductive health. At present, international treatment guidelines are based on expert consensus
opinion, and research efforts are underway to establish the long-term safety and effectiveness of these interventions. Looking
ahead, a revision of the existing WPATH Standards of Care (Coleman, 2012) will be undertaken in the near future, and this next
version is likely to introduce changes in the way children and adolescents with gender dysphoria are managed.
KEY TERMS
cis/cisgender. . . . . . . . . . . . . . . . . . . . . 374 non-binary gender. . . . . . . . . . . . . . . . 385 transition/gender affirmation
gender. . . . . . . . . . . . . . . . . . . . . . . . . . 371 sex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 371 process . . . . . . . . . . . . . . . . . . . . . . . . . 374
gender constancy . . . . . . . . . . . . . . . . 381 sex or gender assigned at birth. . . . . 373 trans man. . . . . . . . . . . . . . . . . . . . . . . . 372
gender expression. . . . . . . . . . . . . . . . 372 sexual orientation. . . . . . . . . . . . . . . . . 372 trans woman. . . . . . . . . . . . . . . . . . . . . 372
gender identity. . . . . . . . . . . . . . . . . . . 372 sexual dimorphism. . . . . . . . . . . . . . . . 381 transsexual . . . . . . . . . . . . . . . . . . . . . . 373
gender dysphoria. . . . . . . . . . . . . . . . . 375 trans and gender diverse (TGD). . . . . 374
gender variance/non-conformity. . . . 373 trans/transgender. . . . . . . . . . . . . . . . . 374
REVIEW QUESTIONS
LO 12.1
12.1 What are the differences between gender identity, sex and sexuality?
12.2 What are the current controversies related to the diagnosis of gender dysphoria?
12.3 Why are differential diagnoses important to consider in assessing gender dysphoria?
LO 12.2
12.4 Describe recent changes in the prevalence of people identifying as TGD, and outline likely reasons for
these trends.
12.5 What mental health problems are commonly observed in TGD individuals, and why might these arise?
LO 12.3
12.6 Briefly discuss the aetiology of gender dysphoria.
LO 12.4
12.7 List some of the key guiding principles in treating gender dysphoria.
12.8 In clinical practice, what can be done to help ensure an environment that is affirming for TGD individuals?
12.9 Describe some of the issues for which TGD individuals may wish to seek psychological support.
12.10 What are the different hormonal treatment options for gender dysphoria?
REFERENCES
ACON (2013). Submission to ABS Census Consultation on Context American Psychiatric Association (1980). Diagnostic and statistical
and Procedures 2016. Canberra: Australian Government. manual of mental disorders (3rd ed.). Washington, DC: Author.
Aghabikloo, A., Bahrami, M., Saberi, S. M., & Emamhadi, M. A. American Psychiatric Association (1987). Diagnostic and statistical
(2013). Gender identity disorders in Iran: Request for sex manual of mental disorders (3rd ed. text rev.). Washington, DC:
reassignment surgery. International Journal of Medical Toxicology Author.
and Forensic Medicine, 2, 128–134. American Psychiatric Association (1994). Diagnostic and statistical
American Psychiatric Association (1952). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.
manual: Mental disorders. Washington, DC: Author. American Psychiatric Association (2000). Diagnostic and statistical
American Psychiatric Association (1968). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC:
manual of mental disorders (2nd ed.). Washington, DC: Author. Author.
rie66620_ch12_369-398.indd 395 07/29/17 02:09 PM

American Psychiatric Association (2013). Diagnostic and statistical Cohen-Bendahan, C. C., van de Beek, C., & Berenbaum, S. A.
manual of mental disorders (5th ed.). Arlington: Author. (2005). Prenatal sex hormone effects on child and adult sex-typed
Andrology Australia (2015). PBS criteria for testosterone behavior: Methods and findings. Neuroscience and Biobehavioral
prescribing: A few suggestions on implementation. Retrieved from Reviews, 29, 353–384.
https://www.andrologyaustralia.org/wp-content/uploads/PBS- Cohen-Kettenis, P. T., & Kuiper, A. J. (1984). Transseksualiteit en
testosterone-implementation-2015.pdf. psychothérapie. Tìjdschrift Voor Psychotherapie, 10, 153–166.
Australian and New Zealand Professional Association for Cohen-Kettenis, P. T., & Pfafflin, F. (2010). The DSM diagnostic
Transgender Health (2016). ANZPATH supports the World criteria for gender identity disorder in adolescents and adults.
Professional Association for Transgender Health’s statement on Archives of Sexual Behavior, 39, 499–513.
de-psychopathologisation of gender variance. Retrieved from Coleman, E., Bockting, W., Botzer, M., Cohen-Kettenis, P.,
http://anzpath.org/about/statements DeCuypere, G., Feldman, J., . . . Meyer, W. J. (2012). Standards
Australian Psychological Society (2016). Australian Psychological of care for the health of transsexual, transgender, and gender-
Society recommends mental health practices that affirm nonconforming people, version 7. International Journal of
transgender people’s experiences. Retrieved from http://www. Transgenderism, 13, 165–232.
psychology.org.au/Content.aspx?ID=5638 Connell, R., & Pearse, R. (2014). Gender: In world perspective
Bagga, H., & Erasmus, J. (2014). Prevalence data research in (3rd ed.). Cambridge: Polity Press.
transgender health care. Paper presented at the Australia New Conron, K. J., Scott, G., Stowell, G. S., & Landers, S. J. (2012).
Zealand Professional Association for Transgender Health Transgender health in Massachusetts: Results from a household
Conference Adelaide. probability sample of adults. American Journal of Public Health,
Bailey, J. M. (2003). The man who would be queen: The science 102, 118–122.
of gender-bending and transsexualism. Washington, DC: Joseph Couch, M. (2007). Tranznation: A report on the health and wellbeing
Henry Press. of transgender people in Australia and New Zealand. Melbourne:
Bandini, E., Fisher, A. D., Ricca, V., Ristori, J., Meriggiola, M. C., Australian Research Centre in Sex, Health and Society, LaTrobe
Jannini, E. A., . . . Maggi, M. (2011). Childhood maltreatment in University.
subjects with male-to-female gender identity disorder. International De Cuypere, G., Van Hemelrijck, M., Michel, A., Carael, B.,
Journal of Impotence Research, 23, 276–285. Heylens, G., Rubens, R., . . . Monstrey, S. (2007). Prevalence and
Bentz, E. K., Pils, D., Bilban, M., Kaufmann, U., Hefler, L. A., demography of transsexualism in Belgium. European Psychiatry,
Reinthaller, A., . . . Tempfer, C. B. (2010). Gene expression 22, 137–141.
signatures of breast tissue before and after cross-sex hormone Devor, H. (1997). FTM: Female-to-male transsexuals in society.
therapy in female-to-male transsexuals. Fertility and Sterility, 94, Bloomington: Indiana University Press.
2688–2696. Dhejne, C., Oberg, K., Arver, S., & Landen, M. (2014). An analysis
Blanchard, R. (1985). Typology of male-to-female transsexualism. of all applications for sex reassignment surgery in Sweden,
Archives of Sexual Behavior, 14, 247–261. 1960–2010: Prevalence, incidence, and regrets. Archives of Sexual
Blanchard, R. (1989). The concept of autogynephilia and the typology Behavior, 43, 1535–1545.
of male gender dysphoria. Journal of Nervous Mental Diseases, Dhejne, C., Van Vlerken, R., Heylens, G., & Arcelus, J. (2016).
177, 616–623. Mental health and gender dysphoria: A review of the literature.
Blanchard, R. (2008). Deconstructing the feminine essence narrative. International Review of Psychiatry, 28, 44–57.
Archives of Sexual Behavior, 37, 434–438. Diamond, M., & Sigmundson, H. K. (1997). Sex reassignment at
Bockting, W. (2008). Psychotherapy and the real-life experience: From birth. Long-term review and clinical implications. Archives of
gender dichotomy to gender diversity. Sexologies, 17, 211–224. Pediatric and Adolescent Medicine, 151, 298–304.
Bockting, W. O., & Goldberg, J. (Eds.) (2006). Guidelines for Drescher, J. (2010). Transsexualism, gender identity disorder and the
transgender care. Binghamton, NY: Haworth Medical Press. DSM. Journal of Gay & Lesbian Mental Health, 14, 109–122.
Brizendine, L. (2006). The female brain. New York: Morgan Road Drescher, J., Cohen-Kettenis, P. T., & Reed, G. M. (2016). Gender
Books. incongruence of childhood in the ICD-11: Controversies, proposal,
Brizendine, L. (2010). The male brain. New York: Broadway Books. and rationale. The Lancet Psychiatry, 3, 297–304.
Butler, J. (1990). Gender trouble. London: Routledge. Drescher, J., Cohen-Kettenis, P., & Winter, S. (2012). Minding
Cavanaugh, T., Hopwood, R., & Lambert, C. (2016). Informed consent the body: situating gender identity diagnoses in the ICD-11.
in the medical care of transgender and gender-nonconforming International Review of Psychiatry, 24, 568–577.
patients. AMA Journal of Ethics, 18, 1147–1155. Eden, K., Wylie, K., & Watson, E. (2012). Gender dysphoria:
Chung, W. C., De Vries, G. J., & Swaab, D. F. (2002). Sexual recognition and assessment. Advances in Psychiatric Treatment,
differentiation of the bed nucleus of the stria terminalis in 18, 2–11.
humans may extend into adulthood. Journal of Neuroscience, 22, Elaut, E., Heylens, G., De Cuypere, G., Van Hoorde, B., & Baetens,
1027–1033. K. (2016). DSM-IV-TR versus DSM-5: Do the new criteria for
Clark, T. C., Lucassen, M. F., Bullen, P., Denny, S. J., Fleming, gender dysphoria lead to different diagnostic outcomes? Paper
T. M., Robinson, E. M., & Rossen, F. V. (2014). The health and presented at the World Professional Association for Transgender
well-being of transgender high school students: Results from the Health Symposium, Amsterdam.
New Zealand adolescent health survey (Youth’12). Journal of Erasmus, J., Harte, F., Bagga, H., Davies, D., & Cowling, S. (2014).
Adolescent Health, 55, 93–99. An exploratory investigation into the quality of life of patients
rie66620_ch12_369-398.indd 396 07/29/17 02:09 PM

with gender dysphoria at various stages during their transition: characteristics in transsexual individuals: Multicentre study in four
An Australian perspective. Paper presented at the World European countries. British Journal of Psychiatry, 204, 151–156.
Professional Association for Transgender Health Symposium, Hyde, Z., Doherty, M., Tilley, P., McCaul, K., Rooney, R., & Jancey,
Bangkok. J. (2014). The first Australian national trans mental health study:
Fausto-Sterling, A. (2000). Sexing the body: Gender politics and the Summary of results. School of Public Health, Curtin University,
construction of sexuality (1st ed.). New York: Basic Books. Perth.
Fernandez, R., Esteva, I., Gomez-Gil, E., Rumbo, T., Almaraz, M. C., Inch, E. (2016). Changing minds: The psycho-pathologization of
Roda, E., . . . Pasaro, E. (2014a). Association Study of ERbeta, trans people. International Journal of Mental Health, 45, 193–204.
AR, and CYP19A1 Genes and MtF Transsexualism. Journal of Kerry, S. C. (2014). Sistergirls/brotherboys: The status of Indigenous
Sexual Medicine, 11, 2986–2994. transgender Australians. International Journal of Transgenderism,
Fernandez, R., Esteva, I., Gomez-Gil, E., Rumbo, T., Almaraz, M. C., 15, 173–186.
Roda, E., . . . Pasaro, E. (2014b). The (CA)n polymorphism of Kruijver, F. P., Zhou, J. N., Pool, C. W., Hofman, M. A.,
ERbeta gene is associated with FtM transsexualism. Journal of Gooren, L. J., & Swaab, D. F. (2000). Male-to-female transsexuals
Sexual Medicine, 11, 720–728. have female neuron numbers in a limbic nucleus. Journal of
Fine, C. (2010). Delusions of gender: The real science behind sex Clinical Endocrinology and Metabolism, 85, 2034–2041.
differences. London: Icon Books. Lane, R. (2011). Trans, science and society: The politics of knowledge
Fine, C. (2017). Testosterone rex: Myths of sex, science, and society. of the brain sex theory of trans (doctoral dissertation). La Trobe
New York: W. W. Norton. University, Melbourne. Retrieved from http://arrow.latrobe.edu.au:
Gelder, M. G., & Marks, I. M. (1969). Aversion treatment in 8080/vital/access/manager/Repository/latrobe:34019;jsessionid=
transvestism and transsexualism. In R. Green & J. Money (Eds.), 7FD8AE94B3AD084859BBDBF7ECB05308.
Transsexualism and sex reassignment (pp. 383–413). Baltimore: Lawrence, A. A. (2003). Factors associated with satisfaction or regret
Johns Hopkins University Press. following male-to-female sex reassignment surgery. Archives of
GLBTI Health and Wellbeing Ministerial Advisory Committee Sexual Behavior, 32, 299–315.
(2014). Transgender and gender diverse health and wellbeing: Leonard, W., Pitts, M., Mitchell, A., Lyons, A., Smith, A., Patel, S.,
Background paper. Retrieved from http://www.health.vic.gov.au/ Barrett, A. (2012). Private Lives 2: The second national survey of
diversity/index.htm. the health and wellbeing of gay, lesbian, bisexual and transgender
Glidden, D., Bouman, W. P., Jones, B. A., & Arcelus, J. (2016). Gender (GLBT) Australians. Melbourne: Australian Research Centre in
dysphoria and autism spectrum disorder: A systematic review of the Sex, Health and Society, La Trobe University.
literature. Sexual Medicine Reviews, 4, 3–14. Lev, A. I. (2004). Transgender emergence: Therapeutic guidelines for
Godwin, R. (2016). Andreja Pejić on becoming the most famous working with gender-variant people and their families. New York:
transgender model in the world. Retrieved from http://www. Haworth Clinical Practice Press.
standard.co.uk/lifestyle/esmagazine/andreja-peji-on-becoming- Lev, A. I. (2009). The ten tasks of the mental health provider:
the-most-famous-transgender-model-in-the-world-a3288581.html. Recommendation for revision of the World Professional Association
Gooren, L. (2006). The biology of human psychosexual for Transgender Health’s Standards of Care. International Journal
differentiation. Hormones and Behavior, 50, 589–601. of Transgenderism, 11, 74–99.

Grant, J., Mottet, L., & Tanis, J. (2011). Injustice at every turn: Lombardo, F., Toselli, L., Grassetti, D., Paoli, D., Masciandaro, P.,
A report of the National Transgender Discrimination Survey. Valentini, F., . . . Gandini, L. (2013). Hormone and genetic study
Retrieved from www.thetaskforce.org/downloads/reports/reports/ in male to female transsexual patients. Journal of Endocrinological
ntds_full.pdf. Investigation, 36, 550–557.
Hakeem, A. (2012). Psychotherapy for gender identity disorders. Marshall, B. D. L., Socías, M. E., Kerr, T., Zalazar, V., Sued, O., &
Advances in Psychiatric Treatment, 18, 17–24. Arístegui, I. (2016). Prevalence and correlates of lifetime suicide
Hare, L., Bernard, P., Sánchez, F. J., Baird, P. N., Vilain, E., attempts among transgender persons in Argentina. Journal of
Kennedy, T., & Harley, V. R. (2009). Androgen receptor Homosexuality, 63, 955–967.
repeat length polymorphism associated with male-to-female Meerwijk, E. L., & Sevelius, J. M. (2017). Transgender population
transsexualism. Biological Psychiatry, 65, 93–96. size in the United States: A meta-regression of population-based
Harte, F. (2012). Gender dysphoria: Shifting diagnostic and treatment probability samples. American Journal of Public Health: February,
paradigms: A report from a meeting of an Australian Psychiatrist 107, e1–e8.
Expert Group. Melbourne: Psychiatry in Australia. Meier, S. C., & Labuski, C. M. (2013). The demographics of the
Henningsson, S., Westberg, L., Nilsson, S., Lundstrom, B., Ekselius, transgender population. In A. K. Baumle (Ed.), International
L., Bodlund, O., . . . Landen, M. (2005). Sex steroid-related genes handbook on the demography of sexuality (pp. 289–327). New York,
and male-to-female transsexualism. Psychoneuroendocrinology, NY: Springer.
30, 657–664. Money, J. (1975). Ablatio penis: Normal male infant sex-reassigned
Heylens, G., De Cuypere, G., Zucker, K. J., Schelfaut, C., Elaut, as a girl. Archives of Sexual Behavior, 4, 65–71.
E., Vanden Bossche, H., . . . T’Sjoen, G. (2012). Gender identity Money, J., & Ehrhardt, A. A. (1972). Man and woman, boy and
disorder in twins: A review of the case report literature. Journal of girl: The differentiation and dimorphism of gender identity from
Sexual Medicine, 9, 751–757. conception to maturity. Baltimore: Johns Hopkins University Press.
Heylens, G., Elaut, E., Kreukels, B. P., Paap, M. C., Cerwenka, Namaste, V. K. (2000). Invisible lives: The erasure of transsexual and
S., Richter-Appelt, H., . . . De Cuypere, G. (2014). Psychiatric transgendered people. Chicago: University of Chicago Press.
rie66620_ch12_369-398.indd 397 07/29/17 02:09 PM

Nuttbrock, L., Bockting, W., Mason, M., Hwahng, S., Rosenblum, Stryker, S. (2008). Transgender history. Berkeley: Seal Press.
A., Macri, M., & Becker, J. (2011). A further assessment of Telfer, M., Tollit, M., & Feldman, D. (2015). Transformation of
Blanchard’s typology of homosexual versus non-homosexual or health-care and legal systems for the transgender population: The
autogynephilic gender dysphoria. Archives of Sexual Behavior, 40, need for change in Australia. Journal of Paediatrics and Child
247–257. Health, 51, 1051–1053.
Pauly, I. B. (1965). Male psychosexual inversion: Transsexualism: A Ujike, H., Otani, K., Nakatsuka, M., Ishii, K., Sasaki, A., Oishi, T., . . . 
review of 100 cases. Archives of General Psychiatry, 13, 172–181. Kuroda, S. (2009). Association study of gender identity
Phoenix, C. H., Goy, R. W., Gerall, A. A., & Young, W. C. (1959). disorder and sex hormone-related genes. Progress in Neuro-
Organizing action of prenatally administered testosterone Psychopharmacology and Biological Psychiatry, 33, 1241–1244.
propionate on the tissues mediating mating behavior in the female Veale, J. F. (2014). Evidence against a typology: A taxometric
guinea pig. Endocrinology, 65, 369–382. analysis of the sexuality of male-to-female transsexuals. Archives
Reed, B., Rhodes, S., Schofield, P., & Wylie, K. (2009). Gender of Sexual Behavior, 43, 1177–1186.
variance in the UK: Prevalence, incidence, growth and geographic Vujovic, S., Popovic, S., Mrvosevic Marojevic, L., Ivovic, M.,
distribution. Retrieved from https://www.gires.org.uk/assets/ Tancic-Gajic, M., Stojanovic, M., . . . Micic, D. (2014). Finger
Medpro-Assets/GenderVarianceUK-report.pdf. length ratios in Serbian transsexuals. Scientific World Journal,
Reed, T. (2006). Atypical gender development: A review. International 2014, article ID 763563.
Journal of Transgenderism, 9, 29–44. Williams, M., Chesterman, J., & Grano, P. (2014). Re Jamie (no 2):
Riggs, D. W., Coleman, K., & Due, C. (2014). Healthcare experiences A positive development for transgender young people. Journal of
of gender diverse Australians: A mixed-methods, self-report Law and Medicine, 22, 90–104.
survey. BMC Public Health, 14, 230. Winter, S. (2006). Thai transgenders in focus: Their beliefs about
Robles, R., Fresán, A., Vega-Ramírez, H., Cruz-Islas, J., Rodríguez- attitudes towards and origins of transgender. International Journal
Pérez, V., Domínguez-Martínez, T., & Reed, G. M. (2016). of Transgenderism, 9, 47–62.
Removing transgender identity from the classification of mental Winter, S. (2016). Should the diagnosis of gender incongruence in
disorders: A Mexican field study for ICD-11. The Lancet childhood (GIC) be included in the ICD-11? In favour Morris
Psychiatry, 3, 850–859. Bersin; against Sam Winter. Amsterdam June 2016. Paper
Ross, M. W., Wålinder, J., Lundströ, B., & Thuwe, I. (1981). presented at the World Professional Association for Transgender
Cross-cultural approaches to transsexualism. Acta Psychiatrica Health Symposium, Amsterdam.
Scandinavica, 63, 75–82. World Health Organization (1978). International classification of
Russo, F. (2017). Where transgender is no longer a diagnosis. diseases; manual of the international statistical classification of
Scientific American (6 January). diseases, injuries, and causes of death. Adopted by the 29th World
Saraswat, A., Weinand, J. D., & Safer, J. D. (2015). Evidence Health Assembly.
supporting the biologic nature of gender identity. Endocrine World Professional Association for Transgender Health Symposium
Practice, 21, 199–204. (2010). WPATH de-psychopatholisation statement. Retrieved from
Schneider, H. J., Pickel, J., & Stalla, G. K. (2006). Typical http://www.wpath.org/site_page.cfm?pk_association_webpage_
female 2nd–4th finger length (2D:4D) ratios in male-to-female menu=1351&pk_association_webpage=3928.

transsexuals: Possible implications for prenatal androgen exposure. Wylie, K., Eden, K., & Watson, E. (2012). Gender dysphoria:
Psychoneuroendocrinology, 31, 265–269. Treatment and outcomes. Advances in Psychiatric Treatment, 18,
Slaby, R. G., & Frey, K. S. (1975). Development of gender constancy 12–16.
and selective attention to same-sex models. Child Development, Youth Coalition of the ACT (2010). Policy platform: Gay, lesbian,
46, 849–856. bisexual, transgender and/or intersex young people. Canberra:
Smith, E., Jones, T., Ward, R., Dixon, J., Mitchell, A., & Hillier, Author.
L. (2014). From blues to rainbows: The mental health and well- Zhou, J. N., Hofman, M. A., Gooren, L. J., & Swaab, D. F. (1995). A
being of gender diverse and transgender young people in Australia. sex difference in the human brain and its relation to transsexuality.
Melbourne: La Trobe University. Nature, 378, 68–70.
Starcevic, V., Monti, M. R., D’Agostino, A., & Berle, D. (2013). Will Zucker, K. J. (2010). The DSM diagnostic criteria for gender identity
DSM-5 make us feel dysphoric? Conceptualisation(s) of dysphoria disorder in children. Archives of Sexual Behavior, 39, 477–498.
in the most recent classification of mental disorders. Australian Zuckerman, B. (2014). Andrej Pejic now Andreja after sex
and New Zealand Journal of Psychiatry, 47, 954–955. reassignment surgery. Retrieved from http://people.com/celebrity/
Stoller, R. J. (1967). Etiological factors in male transsexualism. andrej-pejic-now-andreja-after-sex-reassignment-surgery/.
Transactions of the New York Academy of Sciences, 29, 431–434.
Stoller, R. J. (1971). Transsexualism and transvestism. Psychiatric
Annals, 1, 60–72.
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CHAPTER 13
Personality disorders
Louise McCutcheon
Carol Hulbert
Martina Jovev
Catharine McNab
CHAPTER OUTLINE
●
The definition of personality and personality disorder
● The diagnosis of personality disorder
● The epidemiology of personality disorders
● General models of the aetiology and treatment of personality disorders
● The aetiology and treatment of specific personality disorders
● Summary

13.1 Outline the factors differentiating normal from dysfunctional personality functioning.
13.2 Describe the two classification systems for diagnosing personality disorders, including their similarities and
differences.
13.3 Summarise and critically evaluate research on the prevalence of personality disorders.
13.4 Describe prominent models regarding the aetiology and treatment of personality disorders in general.
13.5 Describe prominent models regarding the aetiology and treatment of specific personality disorders.
PERSONALITY DISORDERS: AN AUSTRALASIAN FOCUS

The study of personality and personality dysfunction is a source of great interest within the field of psychology and the
broader community. Sources of community interest include the desire to better understand our own and others’ actions,
experiences and even instances of extreme behaviours brought to public attention through the media. Notable among
these behaviours are aggressive and cruel acts, such as those carried out by individuals with antisocial personality
disorder, as well as the self-harming (e.g., cutting or overdosing using prescribed medication) and other risky behaviours
(e.g., promiscuity and misuse of drugs and alcohol) associated with borderline personality disorder. Such extreme
behaviours are not easily explained by lay accounts of human nature, requiring the development of more complex
clinical models of classification, aetiology and treatment. An example of personality disorder in the Asia-Pacific context is
that of Clayton Weatherston (Hartevelt, 2009).
Clayton Weatherston was a tutor and recent PhD graduate in the Economics department at Otago University in
Dunedin, New Zealand. In June 2007, when he was 31, he began a relationship with Sophie Elliott, a 22-year-old
undergraduate student in the same department. Their six-month relationship was tumultuous, and reportedly included
instances of Weatherston assaulting and verbally abusing Elliott (including belittling her in university tutorials that
he tutored) and Elliott having relationships with other men and damaging Weatherston’s property. They broke up in
December 2007.
continued
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On 9 January (Weatherston’s 32nd birthday), Weatherston went

to Elliott’s house in Dunedin, where she lived with her family, to self-
reportedly return gifts Elliott had given him and to make her behave
better through ‘some sort of insulting gesture’. He parked his car
on the road, rather than closer to the house, and carried a kitchen
knife in his laptop case. Elliott’s mother let him in, and Elliott and
Weatherston proceeded to Elliott’s bedroom to talk. Soon afterwards,
Mrs Elliott heard screams from her daughter, and attempted to enter
Elliott’s bedroom only to find the door was locked. Mrs Elliott called
the police and on returning to the bedroom, managed to open the
door. She briefly saw Weatherston straddling Elliott and stabbing her,
before Weatherston closed the door in Mrs Elliott’s face.
When the police arrived, Weatherston admitted to killing Elliott,
giving as the reason ‘the emotional pain that she [had] caused [him]
over the past year’. Elliott died of massive blood loss after sustaining
seven blunt force injuries and 216 stab or cut wounds, some from
the kitchen knife and others from a pair of scissors found in Elliott’s
bedroom. The judge ruled that, in his actions, Weatherston had
focused on damaging aspects of Elliott’s beauty and sexuality (e.g.,
the number of stab wounds to Elliott’s eyes, neck, breasts and pubic
area; and the cutting off of Elliott’s hair, of which she had been proud).
DAL
In his trial, Weatherston used the provocation defence, saying that
he had lost his self-control when Elliott had criticised his mother and Clayton Weatherston, who was convicted of
attacked him with a pair of scissors, causing his glasses to fall off, killing his ex-girlfriend in New Zealand.
and that these actions had led to him losing his self-control.
Evidence at the trial suggested that Weatherston had a largely unremarkable upbringing, and had a history of
some successful romantic relationships and friendships in his rugby team. He was reported to be capable of ‘kind and
generous’ acts, such as helping overseas students to become familiar with Dunedin, where he had lived all his life.
However, it was also reported that he saw himself as a ‘big fish in a small pond’ at school and that he often boasted of his
achievements throughout school. This inflated sense of his own importance and exaggeration of his accomplishments
was also noted by his colleagues and the forensic psychiatrists who interviewed him. His colleagues also described him
as competitive, saying ‘he liked to put other people down’ and that he accused others of stealing his ideas. He boasted
that completing his PhD had been ‘easy’, even though in reality he had never studied full time because he found it
too stressful. He had been expecting to get a job in the Economics department, but seemed to have no idea that his
behaviour towards his colleagues had made this very unlikely.
A previous girlfriend reported that while Weatherston had a loving side, he also had a ‘nasty and mean demeanour on
the other’. He was dismissive and bullying once the relationship broke up, later returning in tears, begging forgiveness
and stating that he had ‘messed everything up’. He conceded that he had physically assaulted a previous girlfriend, who
reported that he had tried to blame her for the incident, and a professor in his department reported that Weatherston had
pushed Elliott down the stairs while boasting that he now had a new girlfriend who was ‘such a step up’ from her. Friends
of Weatherston’s reported that he had not shown any affection or care for Elliott during their relationship. Furthermore,
throughout the trial Weatherston continued to blame Elliott for provoking him into killing her, showed anger and envy
over the sympathy and attention afforded Elliott and her ‘contrived legacy’ (Elliott’s parents set up the Sophie Elliott
Foundation to raise awareness of the signs of partner abuse). In his testimony, he stated, ‘I was in a relationship and I
wasn’t going to be controlled. So I left it. That’s all there is, there’s nothing more to it. And now I’m free of the relationship.’
He showed no remorse for the murder, and the most he conceded was that he ‘played a part’ in the death and mutilation
of Ms Elliott.
Many observers noted the arrogance and contempt with which he treated the Crown prosecutors, his workmates and
others in court. He made statements such as ‘I can’t believe we are talking about this. You’re really scraping the barrel.’
Other evidence from previous counselling suggested that he was fragile in the face of challenge and ‘(longed) to get the
best evaluations from students. Trying to be adored.’ During the trial he reported a history of anxiety about the size of his
genitalia and of seeking reassurance from previous partners about this. Two senior psychiatrists gave evidence for the
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Chapter 13 Personality disorders 401
defence that they believed Weatherston had a personality disorder, and many aspects of his character and behaviour
described by those who knew him or observed him in court are consistent with this. Specifically, he displayed a number
of features consistent with narcissistic personality disorder. These included his inflated sense of his own importance, the
belief that he was ‘special’ and his sense of entitlement, his need for others’ admiration, the exploitative nature of many
of his relationships, his lack of empathy, his haughty and arrogant behaviour, and his jealousy and envy.
Co-occurrence of personality disorders is common and, consistent with this, it is likely that some of the other
longstanding personality features Weatherston demonstrated were consistent with features of other personality
disorders (e.g., the relational instability described by previous partners is a feature of a borderline personality disorder).
Weatherston’s actions could be understood as narcissistic rage consequent to feeling humiliated, spurned or threatened.
The jury rejected Weatherston’s provocation defence and found him guilty of murder. The judge concluded that the
killing of Elliott was a ‘deliberate and controlled attack on a young woman whom, [Weatherston] had made known to
others, he hated’. Weatherston was sentenced to a minimum term of 18 years.
This chapter will address the terms ‘personality’ and ‘personality disorder’ and examine the main characteristics of
the various personality disorders according to current classification systems. Research findings regarding the prevalence
of personality disorders will then be provided, and discussion of the aetiology and treatment of personality disorders will
be presented. General models of aetiology and treatment of personality disorders will be described, and treatments for
specific personality disorders will be outlined. Finally, the challenges and controversial issues in the field of personality
disorder will be examined.
LO 13.1 The definition of personality

and personality disorder
Personality
Personality is defined in terms of consistency in patterns of thinking, feeling and behaving that are
pervasive across life domains and enduring over time. The influential and well-validated model, the
five factor model (Costa & Widiger, 2002; McCrae & Costa, 1984), identifies five personality traits: five factor model
neuroticism, extroversion, openness to experience, conscientiousness and agreeableness. Personality theory
which proposes
∙ Neuroticism (N) encompasses the general level and stability of an individual’s emotional that any
adjustment—individuals high in N are prone to psychological distress and a reliance on maladaptive individual’s
coping skills. personality is
∙ Extroversion (E) describes an individual’s preferred quantity and intensity of interpersonal organised along
five broad
interactions, activity levels, need for stimulation and capacity for joy—individuals high in E are
dimensions:
sociable, talkative, active and optimistic. neuroticism,
∙ Openness to experience (O) is the degree to which an individual actively seeks and appreciates extroversion,
different experiences—individuals high in O are curious, imaginative and open to novel and openness to
unconventional ideas and behaviours. experience,
∙ Conscientiousness (C) refers to the degree to which an individual is organised, persistent and agreeableness and
motivated in goal-directed behaviour—individuals high in C are organised, reliable, hard-working, conscientiousness.
self-directed and punctual.
∙ Agreeableness (A) encompasses the interpersonal interactions preferred by an individual on a
continuum from compassion to antagonism—individuals high in A are good-natured, trusting,
helpful, forgiving and altruistic.
Cross-cultural research has validated the five factor model across diverse national and ethnic
populations. The dimensions making up the five factor model have been consistently demonstrated. In
addition, robust research findings indicate that personality functioning exists on a continuum, with no
clear or easily detectable point of division between normality and pathology.
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Personality disorder
The definition of personality disorder remains a controversial issue. The work of the late Theodore
Millon, a major theorist and researcher in the area of personality disorder, helpfully spelt out three
core and enduring characteristics that differentiate disordered personality from normal-range
problematic behaviours. The three core features are (a) functional inflexibility; (b) self-defeating
patterns of behaviour; and (c) unstable functioning in the face of stress (Millon, 1981). ‘Functional
inflexibility’ refers to a failure to adapt to changing and varied life experiences and is characterised
by the tendency to rigidly apply a range of behavioural strategies or responses across diverse life
situations, even when the behaviour is clearly inappropriate. ‘Self-defeating behaviour patterns’ are
typical ways of responding or coping that worsen the current situation or are highly damaging for the
person involved. Despite this, the person demonstrates limited capacity to learn from experience and
alter harmful or maladaptive behaviours. Finally, the individual with a personality disorder is likely to
demonstrate what Millon refers to as ‘tenuous stability under stress’, evident in marked instability in
mood, thinking and behaviour during challenging life events.
CASE STUDY: PERSONALITY DISORDER

The case of Eve, a 28-year-old single woman with borderline personality disorder, illustrates the three core features
of personality disorder. Eve’s family had migrated to Australia before she was born. Her parents had a very chaotic
relationship that was characterised by loud arguments and some physical violence. Eve was bright and did well at school.
She recalled feeling jealous of the attention her older disabled brother received from her parents, but felt guilty about
this. She recalled feeling lonely and that she struggled to find ways to please her parents. On starting school, she
excelled and quickly found satisfaction in the praise she received from her teachers. By the middle of high school,
she found studying had ceased to be enough for her and she realised she had few friends. She then tried to fit in with
her peers by going out to parties and experimenting with drinking and taking drugs. She was very competitive, which
resulted in her struggling to maintain friendships with girls. Her relationships with boys were easier to initiate, but also
rarely lasted after the first sexual encounter, leaving her feeling exploited and alone. She dropped out of her final year of
school after being sexually assaulted at a party.
As an adult, Eve continues to struggle with alcohol, often getting herself into embarrassing and potentially dangerous
situations. She reports that her moods seem to change constantly. When lonely and upset, she binge eats or goes on
excessive spending sprees, which add to her financial problems. When very distressed, she cuts herself or overdoses on
prescription medication. Eve’s difficulties in managing her own moods and use of maladaptive coping strategies when
experiencing challenges are an example of Millon’s definition of ‘tenuous stability under stress’.
Her substance misuse, spending problems and binge eating are all examples of Millon’s self-defeating patterns of
behaviour, and are likely to make her situation even worse. As people distance themselves from her, she has fewer
opportunities to experience trustful, respectful, mutually supportive and stable relationships that might provide
opportunities for her to learn more adaptive behaviours.
Despite her natural abilities, she drifts from job to job, often leaving after an altercation or because she has done
something in front of colleagues she feels ashamed about. She tends to blame this on her colleagues or friends and is
not able to learn how to manage these relationships better over time. The repeated difficulties she has with work and
social relationships illustrate Millon’s definition of functional inflexibility.
LO 13.2 The diagnosis of personality disorder

There are two major current classification systems that include personality disorders, namely the
Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published by the American
Psychiatric Association (APA, 2013), and the International Classification of Diseases and Health
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Related Problems (ICD-10), prepared by the World Health Organization (WHO, 1992). According
to the DSM-5, personality disorders are defined as enduring patterns of perceiving, relating to and
thinking about the environment and oneself that are exhibited in a wide range of social and personal
contexts. These enduring patterns must differ markedly from the expectations of the individual’s
cultural group and cause significant personal distress and impairment in functioning. Personality
functioning is highly complex and it is not uncommon for a person’s behaviour to be quite disturbed in
one area (such as family life and close relationships) while in other domains (such as work and study)
the person might function relatively effectively.
The DSM-5 refers to 10 personality disorders that have been grouped into three clusters:
∙ Cluster A comprises paranoid, schizoid and schizotypal personality disorders, which are
characterised by odd or eccentric traits and behaviours.
∙ Cluster B comprises antisocial, borderline, histrionic and narcissistic personality disorders, which
are defined by dramatic, emotional or erratic traits and behaviours.
∙ Cluster C comprises avoidant, dependent and obsessive-compulsive personality disorders, which
are defined in terms of anxious and fearful traits and behaviours.
As shown in Table 13.1, the nine specific personality disorders included in the ICD-10
approximate to the 10 listed in the DSM-5. This chapter will focus on the personality disorders
defined by the DSM-5, as this is the most widely used classification system in Australasian mental
health settings.
TABLE 13.1 Comparison of the DSM and ICD classification systems for personality disorders
DSM ICD
Diagnostic criteria Diagnostic criteria refer to behaviours or traits Diagnostic criteria include a variety of conditions
that are characteristic of the person’s recent and that indicate a person’s characteristic and enduring
long-term functioning since adolescence or early patterns of inner experience (cognition and affect)
adulthood. and behaviour that differ markedly from a culturally
Personality disorder describes a constellation of expected and accepted range.

behaviours or traits that cause either significant
impairment in social or occupational functioning or
subjective distress.
CLASSIFICATION THREE MAIN CLUSTERS NINE MAIN TYPES
Cluster A:
Paranoid Paranoid
Schizoid Schizoid
Schizotypal
Cluster B:
Antisocial Dissocial
Borderline Emotionally unstable:
Histrionic Impulsive type
Narcissistic Borderline type
Histrionic
Cluster C:
Avoidant Anxious (avoidant)
Dependent Dependent
Obsessive-compulsive Anankastic
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The clinical features for the DSM-5 (APA, 2013) personality disorders cover a wide range of
dispositions and behaviours. Using the three clusters described above, some broad predictions can be
made in terms of the likely problems and management difficulties of individuals with these various
personality disorders. For example, individuals with Cluster A traits may present with a range of
odd or eccentric behaviours. They are likely to be mistrusting of the motives of treating clinicians
and difficult to engage in treatment. In contrast, those with Cluster C traits are likely to present as
anxious, avoidant and/or dependent. Those with high levels of dependency may readily become over-
reliant on health practitioners. They may forgo engagement in challenging situations and interactions,
often relying on a small number of relationships (even if these relationships are unhealthy) to meet
their needs. Cluster B personality traits present the greatest challenge to clinicians, being associated
with more dramatic and confronting behaviours, including verbal aggression, inappropriate demands,
angry behaviour, drug use, repeated self-harm and inappropriate flirtation and/or sexual advances.
While assessing and diagnosing personality disorder is generally more complex and time-consuming
than diagnosing mental state disorders (such as major depressive disorder), clinicians can be trained
in this process. The essential challenge is to distinguish phenomena likely to be more transient, which
are probably related to a mental state disorder, from those that are more persistent and enduring, thus
representing the way the individual usually responds to situations, and therefore personality-related.
Semi-structured instruments used in face-to-face interviews are likely to be the most accurate way
to assess personality disorder but these might be too time-consuming for clinical settings. To assist
in the identification of individuals for whom a more intensive assessment of personality disorder is
warranted in the form of a semi-structured interview, there are briefer screening tools that can be used.
schizotypal Clinicians should be encouraged to consider the possible presence of a personality disorder when
personality conducting assessments. The benefit of doing this is that clinicians will be better informed when
disorder engaging in treatment planning, and patients will be more likely to receive appropriate treatment for
Pervasive pattern their difficulties. For example, treatment of a disorder such as depression can be compromised when
of inhibited or the clinician treats the presenting problem without recognising that there is a longstanding personality
inappropriate
disorder underlying the depression, while a patient with avoidant personality disorder may find it
emotion
and social extremely difficult to seek the level of social support needed to support his/her recovery from depression.
behaviour as
well as aberrant The Cluster A personality disorders
cognitions and
disorganised The three Cluster A personality disorders are all typified by high levels of introversion (i.e., low
speech. extroversion). Schizotypal personality disorder is characterised by marked discomfort with close
relationships, as well as a range of perceptual and cognitive distortions and odd behaviour. This
paranoid
constellation of symptoms might include having few close friends, being anxious around others as
personality
disorder
a result of paranoid fears that others are trying to hurt them, experiencing odd ideas (e.g., a belief
Pervasive, in clairvoyance) and speech (e.g., over-elaborate speech), having constricted or inappropriate affect
unwarranted and unusual perceptual experiences (e.g., sensing that another person is present). In other words,
mistrust and individuals with the disorder manifest a number of positive and negative psychotic symptoms;
suspicion of however, these tend to be of a more transient nature (lasting minutes to hours) than would warrant a
others. diagnosis of a psychotic disorder.
schizoid Even more intense paranoia is seen among those with paranoid personality disorder. These
personality individuals exhibit a pervasive pattern of suspiciousness and distrust, and are hypervigilant for signs of
disorder others trying to harm them in some way. They misinterpret events and the actions of others, perceiving
Pervasive pattern malevolence when it is not present. They are unforgiving and persistently hold grudges regarding real
of lack of interest or imagined insults or slights towards them, and may repeatedly doubt the fidelity of their spouse or
in and avoidance partner when this has no justification. These beliefs are chronic and persistent over time rather than
of interpersonal
being episodic, as is the case for someone with a psychotic disorder. The beliefs of a person with
relationships as
well as emotional paranoid personality disorder are also less bizarre or delusional in nature than those seen in someone
coldness in with a psychotic disorder.
interactions with Those with schizoid personality disorder exhibit a low desire for connection with other human
others. beings and no interest or pleasure in social activities, including sex. Emotionally cold with a restricted
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CASE STUDY: PARANOID PERSONALITY DISORDER

Tony is a 25-year-old single man who has been unemployed for the past five months. While being assessed by a
psychologist, he appears uncomfortable with personal questions and asks who will be able to read the psychologist’s
notes. He reports that he does not have any credit cards because he worries about people getting hold of his personal
information and using it against him. He also reports that his last job involved working in a small carpeting company,
which had been reasonable until the relationship with his boss broke down and Tony was asked to leave. He mentions
several years of growing disputes with his boss over his rates of pay, the menial tasks he was asked to perform and
other incidents that Tony thought were evidence of targeted discrimination. Although his boss had provided Tony with an
explanation for his decisions, Tony refused to believe that he was not the victim of discrimination and then angrily sat in
his car outside his employer’s house every evening for three weeks until the police threatened to charge him.
Tony says he has been let down by so many people that he rarely trusts others to keep their promises. He says he can
recall everyone who has ‘insulted or screwed me over’ since he was in primary school. He reports ending his relationship
with his girlfriend recently because he was unable to shake the thought that she was cheating on him, despite her
repeated protests that she had always been faithful to him. Tony has now sought help from a psychologist for his feelings
of depression, but his longstanding mistrust of organisations and others make it difficult for him to engage in treatment.
He drops out after three sessions and does not return the psychologist’s phone calls.
range of emotional responses, they almost always choose solitary work and leisure activities, and
show indifference when praised or criticised by others. Individuals with these characteristics are not
motivated to fit in with social expectations, and therefore sometimes appear to others as odd or strange,
or like extreme examples of the ‘loner’ or ‘computer nerd’ stereotypes.
The Cluster B personality disorders

Those with Cluster B personality disorders are narcissistic
labelled as dramatic, acting out or flamboyant. personality
Four personality disorders fall under this rubric. disorder
Individuals with narcissistic personality disorder Pervasive pattern

are arrogant and concerned with their own power of experiencing
and abilities. They show disdain and disregard inflated thoughts
for people, are interpersonally exploitative (i.e., of one’s own
worth as well as
approaching relationships in terms of what they
an obliviousness
can take from them rather than engaging in the to others’
give-and-take of healthy relationships), manifest needs and an
a sense of self-entitlement (i.e., believing that exploitative,
they deserve special treatment), and are often arrogant
envious of others or believe that others are demeanour.
envious of them. Other people are treated merely histrionic
AF ARCHIVE/ALAMY STOCK PHOTO
as an audience to appreciate the narcissistic personality

individual’s supposed greatness rather than as disorder
persons with their own needs. Individuals with Pervasive pattern
this disorder lack empathy and are callous. of excessive
Histrionic personality disorder is partly emotionality and
characterised by a pattern of excessive attention- an intense need
for attention and
seeking. People with the disorder like being the
approval, which is
centre of attention and are uncomfortable when sought by means
they are not. For instance, the individual might The Mean Girls (2004) character Regina George, of overly dramatic
use his/her physical attractiveness or sexuality played by Rachel McAdams, displays features of and seductive
in order to gain the attention of others. Their histrionic personality disorder. behaviour.
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emotions are shallow, they can be easily influenced by others, and they consider their relationships to
be more intimate than they really are. Their behaviour is described as superficial and lacking in depth.
An example of an individual who displays many of these features is the character of Regina George in
the film Mean Girls.
borderline Characteristics of individuals with borderline personality disorder include instability in terms of
personality emotions, sense of identity and interpersonal relationships. Individuals with borderline personality
disorder disorder report changeable moods (feeling low/dysphoric, irritable or anxious) that last hours, or days
Pervasive pattern rather than weeks. Some exhibit episodes of inappropriate or extreme anger, and they can lack a solid
of unstable mood, sense of self or identity. Their interpersonal relationships are often unstable because they oscillate
self-concept,
between intense emotions such as idealising and then devaluing others, and engage in behaviours
interpersonal
relationships and aimed at avoiding real or imagined abandonment. They may engage impulsively in potentially self-
impulse control. destructive behaviours, such as substance abuse, gambling, risk-taking behaviours (e.g., unsafe sexual
practices), self-mutilation (e.g., self-cutting) and suicidal acts. Those with the disorder may also report
antisocial
chronic feelings of emptiness, and may experience brief periods of paranoia or dissociation during
personality stressful situations. Individuals with borderline personality disorder have a high risk of experiencing
disorder other mental health problems, especially depressive disorders and substance use disorders. The parents
Pervasive pattern of singer Amy Winehouse reportedly stated that she had been diagnosed with borderline personality
of criminal, disorder. Her much-publicised risk-taking behaviour, including misuse of drugs and alcohol and
impulsive, callous interpersonal problems, is consistent with this assertion.
and/or ruthless Antisocial personality disorder is essentially conduct disorder (often described as juvenile
behaviour delinquency) continued into later teenage and adult years. It overlaps with other Cluster B personality
predicated upon
disorders yet focuses on overt antisocial or criminal behaviour. The disorder is characterised
disregard for the
rights of others fundamentally by a pattern of behaviour that does not conform to social norms or the law, including
and an absence lying, stealing, cheating, fighting, cruelty to humans and animals, and fire-setting. In addition, there is
of respect for a lack of remorse for such behaviour. People with this personality disorder are also highly impulsive,
social norms. irritable and aggressive, with limited regard for the safety of themselves or others.
CASE STUDY: ANTISOCIAL PERSONALITY DISORDER

The case of James exemplifies an individual with antisocial personality disorder. James is a 42-year-old unemployed man
who lives with his mother following a split from his girlfriend. He was referred to a psychologist for treatment of substance
use. He presents as confident, extroverted and superior. He is the eldest of three children. His father, who was largely
absent during his childhood, working long hours to support the family, died when James was 12 years old. He describes his
mother as ‘weak’ in that she was not able to discipline him or his younger siblings. James describes being ‘out of control’
in his adolescence, engaging in truancy from school, physical fights, lying about his age, binge drinking, illicit drug sale and
use. Despite this, he reports getting good grades and getting by on his ‘natural ability’. James briefly attended university,
but dropped out as he wanted to start his own business.
Since then, he has had numerous business ventures. He reports making money in the hospitality industry but
is vague when asked about his current financial situation. He reports being investigated by the tax office following
a recent audit of his businesses. In the session with the psychologist, he describes feeling unfairly treated by his
business partners over the years, which escalated into verbal aggression and physical assaults on a number of
occasions. When asked about these altercations, James shows little remorse and rationalises his actions by blaming
others. He is open and matter-of-fact about currently using drugs, and boasts about getting free drugs and entry into
nightclubs. He also boasts about having sexual relationships with many women, and hints that this has led to the
break-up of his recent relationship. He emphasises that his attendance at the clinic today was his ex-partner’s idea,
adding that he is considering getting back with her as he was living at her house rent-free and she was doing all of the
household chores. When asked why they broke up, he indicates that ‘she was being too needy’. James also exemplifies
some of the core features of the psychopathic personality (psychopathy), which is related to the concept of antisocial
personality disorder.
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UNDERSTANDING PSYCHOPATHY
Psychopathy is not listed as a disorder in the DSM-5 (APA, 2013) but is closely related to antisocial psychopathy
personality disorder. It is currently understood as a cluster of behaviours and personality traits that Set of personality
describe callous individuals who are aware of their antisocial behaviour but lack remorse. They traits including
superficial charm,
fail to accept responsibility for their actions and pride themselves on having the skill to avoid
a grandiose
capture by the authorities (Cleckley, 1982). Psychopathy was first described in the nineteenth sense of self-
century by the French psychiatrist Philippe Pinel (1745–1826), who used the term ‘madness worth, a tendency
without delirium’ to describe behaviour that was marked by remorselessness. Yet it was not until towards boredom
the twentieth-century contribution of Hervey Cleckley in his 1941 book The Mask of Sanity that and need for
the interpersonal, affective and behavioural features of psychopathy were described in detail. stimulation,
These features (as exemplified in the description of James in the case study) include a desire for pathological
dominance, manipulation, callousness and a lack of empathy and remorse. However, psychopathy lying, an ability
to deceive
is not restricted to individuals showing criminal or deviant behaviour; it can also be found in
others and be
seemingly socially well-adjusted and successful individuals. manipulative,
The DSM-5 criteria for antisocial personality disorder are mostly restricted to the description of and a lack of
criminal and socially deviant behaviour. The difference between antisocial personality disorder and remorse; similar
psychopathy is best illustrated by the pattern of scores on the Psychopathy Checklist-Revised (PCL-R; to antisocial
Hare, 1991). The PCL-R is a standardised, semi-structured interview that currently constitutes the most personality
widely accepted instrument for diagnosing psychopathy. The PCL-R comprises two factors: ‘emotional disorder but with
less emphasis on
detachment’ (which includes items that describe the core personality traits of psychopathy such as
behaviour.
callousness, manipulativeness and remorselessness) and ‘antisocial behaviour’ (which includes a history
of antisocial behaviour, impulsiveness and violence). A psychopath may score highly on both factors
of the PCL-R, but particularly in terms of the emotional detachment factor, whereas someone with
antisocial personality disorder may score highly on the antisocial behaviour factor alone. The diagnosis
of antisocial personality disorder can therefore be applied to the majority of the prison population, with
nearly 75 per cent of such individuals meeting the DSM-5 criteria for this disorder, while the prevalence
of psychopathy is much lower, namely about one-quarter of the 75 per cent of prison inmates with
dependent
antisocial personality disorder (Hare, 2006). Since the concept of psychopathy does not require a
personality
history of criminality, many of those with psychopathy would not have been included in this research.
disorder
Moreover, because many psychopaths are endowed with higher socioeconomic status, are socially
Pervasive need
skilled, and may possess high intelligence, they may not come to the attention of the authorities (unlike to be cared
those with antisocial personality disorder). Indeed, psychopaths may be part of the establishment, for and fear of
found in the legal system, business, politics, the military and academia (Blackburn, 2007; Millon & rejection, which
Davis, 1996). This group has escaped systematic attention by researchers and, as such, it is premature lead to total
to conclude that they are accurately identified through the criteria for antisocial personality disorder. dependence on
and submission
to others.
The Cluster C personality disorders avoidant
personality
Cluster C includes dependent, avoidant and obsessive-compulsive personality disorders. People with
disorder
dependent personality disorder have a strong need to be taken care of, including maintaining physical
Pervasive
closeness to others, needing others to do things and make decisions for them and help them initiate anxiety, sense
projects/tasks. They often experience intense anxiety when alone and are constantly fearful of being of inadequacy
abandoned or losing the support of others. Due to their fear of losing others, they engage in clingy and fear of
and self-sacrificing behaviours such as volunteering to do things that are unpleasant and avoiding being criticised
expressing any disagreement with others so as to maintain the relationship. that lead to
Individuals with avoidant personality disorder are preoccupied with and fearful of being negatively the avoidance
of most social
evaluated, criticised and rejected by others, tending to avoid social and intimate situations, particularly
interactions with
if they are not certain they will be liked. This behaviour arises from core beliefs of the self as others and to
inadequate, inferior, socially inept and unappealing. Hence, those with the disorder tend to engage in restraint and
solitary work roles and leisure activities and shun new activities in order to avoid criticism, disapproval nervousness in
or embarrassment, even if this means forgoing desired opportunities. social situations.
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obsessive- Individuals with obsessive-compulsive personality disorder are rigid, moralistic and perfectionistic
compulsive to the point where their preoccupation with minor details, rigidly abiding by the rules and getting
personality things perfect results in them losing the point of the activity at hand and interferes with their ability
disorder to complete tasks on time. They are rigid and stubborn and like things to be done their way. These
Pervasive rigidity individuals are often viewed as ‘workaholics’ because they have difficulty delegating tasks and have
in one’s activities
little time for leisure and social pursuits. They also tend to hoard worn-out or useless objects and are
and interpersonal
relationships; miserly with money, preferring to save it in case of a future catastrophe. Summary descriptions of each
includes personality disorder are presented in Table 13.2.
characteristics
such as emotional
TABLE 13.2 Summary of the 10 personality disorders contained in the DSM-5
constriction,
extreme
PERSONALITY DISORDER DESCRIPTION
perfectionism and
anxiety resulting 1 Paranoid A pattern of distrust and suspiciousness such that others’ motives are
from even slight interpreted as malevolent
disruptions to
one’s routine. 2 Schizoid A pattern of detachment from social relationships and a restricted range
of emotional expression
3 Schizotypal A pattern of acute discomfort in close relationships, cognitive or
perceptual distortions and eccentricities of behaviour
4 Antisocial A pattern of disregard for, and violation of, the rights of others.
5 Borderline A pattern of instability in interpersonal relationships, self-image and
affect, and marked impulsivity
6 Histrionic A pattern of excessive emotionality and attention-seeking
7 Narcissistic A pattern of grandiosity, need for admiration and lack of empathy
8 Avoidant A pattern of social inhibition, feelings of inadequacy and hypersensitivity
to negative evaluation
9 Dependent A pattern of submissive and clinging behaviour related to an excessive
need to be taken care of

10 Obsessive-compulsive A pattern of preoccupation with orderliness, perfectionism and control
CASE STUDY: OBSESSIVE-COMPULSIVE PERSONALITY DISORDER

The personal history of Dion, a 21-year-old economics and commerce student, exemplifies many of the features of
obsessive-compulsive personality disorder and some possible contributing factors. An international student studying in
Australia, Dion presents to the psychologist as well groomed, articulate and intelligent, though she does appear quite
controlled and guarded, with little warmth in her manner. An only child of high-achieving parents, she states that she was
raised to be ‘a perfectionist and workaholic just like them’. In her home country of Singapore, she said she experienced a
rigorous educational regimen from kindergarten onwards, with her parents’ high expectations made very clear to her. One
or both of her parents were often working overseas so that Dion had only the maid and nanny for company. She excelled in
her studies and ballet training, which she describes as her only outlet as a child. She notes she rarely has time for dance or
for socialising these days. Like her parents, she works long hours and takes few holidays, stating that she prefers to make
her time productive. She has mainly social media contact with a few school friends and with other international students
and says she does not mind this as she does not see the point of endless chatting. She does, though, report becoming
concerned about a recent increase in anxiety (manifesting as tension, tiredness and headaches) that coincides with the start
of her Honours year. She asks the psychologist for some strategies to manage her anxiety, adding that she does not want
‘to go too deep. The way I am gets results.’ Dion’s account of her history and current presentation raise important questions
about the intersection between genetic, family environmental and cultural factors in the development of personality.
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The dimensional approach to personality dysfunction

During the preparation of the DSM-5 there was widespread support for a dimensional model of
personality disorder to replace the use of distinct categories of personality disorders. The dimensional
approach maintains that the various personality characteristics exist on a continuum from low to high,
with those currently defined as having a ‘disorder’ occupying the extreme end of this continuum. This
alternative conceptualisation arose from challenges to the categorical approach. For instance, there is
a high level of comorbidity between personality disorders and other mental disorders, which can be
seen as supporting a dimensional approach (e.g., social phobia often occurs in those with avoidant
personality disorder such that social phobia might be a milder form of avoidant personality disorder)
(Hummelen, Wilberg, Pedersen, & Karterud, 2007).
However, during the preparation of the DSM-5, problems with the dimensional approach emerged,
including difficulty in reaching agreement as to which dimensional model should be used and concern
that dimensional models are too complex. This controversy resulted in the categorical approach being
retained in the main body of the DSM-5, while a proposed dimensional-categorical hybrid model was
placed in a section on ‘Emerging Measures and Models’ for further research.
The DSM-5 dimensional-categorical hybrid model begins with an overall rating of personality
in terms of the individual’s self and interpersonal functioning, ranging from ‘healthy, adaptive
functioning’ to ‘extreme impairment’. In the dimensional component, pathological personality is
assessed in terms of five broad domains (negative affectivity, detachment, antagonism, disinhibition
and psychoticism), which in turn comprise 25 traits. In the categorical component, six specific
personality disorders are identified, namely, schizotypal, borderline, antisocial, narcissistic, obsessive-
compulsive and avoidant. These proposed types differ from the existing DSM-5 personality disorders
which bear the same names in that they are partly defined by a subset of traits (e.g., antisocial
personality disorder is defined in part by traits from the antagonism and disinhibition domains). The
proposed model for the upcoming ICD-11 is likely to be based on a simplified dimensional model
(Tyrer, Reed, & Crawford, 2015).
What is the role of culture in the development

of personality disorders?
There is a growing body of evidence indicating that
culture contributes to the development of personality
disorders via gene–environment interactions,
supporting the expression or suppression of
biologically driven temperamental factors (Ryder,
Sunohara, & Kimayer, 2015). Cultural influences
result, first, in differences in the prevalence and types
of personality disorders between contemporary
societies across the world and, secondly, in changes
in personality disorders over time within a single
nation (i.e., the ‘cohort effect’).
PERSONALITY DISORDERS ACROSS

CULTURES
The limited available research has identified some
DAL
differences in the prevalence rates of personality

disorders across ethnic groups and cultures. Such Lower rates of antisocial personality disorder in certain cultures, such
results are often explained using the ‘ecological as those of Japan and Taiwan, may be because of the value those
niche’ model (Parker, 1997)—that is, the notion cultures place upon social cohesion, loyalty and mutual obligation
that certain personality styles (and even disorders) rather than individualism and antisocial behaviours.
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fit certain cultures or occupations, while others are not tolerated or are actively discouraged. For
example, it has been argued that the higher rates of antisocial personality disorder in Korea than
in Japan and Taiwan reflect the value Japanese and Taiwanese cultures place upon social cohesion,
loyalty and mutual obligation rather than individualism and antisocial behaviours (Paris, 1998). In
contrast, Western societies are more likely to reward individuality and a strong commitment to the
work ethic, and to place less importance on dependency. In fact, obsessive-compulsive personality
disorder demonstrated the highest prevalence of all personality disorders in a national epidemiological
study in Australia (Jackson & Burgess, 2004).
PERSONALITY DISORDERS WITHIN CULTURES OVER TIME

Research in the United States investigating personality disorders over time points to an increase in
the prevalence of antisocial personality disorder (Kessler, 1994) and borderline personality disorder
(Millon & Davis, 1996; Paris, 1998) since the middle of the last century. The increase in these
disorders has been explained in terms of a broader cultural de-emphasis on community, including
on families (with increased working lives possibly leading to less practical and emotional support
available for immediate and extended family) and on broader communities such as formal spiritual
communities. There is evidence, also, that narcissism may be increasing in prevalence in Western
countries, partly because individualistic work-oriented cultures may be increasingly valuing and
reinforcing grandiosity, both in the rise of social media, in popular culture (such as in song lyrics)
(De Wall, Pond, Campbell, & Twenge, 2011) and in parental responses to their children (Twenge &
Campbell, 2009). Twenge and Campbell made headlines in the media when, based on their research,
they linked certain parental behaviours to findings of increasing levels of narcissism in American
college students. These parental behaviours might include providing extravagant praise for actions that
do not accurately reflect the child’s own effort, ability or achievement or which might even include
inappropriate behaviours.
THE LABELLING EFFECT

Culture also influences whether particular behaviours or traits are seen as aberrant or not and may
influence how clinicians or researchers assess personality and personality disorders. It is suggested that
the ‘labelling effect’ makes it more likely that assessors will define behaviour as ‘disordered’ if it is
inconsistent with an individual’s culture of origin, and less likely to define a behaviour as pathological
if it seems consistent with that culture. Supporting this view, Castaneda and Franco (1985) found that
American interviewers misinterpreted symptoms such as histrionic behaviour, low control of emotion
and impulsivity in Latin American females as a result of cultural differences rather than reflecting a
disorder. As Paris (1998) states: ‘When personality profiles correspond to social expectations, certain
traits may not be considered pathological unless they seriously interfere with functioning’ (p. 289).
LO 13.3 The epidemiology of personality disorders

Large-scale epidemiological studies on the prevalence of personality disorders in the community
have provided varying estimates ranging from 4.4 to 21.9 per cent. Methodological shortcomings
are likely to have contributed to these inconsistent findings. Some studies have attempted to address
these methodological issues through the use of nationwide samples and semi-structured interviews to
better assess personality disorder. One methodologically sound Australian study reported a prevalence
rate of 6.5 per cent (Jackson & Burgess, 2004). A study of 10 different countries reported rates from
2.4 per cent (Western Europe) to 7.6 per cent (United States) (Huang et al., 2009; Tyrer et al., 2010).
In clinical settings, the prevalence of personality disorders increases dramatically to 25–40 per cent
(Grant et al., 2009; Newton-Howes et al., 2010).
Prevalence rates for each of the specific personality disorders across various countries are shown
in Table 13.3. In community samples, the prevalence of each of the specific personality disorders
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is around 1–2 per cent, with the exception being obsessive-compulsive personality disorder, which
has a prevalence figure of around 2–4 per cent. The prevalence of personality disorders can also
vary somewhat across the life cycle, with borderline personality disorder being highest (up to 3%) in
adolescents and young adults (Sharp & Fonogy, 2016).
Studies consistently report that people with borderline personality disorder have the highest level
of disability and the poorest levels of psychosocial functioning of all the personality disorders and that
those with obsessive-compulsive personality disorder have the least (Jackson & Burgess, 2004; Jovev
& Jackson, 2006; Skodol et al., 2002a; 2002b). Further, the functional disability noted in borderline
personality disorder has been found to persist for years, despite symptomatic improvement (Gunderson
et al., 2011; Zanarini, Frankenburg, Reich, & Fitzmaurice, 2010). Across studies, the disorder is found
in about 2 per cent of the general population, about 10 per cent in outpatient services, and up to
24 per cent in inpatient services (Newton-Howes et al., 2010). It is associated with psychiatric
comorbidity including depressive disorders, anxiety disorders and substance use disorders (Coid et
al., 2009; Grant et al., 2009; Quirk et al., 2014). Also, people with borderline personality disorder are
at significantly greater risk for self-harm and have a suicide rate of 8–10 per cent (Pompili, Girardi,
Ruberto, & Tatarelli, 2005). In Australia, those with the disorder have been found to be frequent users
of general health and mental health services, having the highest rates of consultations with general
practitioners, psychiatrists and psychologists compared to people with other personality disorders
(Jackson & Burgess, 2004).
TABLE 13.3 Prevalence (%) of personality disorders in community samples from Australia, the United States and Norway
OBSESSIVE-
PARANOID SCHIZOID SCHIZOTYPAL ANTISOCIAL BORDERLINE HISTRIONIC NARCISSISTIC AVOIDANT DEPENDENT COMPULSIVE
Australia
(1997)* 1.3 1.9 n/a n/a 1.0 0.5 n/a n/a 1 3.1
United
States
(1997)** 1.0 1.0 1.6 0.6 1.3 2.9 2.7 1.0 0.6 1.3
Norway
(2001)*** 2.4 1.7 0.7 0.7 0.7 2.0 0.8 5.0 1.5 2.0
*Jackson & Burgess (2000)

**Lenzenweger, Loranger, Korfine, & Neff (1997)
***Torgersen, Kringlen, & Cramer (2001)
Source: Adapted from Sansone, R.A., & Sansone, L.A. (2011). Personality disorders: A nation-based perspective on prevalence. Innovations in Clinical
Neuroscience, 8, 13–18.
LO 13.4 General models of the aetiology

and treatment of personality disorders
In this section, prominent models that contribute to an understanding of the nature, origin and
treatment of personality disorders are discussed. This will be followed by a consideration of current
theories and research in relation to the aetiology and treatment of each of the DSM-5 (APA, 2013)
personality disorders presented according to the Cluster A, B or C groupings.
The full range of available models regarding the aetiology and treatment of personality disorders
includes diverse theoretical orientations (e.g., psychodynamic and cognitive behavioural approaches) and
domains of interest (e.g., neurobiological, psychological and integrated biopsychosocial approaches).
Millon and Davis (1996) have pointed out that this diversity of explanations for personality dysfunction
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is not accidental but, rather, reflects the complexity of the aetiology and clinical presentation of
personality pathology. The majority of these models, however, have not been empirically tested.
Based on the available evidence, it seems that, in conjunction with a genetic predisposition,
it is the nature, timing and intensity of life events and influences that will result in some people
developing pathological personalities and others acquiring adaptive ones. Major environmental
factors broadly implicated in the aetiology of disordered personality include disrupted attachment
experiences with primary caregivers, and trauma, neglect and deprivation in childhood. It should
be emphasised, though, that the experience of significant childhood adversity is not specific to the
development of personality dysfunction but has been shown to be generally predictive of a wide
range of mental health problems in adulthood, such as depression, anxiety disorders, psychosis and
substance use disorders.
An illustration of the complex interaction between genetic and environmental influences comes from
researchers in New Zealand who are conducting an ongoing longitudinal study of over 1000 children
(Caspi et al., 2002). The study identified much higher levels of aggressive behaviour in maltreated
children with low activity of the monoamine oxidase A (MAOA) gene than in those with the same genetic
predisposition but little or no experience of childhood abuse or neglect. The MAOA gene metabolises
neurotransmitters, such as noradrenaline, serotonin and dopamine, which powerfully influence thoughts,
feelings and behaviours. Thus, it was the link between a certain genetic profile and adverse early life
experiences that explained the occurrence of aggressive behaviour in these 11-year-old children.
FACTOR APPROACHES
Factor approaches maintain that personality can be understood in terms of the degree to which an
individual manifests certain traits and combinations of traits. Personality disorders are believed to
comprise extremely high or low levels of these traits. The number and type of traits believed to capture
the full range of personality varies across the different factor approaches. Mention has already been
made of the highly influential five factor model (McCrae & Costa, 1984), which consists of neuroticism,
extroversion, openness, agreeableness, and conscientiousness. Four of these five (excluding openness)
have been found to characterise disordered personality, with the trait of openness to experience being
found to be unrelated to personality disturbance (Costa & Widiger, 2002).
The significant heritability of the core personality traits is firmly established, with estimates
of the degree to which various personality traits are inherited ranging from 40 to 60 per cent
(Livesley, 2008). In a seminal report, Livesley, Jang, Jackson, and Vernon (1998) presented findings
showing that the environment acts to influence the extent to which genetically based personality
predispositions are expressed as well as to shape the behaviours through which given traits are
epigenetic expressed. Epigenetic research suggests that experiences, such as sustained deprivation and trauma,
Related to might alter the genetic code of the sufferer and that the resulting changes to DNA are then transmitted
influences over subsequent generations (Livesley et al., 1998).
on gene
expression that BECK’S COGNITIVE MODEL
do not involve The key component in cognitive models of psychopathology is the presence of dysfunctional core
changes in DNA
beliefs that influence people’s understanding of themselves, others and the world (Beck & Freeman,
sequencing.
1990). The cognitive theory of personality disorders relies on two key premises. First, each personality
disorder is thought to be characterised by specific maladaptive core beliefs. Second, these beliefs
influence the processing of social information in such a way as to maintain the person’s dysfunctional
beliefs by filtering out inconsistent information and interpreting ambiguous information as consistent
with the dysfunctional belief.
Cognitive behaviour therapy (CBT) for personality disorders begins with the development
of a cognitive case formulation. The cognitive case formulation involves drawing together theory,
research and the client’s experiences in order to explain the causal and maintaining factors relating
to his/her problems (Persons, 2008). It is a collaborative endeavour between the therapist and client,
with both working together to describe the factors maintaining the client’s problems and develop a
treatment plan based on this shared understanding. Additional CBT interventions include cognitive
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restructuring (identifying and challenging dysfunctional cognitions that give rise to negative feelings
and behaviours) and supporting behavioural change (using strategies such as learning the skills of
problem solving to decrease unhelpful behaviours and increase adaptive solutions to problems).
However, while evidence suggests the effectiveness of CBT in working with other psychological
disorders, many of its assumptions are not readily met by people with a personality disorder. Some of
the key assumptions of standard short-term CBT that are not met in the case of personality disorders,
and therefore need to be altered for the treatment of personality disorders, are outlined in Table 13.4.
TABLE 13.4 Assumptions of short-term CBT that are often not met by individuals with personality disorders
ASSUMPTION REALITY
Patients are motivated to reduce symptoms, build skills and Motivation to change may be lacking in individuals with a
solve current problems. personality disorder due to factors such as seeing others
(rather than themselves) as in need of changing or lacking
confidence that they can successfully change.
Patients will comply with standard treatment approaches Many factors may make it difficult for those with a personality
(e.g., the need to practise skills between sessions in the form disorder to comply with standard treatment techniques (e.g.,
of homework tasks). their lives may be too chaotic to complete homework tasks).
Patients are able to identify their cognitions and emotions and Individuals with a personality disorder may be more likely to
report them to the therapist. block/avoid distressing thoughts and feelings so that they
cannot easily identify and report them.
Patients will readily engage in a collaborative relationship with Those with a personality disorder may be hostile or fearful
the therapist aimed at achieving the agreed goals of therapy. and avoidant or overly dependent in relationships, which
makes it difficult for them to establish a strong working
relationship with the therapist.
Patients will have problems that readily lend themselves to The problems of individuals with a personality disorder are
goal-focused treatment. more likely to be pervasive and diffuse, affecting broad areas
of their functioning, which makes it difficult to limit the focus

to any one problem area.
Patients will have the capacity to challenge cognitions that The rigidity that typifies all personality disorders likely extends
are unrealistic and/or unhelpful. to cognitive rigidity, making challenging these rigid beliefs
difficult, which can in turn leave people with the disorder
feeling invalidated and inadequate.
Source: Adapted from Young, J. E., Klosko, J. S., & Weishaar, M. E. (2003). Schema therapy: A practitioner’s guide. New York: Guilford Press.
YOUNG’S SCHEMA THERAPY MODEL

Jeffrey Young (Young, 1990; Young, Klosko, & Weishaar, 2003) has further developed cognitive
therapy for personality disorders by extending the construct of the schema beyond cognition schema
(i.e., negative beliefs about the self, others and the world) to also include emotions, behaviours and Cognitive
bodily sensations. In this approach, schemas refer to an organised collection of multidimensional framework
for organising
information in memory that, once established, operate automatically to influence information
information about
processing and responding. Young’s model identifies 18 schemas. He proposes that schemas develop the world.
early and so are named ‘early maladaptive schemas’, since they are believed to develop as a result
of a mixture of biological dispositions and repeated interpersonal distress with significant others in
childhood. Specifically, these early negative interactions result in a failure to meet the child’s core
emotional needs, which in turn results in the development of various early maladaptive schema
(depending on the nature of the unmet need). The various core emotional needs and the early
maladaptive schemas they give rise to if unmet are outlined in Table 13.5.
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TABLE 13.5 Core emotional needs of the child and the associated early maladaptive
schemas that can develop when these needs are unmet
CHILDHOOD NEED EARLY MALADAPTIVE SCHEMA
Secure attachment Abandonment/instability

with others ‘I worry that people I feel close to will leave me or abandon me.’
Mistrust/abuse
‘I feel that people will take advantage of me.’
Emotional deprivation
‘I haven’t someone to nurture me, share him/herself with me, or care
deeply about everything that happens to me.’
Defectiveness/unlovability
‘No one I desire would want to stay close to me if s/he knew the real me.’
Social isolation
‘I always feel on the outside of groups.’
To develop a sense of Dependence/incompetence

identity, competence and ‘I don’t feel confident about my ability to solve everyday problems that
independence come up.’
Vulnerability to harm or illness
‘I feel a disaster could strike at any minute.’
Enmeshment/underdeveloped self
‘I often feel I do not have a separate identity from my parents or partner.’
Failure to achieve
‘Most other people are more capable than I am in areas of work and
achievement.’
To express one’s desires Subjugation

and emotions ‘I have a lot of trouble demanding that my rights be respected and that
my feelings be taken into account.’
Self-sacrifice
‘Other people see me as doing too much for others and not enough for
myself.’
Approval-seeking/recognition-seeking
‘Accomplishments are most valuable to me if other people notice them.’
To have realistic limits set Entitlement/grandiosity

by others so as to learn ‘I feel that I shouldn’t have to follow the normal rules or conventions that
self-control other people do.’
Insufficient self-control/self-discipline
‘I can’t force myself to do things I don’t enjoy, even when I know it’s for
my own good.’
For spontaneity and play Negativity/pessimism

‘Even when things seem to be going well, I feel that it’s only temporary.’
Emotional inhibition
‘I find it embarrassing to express my feelings to others.’
Unrelenting standards/hypercriticalness
‘I must be the best at most of what I do; I can’t accept second best.’
Punitiveness
‘If I make a mistake, I deserve to be punished.’
Source: Adapted from Young, J. E., Klosko, J. S., & Weishaar, M. E. (2003). Schema therapy: A practitioner’s guide. New York: Guilford Press.
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The main characteristics of early maladaptive schemas are that they are rigid, resistant to change,
associated with high levels of affect, and significantly impair the functioning of the individual. While
not always consciously available, they may be triggered in day-to-day functioning by a range of
external events (e.g., seeing an ex-girlfriend) or by internal stimuli (e.g., ruminating about a failed
relationship in the middle of the night).
Although early maladaptive schemas develop in the context of aversive early childhood experiences,
these schemas are also maintained and even strengthened over time. In Young’s approach, this
tendency for schemas to be strengthened over time is referred to as schema perpetuation. One reason
schemas are perpetuated is that, in accordance with basic cognitive therapy tenets, they influence
information processing such that the individual selectively perceives and interprets information so as
to confirm maladaptive schemas and filters out disconfirming information.
In addition, Young proposes that schemas are perpetuated over time by the individual’s use of
certain schema coping styles. These coping styles, while making life more manageable in the short
term, serve ultimately to reinforce the schema. The coping style of ‘schema surrender’ refers to the
individual accepting the truth of the schema and behaving in consistent ways (e.g., choosing an
abusive partner in the case of someone with a mistrust/abuse schema). This prevents the individual
from having experiences that are inconsistent with the schema and would therefore challenge the
truth of the schema. The coping style of ‘schema avoidance’ involves blocking features of the schema
(such as the associated thoughts, images or feelings) through activities such as substance misuse
because of the distressing nature of the schema content. Schema avoidance might also entail the
individual avoiding situations that trigger the schema (e.g., avoiding relationships in someone with
an abandonment schema). The coping style of ‘schema overcompensation’ entails reacting against the
schema by embodying its polar opposite. For example, for someone with a defectiveness schema, an
example of overcompensation might include arrogance. Not only does this fail to allow the problem
to be recognised and addressed but it risks confirming the core schema because of its interpersonal
consequences of alienation and rejection by others.
There is some preliminary research showing that specific early maladaptive schemas are strongly
associated with specific personality disorders in both clinical and non-clinical populations. For
instance, the abandonment/instability schema is associated with borderline personality disorder, while
the unrelenting standards schema is associated with obsessive-compulsive personality disorder (Carr &
Francis, 2010; Jovev & Jackson, 2004).

schema therapy
Schema therapy includes an extensive assessment phase focused on identifying the patient’s early
Type of
maladaptive schemas and how s/he manages them (i.e., through schema surrender, avoidance and/or psychological
compensation). The next step involves the therapist educating the patient regarding the nature and type treatment
of his/her maladaptive schemas. The change process in schema therapy involves using behavioural, originally
cognitive and experiential techniques, with the aim of creating more adaptive schemas. The developed by
behavioural techniques aim to alter the coping styles used by the patient. For instance, a patient with an Jeffrey Young
emotional deprivation schema may be encouraged to identify and alter his/her use of schema surrender for the treatment
(e.g., choosing cold, unsupportive partners), schema avoidance (e.g., avoiding close relationships) or of personality
disorders; it
overcompensation (e.g., making excessive demands on others to meet his/her needs). One cognitive
focuses on
strategy involves having the patient test the validity of his/her schema by examining the evidence for helping clients
and against it. For instance, a patient with an emotional deprivation schema who sees evidence for change their
this schema in the fact that her husband comes home late from work may, after exploration, be able early maladaptive
to identify several ways in which her husband provides her with emotional connection and support schemas, that
(e.g., weekend trips away together). Experiential strategies aim to trigger the distressing emotions is, certain
associated with maladaptive schemas to encourage emotional change. In one experiential technique, psychological
themes (such
patients are required to write a letter (which may never be sent) to their parent or other significant
as emotional
people who hurt them in childhood, in which they express how they felt as a result of the person’s deprivation) that
behaviour and what they needed from the person then and now. developed during
Schema therapy is an intensive therapy, often expected to continue for five or more years, that has childhood or
been shown to be an effective treatment for borderline personality disorder (Jacob & Arntz, 2013). adolescence.
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It has a low dropout rate, is cost-effective and can be implemented in regular mental healthcare
settings where long-term psychotherapy is supported. Schema therapy was also found to be superior to
‘treatment as usual’ for paranoid, histrionic, narcissistic and cluster C personality disorders (Bamelis,
Evers, Spinhoven, & Arntz, 2014).
LINEHAN’S BIOSOCIAL MODEL AND DIALECTICAL BEHAVIOUR THERAPY

Marsha Linehan’s (1993) biosocial model was developed for borderline personality disorder, but
has also been applied to the treatment of antisocial behaviours, substance use disorders and eating
disorders. The model asserts that the disturbances of borderline personality disorder are primarily
due to dysfunction in the emotion-regulation system. This dysfunction is thought to be a result of the
interaction and cumulative effects over time of (1) a biologically based emotional vulnerability and
(2) negative experiences, hence the term ‘biosocial’.
The biologically based emotional vulnerability includes a temperament high in neuroticism,
increased baseline levels of emotional arousal, an increased intensity of responses to emotional
stimuli, and a slow return to baseline levels of arousal after having experienced emotional distress.
In addition to this biologically based emotional vulnerability, Linehan’s model emphasises the
contribution of what is referred to as ‘drastically invalidating environments’, in which the child may
experience deprivation, neglect and physical and emotional abuse. In such adverse and uncaring
circumstances, the child’s communication of his/her private experience is disregarded or rejected by
parents and caregivers. With the expression of feelings typically being ignored or punished, the child
is left with a limited capacity to identify and cope with his/her own feelings. In short, the features
of borderline personality disorder are seen to be a consequence of dysregulated emotions and the
dialectical maladaptive coping strategies aimed at modifying these painful emotions.
behaviour Linehan (1993) developed dialectical behaviour therapy on the basis of this model, which integrates
therapy (DBT)
biological, social, cognitive and behavioural theories with ideas from Zen Buddhism. ‘Dialectic’
Type of
psychological
refers to the integration of opposing elements in thinking and behaving. An example of a dialectic
treatment in dialectical behaviour therapy is the emphasis on helping the person to find a balance between
originally acceptance of self and the desire to change important aspects of his/her experience. Thus, a person
developed by with borderline personality disorder who typically responds to conflict in relationships by becoming
Marsha Linehan distressed and taking a drug overdose is encouraged to ‘sit with’ the pain (acceptance) and to learn
for borderline more effective strategies for coping with distress (change).
personality A Cochrane review reported that dialectical behaviour therapy is the most widely researched and
disorder;
combines
empirically validated treatment for borderline personality disorder (Stoffers et al., 2012). Treatment
cognitive- is structured to address dysregulation across five domains: that is, emotional, cognitive, behavioural,
behavioural and self and interpersonal (Linehan, 2012). Dialectical behaviour therapy includes weekly individual
Zen techniques therapy and group-based skills training, with some clients having access to after-hours telephone
in four modules coaching to assist their use of new skills. The initial focus is on developing the client’s engagement
including and commitment to treatment, with priority subsequently being given to the reduction of self-harm
mindfulness, and suicidality. Dialectical behaviour therapy views the client as a robust, resourceful individual and
interpersonal
the therapist style is active, matter-of-fact, warm and strongly focused on validation of the client’s
effectiveness,
distress tolerance experience in therapy. Clients are encouraged to use newly gained skills, self-knowledge and therapist
and emotion support to actively solve problems and learn new ways of being in the world.
regulation. In the group sessions, clients receive training in four areas: mindfulness, distress tolerance,
interpersonal effectiveness and emotion-regulation skills. Mindfulness skills are derived from
Cochrane
reviews
elements of Eastern Zen meditation and include the notions of:
Systematic
reviews of ∙ acceptance and taking a non-judgmental stance towards oneself, people and situations
research in ∙ observing rather than needing to immediately act to alter situations such as negative feelings
human healthcare ∙ being in the moment (rather than being overwhelmed by distress related to past experiences or
and policy. future possibilities).
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Distress-tolerance skills are based on the tenet that pain and distress are part and parcel of everyday
life and that one’s unwillingness to accept this in itself causes pain. The skills taught are four-fold:
∙ engaging in activities that compare oneself to those less fortunate
∙ comforting oneself using vision, hearing, smell, taste and touch (e.g., painting one’s nails, listening
to music, lighting a scented candle, baking a cake or having a bubble bath)
∙ improving the moment (e.g., through positive imagery, prayer or relaxation)
∙ being aware of the positive aspects of tolerating distress (e.g., providing an opportunity to become
emotionally stronger) despite its negative aspects (e.g., short-term emotional pain).
The skills of interpersonal effectiveness
include learning how to initiate and maintain good
relationships and learning assertiveness skills.
Finally, emotion regulation skills include learning
ways to identify emotions, reduce vulnerability to
negative emotions, increase positive emotions and
let go of emotional suffering.
COGNITIVE ANALYTIC THERAPY

Cognitive analytic therapy brings together concepts
from cognitive psychology with understandings
from object relations (which developed from
psychoanalytic theory) and other approaches, into
an integrated and effective therapy (Ryle & Kerr,
2002). The model was not specifically developed
DAL
for use with personality disorders and as such
Interpersonal effectiveness involves learning how to initiate and
it has been applied more broadly. However, it maintain good relationships.
has increasingly been seen as a useful model for
personality disorder because it is a time-limited and engaging approach and has a specific model cognitive
explaining the range of problems that are seen in borderline and other personality disorders. analytic therapy
Cognitive analytic therapy takes a collaborative approach, in which an understanding of the Type of
person’s thoughts, behaviours and actions is developed jointly by the therapist and patient, in order psychological
treatment
to shape and guide the therapy. It is also fundamentally a relational model, in which internalised developed by
early relational experiences (derived primarily from interactions with caregivers) are understood Anthony Ryle
to shape later relationships with others as well as the way that people relate to themselves. The that combines
aim in cognitive analytic therapy is to encourage patients to identify and reflect on their relational concepts from
patterns and the ways in which these are enacted with others and towards themselves in a manner cognitive and
that exacerbates and maintains their problems, in order to allow these patterns to be revised and more psychoanalytic
adaptive patterns to be learnt. therapies.
During normal development, children experience their parents as nurturing and, through the process
of internalising these relational experiences as they grow, they learn how to nurture and care for others,
as well as soothe and care for themselves. Conversely, personality disturbance results from a complex
interaction between inherited neurobiological factors and early traumatic or neglectful experiences
that are internalised and lead to the formation of maladaptive patterns of relating to others and the self
(Ryle, 2004). These internalised dyadic relational patterns are called ‘reciprocal roles’. For example,
children who have experienced neglecting and abusive early interactions with carers will internalise
both their own experiences of being ‘victimised’ as well as their carers’ experiences of being ‘abusing’.
These children have internalised both the ‘victim’ and ‘abuser’ roles, and have the capacity to enact
either (or both) in their relationships with others and with themselves. As children grow, they are likely
to find themselves in similar types of relationships with others who abuse and neglect them or who
allow them to be neglecting and abusive. They might also find themselves enacting the role of abuser
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(and therefore victim) towards themselves, perhaps internally via critical thoughts or externally via
physical self-injury. Most people are unaware of the extent to which they are repeating their automatic
early relational experiences, and even when they are aware, do not know how to change them.
Further development led to the multiple self states model (Ryle, 1997), which proposes that there
are three features responsible for the range of problems experienced by individuals with borderline
personality disorder:
1. dissociation between the different aspects of the self (which can cause sudden switching from one
self state to another)
2. a limited repertoire of reciprocal roles, consisting of internalised harsh, punitive or abusing
reciprocal roles
3. a deficient capacity for self-reflection.
This model posits that those with a severe personality disorder are likely to have experienced harsh
and punitive early relational patterns (e.g., abusing/neglecting) that lead the individual to dissociate
and cut off from some aspects of the self (e.g., the part that is enacting the abuser) in order to
cope and survive. These harsh relational patterns (reciprocal roles) are internalised, and then shape
the individual’s interpersonal relationships with others and themselves, resulting in a reliance on self-
damaging and self-defeating patterns of thinking, feeling and behaving, such as using substances and
harming oneself. The lack of an internalised ‘good enough’ experience of care makes it difficult for
those with a personality disorder to form appropriate caring relationships with others and to enact self-
caring patterns. This in turn can lead to poor health, difficulties with vocational and social functioning,
greater need for health care and reliance on welfare. Cognitive analytic therapy has been demonstrated
to produce better outcomes compared to those receiving treatment as usual in adults with a range of
personality disorders (Clarke, Thomas, & James, 2013). Interestingly, many of those receiving the
treatment as usual got worse over the nine months of the trial. Cognitive analytic therapy has also been
demonstrated to be effective and improve outcomes for younger individuals aged 15–18 years with
borderline personality disorder features (Chanen et al., 2008a; 2009).
In conducting cognitive analytic therapy, the therapist takes a collaborative, curious and respectful
stance, in which the patient is seen as ‘doing the best that he/she can do’. The therapy contract is
usually brief, typically up to 24 sessions for complex problems such as personality disorder (Ryle &
Kerr, 2002). The early sessions are focused on the therapist and patient developing a collaborative
shared understanding (the reformulation) of the patient’s history and the problems that have brought
the patient to therapy. This is formulated in terms of the dysfunctional reciprocal role procedures
(relationship patterns and enactments) and seeks to link current difficulties with earlier experiences.
The therapist aims to develop a genuine, compassionate relationship with the patient that models
‘good enough’ care. Letters and diagrams describing the reformulation assist the therapist and patient
to agree on the goals of therapy, to monitor progress during therapy, and to use the therapist–patient
relationship to explore new relationship patterns and to avoid enacting unhelpful patterns. The last
few sessions are spent actively working towards ending treatment. In the final session, the therapist
and patient exchange letters in which they summarise their experience of the therapy process, the
achievements the patient has made and the work still ahead for the patient. The cognitive analytic
therapy case study below highlights how the reformulation outlined in the letter and diagram are used
to help the patient recognise and revise maladaptive patterns.
CASE STUDY: COGNITIVE ANALYTIC THERAPY

Sophia, a 22-year-old student, was diagnosed with borderline personality disorder and referred for treatment. She and her
therapist agreed to have 24 sessions of cognitive analytic therapy with four follow-up appointments over the subsequent
six months. The first three sessions involved a collaborative discussion of her history and presenting problems in order
to develop a shared understanding of the relationship and behavioural patterns causing her most difficulty. These
became the basis of the reformulation letter that Sophia’s therapist read out to her in her fourth session. The aim of the
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reformulation letter is to present the patient’s history in such a way that he/she can feel validated and understood by
the therapist, and can start to make sense of the interpersonal patterns that are having a negative impact on his/her life.
The therapist is careful to use the patient’s descriptions of important events and to suggest possible links or ideas in a
tentative way in order to facilitate collaboration and to model how to take a non-judgmental and self-reflective stance.
The following reformulation letter was read out to Sophia:
Dear Sophia,
I am writing this letter to try and summarise what we have been talking about over the past few weeks. Please
let me know if we need to change any details, in order for it be more accurate.
You decided to come to therapy after ending up in hospital just before your final exams. We have understood
that taking that overdose was your way of getting everything to stop and let you have some time out to think. I hope
that our conversations have also been moments to think and reflect and make sense of things.
Your early memories were not happy ones and you feel very angry towards those who harmed you or didn’t
protect you adequately. You have always felt you received second best and that your brother was favoured by your
parents, particularly your father. This was very hurtful and when you were about 10, you made the decision to cut
your father out of your life. Although your mother was around more often, you felt she ignored and even neglected
your needs. Even though you know that she had her own difficulties and probably struggled to cope with life, it left
you with a hole inside that mostly feels empty and numb. You still see your mother but have managed the feeling of
being let down by becoming cold and by telling yourself you no longer care about her. We have talked about how
this is an understandable attempt to protect yourself, but I wonder whether you continue to feel hurt inside and dis-
connected from those around you? Perhaps this was the start of you beginning to believe that bad things are always
your fault and that you deserve punishment?
As you progressed through school, it seems you were able to find people outside your family to support and
encourage you. You did well and started to feel more confident in your own abilities and to develop a sense of self-
worth. Unfortunately, at 16 when your teacher Ms T left on maternity leave, you again felt hurt and rejected. It seems
like this was the start of a particularly difficult time for you. You engaged desperately in a number of relationships
with boys that seemed to be attempts to fill the void you felt inside. As these didn’t last long, they reinforced to you
that you are ‘unlovable’ and deserve rejection and punishment. The more you felt alone and uncared for, the more
desperately you sought out someone to ‘perfectly care’ for you. Even now, the distress associated with these feel-
ings is so intense that it leads to you holding on tightly to those who show some care, lest they disappear again. You
become more and more anxious and clingy with people important to you and this then sometimes actually drives
them away. We have been able to notice that you have felt so stuck in this pattern over the past few years that you
have felt the only way out has been to consider suicide.
Sophia, we have begun to talk about how these patterns have emerged and how you might find some alternate
ways of managing. We will need to keep our eye on how you are feeling in therapy with me, especially as we get
closer to finishing up. Our aim will be to help you experience a ‘good enough’ ending. This will not be easy, as we
already know you are likely to feel rejected and abandoned by me. Nevertheless, as we have started to do already,
I hope we can talk about these moments when we notice them and find some way through this together.
We will also need to keep our expectations realistic, as I expect that things will not be perfectly sorted out by the
time we finish up. Rather than try for this, perhaps our aim can be to find a way for you to continue to work on these
issues into the future.
We have already made a good start with therapy and I can see you have been working hard to give this a go.
You identified two goals quite quickly:
• to get your studies back on track
• to manage stress better so you don’t need to harm yourself.
I would like to suggest another goal:
• to learn how to care for yourself better.
I am looking forward to hearing what you think of this third goal and to discussing this letter with you.
Regards,
(Therapist)
continued
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After her therapist read the letter out loud to her, Sophia reported feeling validated and understood. Over the next
few sessions, she and her therapist developed a diagram or ‘map’ of these interpersonal themes that continued to
cause her difficulty (see Figure 13.1).
Remember
to OBSERVE Realistic
Rejecting & without soothing &
punishing (a) caring
judgment
F Confident
TO
Hurt & alone (b)
S OU SS & content
Y E
Feel worse WA HE M
T
Overwhelming Escape into

feelings fantasy
(hope for
Punish myself perfect
(cut, overdose) care)
Desperate &
humiliated
It never lasts
Punish Disappointed
others Enraged
FIGURE 13.1 The diagram used in cognitive analytic therapy for Sophia to summarise her problematic interpersonal patterns
Initially, the discussion centred on Sophia’s early experiences of feeling rejected and punished by her parents
and other relatives (a). In response to this, she could identify often feeling alone and hurt (b). Sophia became quickly
overwhelmed in the face of behaviour from others that indicated any hint of rejection or punishing behaviour. From
this overwhelmed state, she had developed several different procedural patterns. Her earliest responses had been to
try to please others (especially teachers and then boyfriends), in the hope that they would respond with kindness and
care. Sophia was able to recognise that what she was really hoping for was an idealised ‘perfect care’ from them. She
sometimes felt this worked for a time, but it always ended in disappointment, with her becoming desperate, humiliated
and clingy, and left her ultimately distressed and back in the original state feeling hurt and alone (b). Alternatively, on
feeling rejected and overwhelmed, she would become enraged and want to punish others. Sophia described a period
in which she would become angry and abusive towards others (particularly family members) and occasions when she
had physically assaulted her mother and brother. This pattern had become less prominent from her mid adolescence,
when she began to feel more desperate and humiliated and she began to punish herself by self-cutting. This strategy
had increasingly been enacted over the past few years and was now also becoming a quick way to force others to care
for her. Although she felt guilty for doing this, she also found that it was effective. This was a difficult topic for Sophia to
talk about, as she was very sensitive to ideas of blame.
An important aspect of this work was developing some capacity for self-reflection. She was initially unable to talk
about her own actions, thoughts and behaviours without feeling at fault. The therapist was able to use the diagram to
demonstrate how to stand back and observe one’s own interpersonal patterns from some distance and helped Sophia
to gradually build up her tolerance and understanding of this in a manageable way. This work led to the discussion of
alternative relationship patterns. The therapist and Sophia discussed their own relationship and what she found helpful
from the therapist. Sophia learned to assess how realistic her expectations of care were, and to practise asking for care
in a clear and reasonable manner. She began to consider the idea that she might be able to meet some of her needs
for care herself.
By the end of therapy, Sophia had ceased self-harming, was no longer depressed and her anxiety had
significantly reduced. She had mixed feelings about completing therapy—on one hand feeling excited about
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trying things more on her own, but also feeling some sadness and loss. She accepted some non-mental health
supports in the form of sharing her needs with some close friends and a tutor. She had a small relapse when she
engaged in some minor deliberate self-harm in the month after her final session, before her first follow-up session.
She stated at her follow-up that she had also partly felt curious about whether this would cause a complete
relapse or whether she was strong enough to keep moving forward. Sophia went on to complete her studies and
at the final follow-up had begun a relationship with a boy that she felt was more respectful and supportive than
past relationships.
MENTALISATION-BASED TREATMENT
Mentalisation-based treatment is another integrative therapy based on object relations theory and
Bowlby’s (1983) attachment theory, first developed to treat borderline personality disorder. This form
of treatment emphasises the role of mentalisation in the development of a person’s sense of self and mentalisation
his/her functioning in relationships. Mentalisation refers to the capacity to think about one’s own Capacity to think
mental state and the mental states of others (such as the other person’s desires, feelings and beliefs) about one’s own
mental state and
(Bateman & Fonagy, 2004).
the mental states
Within the context of safe and secure child–carer relationships, the capacity to mentalise begins of others.
during the first 2–3 years, and is facilitated through the processes of mirroring and marking. Mirroring
is said to occur when the child experiences the carer responding to the child; this is experienced by
the child as evidence of the self as an entity (me) and as characteristically good or bad. In the process
of marking, the carer interprets the child’s state and alters it, for example, with the aim of soothing the
child. The child takes in the reflected marked state and is soothed, and in the process has an implicit
experience of what was in the mind of the carer. However, in the absence of good enough mirroring,
the child internalises the carer’s marked state (e.g., fear, rage or hatred) and an image of the self as
frightening or unmanageable. To achieve a bearable and coherent sense of self, this painful image
is externalised as an ‘alien self’ (as bad, punitive or hostile). Thus, the self-harm and aggression
towards others seen in borderline personality disorder are explained in this model as efforts to destroy
the ‘alien self’.
Mentalisation-based treatment aims to use the therapeutic relationship as a means of stabilising
the person’s sense of self and to enhance his/her capacity to know his/her own mind and that of
others. The treatment encompasses weekly sessions of individual and group therapy. Using a here-
and-now approach, the therapist attempts to maintain a mentalising stance, paying strict attention
to reflecting on the experiences and perceptions of the client. The treatment relies on clear, simple
dialogue as the client and therapist together work through experiences occurring in the session itself
as well as in the client’s day-to-day life. The therapist seeks to assist the client over time to develop
the capacity to make use of mentalisation to better understand his/her own self and others’ emotions,
needs and intentions.
Findings from two randomised controlled trials provide support for the efficacy of mentalisation-
based treatment for borderline personality disorder. In the first trial, people with borderline personality
disorder attending individual and group therapy sessions in a day hospital setting showed decreased
self-harm and suicidality, and improved mood and social functioning after treatment (Bateman &
Fonagy, 2009). These findings were supported by those from a second trial conducted in a community
setting (Bateman, O’Connell, Lorenzini, Gardner, & Fonagy, 2016).
Can the impact of personality disorders be reduced through

early-intervention programs?
Despite longstanding agreement that personality disorders have their roots in childhood and
adolescence (APA, 1980), there is continued reluctance to make these diagnoses in individuals
younger than 18 (Koehne, Hamilton, Sands, & Humphries, 2012). For instance, borderline personality
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disorder is highly stigmatised by professionals as well as by patients themselves (‘self stigma’) and
this provides an obstacle to applying this diagnosis in young people (due to the concern that such
a diagnosis may result in the affected individual being stigmatised) (Aviram, Brodsky, & Stanley,
2006). However, recent guidelines and reviews of the evidence indicate that this is no longer justified
and that the diagnosis of borderline personality disorder in young people is as valid and reliable as
it is in adults (National Collaborating Centre for Mental Health, 2009; National Health and Medical
Research Council, 2013; Paris, 2013).
There is a strong rationale for early intervention for personality disorders. For instance, in the case
of borderline personality disorder, one justification for early intervention is the fact that the disorder
is most prevalent during adolescence and early adulthood. Indeed, as the prevalence of borderline
personality disorder rises after puberty and peaks in early adulthood, declining steadily every decade
after this, it could be argued that it is actually a disorder of younger people (Samuels et al., 2002;
Ullrich & Coid, 2009). Another reason for early intervention is that young people with borderline
personality pathology have particularly poor functioning and longer-term outcomes. That is, having
borderline features in adolescence is uniquely associated with a range of current difficulties, which
include poor general functioning and problems in peer relationships, self-care and family functioning
(Chanen, Jovev, & Jackson, 2007). This disorder also predicts future problems such as increased risk
of other mental disorders, distress, interpersonal problems and reduced quality of life for up to two
decades (Crawford et al., 2008; Winograd, Cohen, & Chen, 2008). In addition, it has been argued that
the period of adolescence is one in which personality features are more malleable and therefore it may
be the optimal time to intervene so as to produce the greatest change (Lenzenweger & Castro, 2005).
In summary, given the greatest prevalence of borderline personality disorder during adolescence and
early adulthood, the high level of distress and dysfunction associated with the disorder, the fact that
it predicts later problems and that the adolescent period offers greater malleability, many have argued
for the disorder’s early identification so that it can be treated and potential problems stemming from
the disorder can be minimised or averted.
Prevention and early-intervention programs for borderline personality disorder aim to promote more
adaptive developmental pathways, to reduce psychopathology and to improve general functioning,
rather than being narrowly focused on the reduction of borderline symptoms given that these naturally
decrease over time (Chanen & McCutcheon, 2013). Given the evidence that even subthreshold
personality disorder features are associated with poorer functioning and outcomes in adulthood, it
is important that early-intervention programs for borderline personality disorder also include young
people with subthreshold forms of the disorder. Two early-intervention programs indicate that such
programs are viable and that even briefer, good-quality treatments can achieve favourable outcomes
for adolescents (Chanen et al., 2009; Schuppert et al., 2009). Both dialectical behaviour therapy and
mentalisation-based therapy have also been adapted for young people with good results (Mehlum et
al., 2014; Rossouw & Fonogy, 2012), indicating that it is likely a range of treatments will prove to
be effective for adolescents and young adults with personality disorders. With increasing support for
the principles of earlier diagnosis and intervention (National Collaborating Centre for Mental Health,
2009; Paris, 2013), there is a clear need for further investigation to understand which approaches can
be most effective.
LO 13.5 The aetiology and treatment of specific

personality disorders
AETIOLOGY OF THE CLUSTER A PERSONALITY DISORDERS: SCHIZOID,
SCHIZOTYPAL AND PARANOID PERSONALITY DISORDERS
There is longstanding acknowledgement of the association between the Cluster A personality
disorders and schizophrenia. Early models of schizophrenia held that it arose out of a personality type
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characterised primarily by aloofness and a lack of interest in connection with others. Labelled variously
as ‘shut in’ (Hoch, 1910) and ‘schizoidie’ (Bleuler, 1924), this personality subtype was codified as
schizoid personality disorder in the DSM. Subsequent research supported Meehl’s (1989) more complex
concept of schizotypy, incorporating a number of psychosis-like features, leading to the inclusion of
schizotypal personality disorder as a distinct category in the DSM and ICD classification systems.
Empirical research has confirmed a common genetic contribution for the Cluster A personality
disorders and schizophrenia. Research has identified genetically based neurological abnormalities
that, together with certain environmental or gene–environment inputs (e.g., low birth weight, low
childhood socioeconomic status and childhood institutionalisation), will predispose the individual to
developing a personality with odd, eccentric or psychotic features and, in extreme cases, schizophrenia
(Lahti et al., 2009; Yang, Ulrich, Roberts, & Coid, 2007).
Findings from various domains (familial, neuropsychological and biological) support the view that
schizotypal personality disorder represents a milder form of schizophrenia. Familial studies have shown
that schizotypal personality disorder is the most prevalent disorder found among the biological relatives
of individuals with schizophrenia (Kendler, Myers, Torgersen, Neale, & Reichborn-Kjennerud, 2007).
In neuropsychological research, individuals with schizotypal personality disorder show similar types
of memory deficits and difficulties in sustaining attention as people with schizophrenia (Woods et al.,
2009). Finally, biological research has found that individuals with this personality disorder have some
of the same anomalies in brain structure and neurophysiology, including the tendency to have higher
levels of the neurotransmitter dopamine, as those with schizophrenia (Siever & Davis, 2004). Genetic
links are also evident between schizophrenia and paranoid personality disorder, but there is only a
small increase in the frequency of schizoid personality disorder found in the relatives of people with
schizophrenia (Maier, Lichtermann, Minges, & Heun, 1994).
TREATMENT OF THE CLUSTER A PERSONALITY DISORDERS: SCHIZOID,

SCHIZOTYPAL AND PARANOID PERSONALITY DISORDERS
There are very few treatment studies on the Cluster A personality disorders. Individuals with these
disorders may be indifferent to interpersonal interactions and find intimacy aversive or they may be
suspicious of others (including therapists) and, hence, rarely present for treatment. As such, they tend
to present for treatment only when they are in crisis and experiencing marked anxiety, depression
or psychotic symptoms. Such crises may be precipitated by stressful life events (e.g., the loss of
employment) and/or the onset of another mental disorder. Additionally, those with these disorders,
particularly schizoid and schizotypal personality disorders, may be so socially and culturally
marginalised due to their difficulties that it is very difficult for them to access treatment (Connolly,
Cobb-Richardson, & Ball, 2008).
Once in treatment, the intimacy and mistrust issues of these patients often make it difficult for
them to develop a strong working relationship with the therapist. Nevertheless, cognitive-behavioural
techniques can be effectively utilised to address therapy goals, including the enhancement of self-
awareness, social skills and general quality of life (e.g., the development of additional hobbies
and interests, ideally with a social component) (Millon & Grossman, 2007). Interventions such
as keeping a record of thoughts and mood on a daily basis can improve the patient’s capacity to
identify or clarify his/her thoughts and feelings. To augment the patient’s existing repertoire of
social behaviours, an educational approach on the part of the therapist is recommended, given
the difficulty these patients have in developing a strong sense of collaboration and closeness in
working with the therapist. For example, in teaching the patient social skills, the therapist can model
the requisite skill, use role playing so that the patient can practise the skill with the therapist, and antipsychotic
medications
videotape the patient in social interactions so that s/he can use this feedback to improve skills.
Drugs used to
Exposure therapy, in which the patient successively enters a series of increasingly difficult social treat psychotic
situations, may also be helpful. symptoms such
Pharmacotherapy is likely to be a useful treatment alone or in combination with psychological as delusions and
treatment. Low doses of antipsychotic medications, including risperidone, olanzapine and clozapine, hallucinations.
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may be useful to treat psychotic symptoms (Millon & Grossman, 2007). For those with concurrent
selective depressive and anxiety symptoms, the addition of selective serotonin reuptake inhibitors (SSRIs)
serotonin antidepressant medications (such as fluoxetine) and low doses of anxiolytic (anxiety-reducing)
reuptake medications (such as alprazolam or diazepam) are recommended (Millon & Grossman, 2007).
inhibitors (SSRIs) However, one study found that patients with a higher number of schizoid traits were less likely to
Class of respond to pharmacological treatment of depression (Mulder, Joyce, Frampton, Luty, & Sullivan,
antidepressant
2006), indicating some limitations in the use of medication in this population.
drugs (such
as fluoxetine)
AETIOLOGY OF THE CLUSTER B PERSONALITY DISORDERS: ANTISOCIAL
that inhibit the
reuptake of PERSONALITY DISORDER
serotonin. Of the Cluster B personality disorders, the literature on antisocial and borderline personality disorders
is considerably greater than on either histrionic or narcissistic personality disorder, or indeed any
other personality disorder. The focus on borderline personality disorder stems from the fact that it is
the most common personality disorder in clinical practice, is considered challenging to work with by
clinicians and is associated with the most reduced psychosocial functioning and high personal costs
(e.g., suicidal behaviours). The high social costs (e.g., criminal behaviour) are likely to have played a
part in motivating research into the causes and treatment of antisocial personality disorder.
Beginning with the biological factors associated with antisocial personality disorder, family, twin
adoption study and adoption studies have confirmed that traits of this disorder, along with substance use disorders
Study of the and criminal activities, are more common in the relatives of those with antisocial personality disorder,
heritability of thus suggesting a genetic contribution. The nature of the genetic vulnerability for the disorder might
a disorder by
be an inherited predisposition to high levels of impulsivity (i.e., the tendency to respond impetuously
finding adopted
people with a
without thinking about negative consequences). Robust research findings confirm a strong association
disorder and then between antisocial personality disorder and the personality trait of impassivity, which is known to
determining the have a significant genetic contribution (Livesley, 2008). The genetic vulnerability might also entail a
prevalence of the form of neurotransmitter or hormonal disturbance (Yildirim & Derksen, 2013). For instance, findings
disorder among from animal and human studies point to an association between lower levels of the neurotransmitter
their biological serotonin and both impulsivity and aggressive behaviour, which is a combination seen in antisocial
and adoptive individuals. Research also suggests that a higher level of the hormone testosterone is associated with
relatives in order
increased aggressive and violent behaviour in adults (Raine, 2002).
to separate
contributing Other studies examining biological risk factors have examined the role of arousal and fearlessness
genetic in antisocial behaviour. Low levels of physiological arousal, as assessed by measures such as skin
factors from conductance and resting heart rate, are strongly associated with antisocial personality disorder.
environmental Abnormally low arousal means that the individual will experience much less fear than others and may
factors. therefore be more willing to engage in risky behaviours (Raine, 1997). Alternatively, under-arousal
testosterone leaves the individual in an ongoing state of discomfort, encouraging risky and extreme behaviours as
Main hormone a way of increasing arousal (Eysenck, 1994).
produced by the There is also some evidence of abnormalities in the frontal and pre-frontal areas of the brain in
testes. individuals with antisocial personality disorder (Glenn, Johnson, & Raine, 2013), although it is not
clear whether these are genetic in origin or due to environmental factors. It is hypothesised that these
brain abnormalities in part account for the cognitive deficits noted in many people with the disorder.
Specifically, pre-frontal regions of the brain are associated with executive functioning abilities so that
dysfunction in this area results in difficulties with impulse control, planning, problem solving and
goal-setting.
Despite the importance of a unique genetic contribution, the more challenging issue concerns
the interaction between genetic and environmental factors in predisposing individuals to antisocial
behaviour. This is best illustrated by a study of 95 male and 102 female adoptees, with at least one
biological parent with antisocial personality. The study showed that parental antisocial personality
predicted increased aggression and conduct disorders in the offspring, thus providing evidence for
genetic processes. But in addition to this, an adverse adoptive home environment was found to interact
with the antisocial personality of the biological parent in predicting increased aggression in the
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offspring, that is, there was a gene–environment interaction (Cadoret, Yates, Troughton, Woodworth,
& Stewart, 1995).
Biological factors other than genetic influences may also interact with environmental factors to
produce antisocial behaviours. Of these, the most often replicated effect involves birth complications
such as anoxia (lack of oxygen) and forceps delivery interacting with negative home environments
(e.g., maternal separation, marital discord, parental mental health problems and paternal absence)
in predisposing offspring to adult violence; there is also evidence that this effect particularly
characterises life-long persistent rather than adolescence-specific antisocial behaviour (Raine, 2002).
Thus, birth complications may not by themselves predispose a person to crime but instead may require
the presence of negative environmental circumstances to trigger antisocial behaviour.
Research into the nature and origins of psychopathy, an overlapping but distinct construct to
antisocial personality disorder, highlights how neurobiology influences antisocial behaviour. The
somatic marker hypothesis by Damasio (1994) and the violence inhibition mechanism model by Blair
(1995) are the two main theories proposed to explain psychopathy.
The somatic marker hypothesis proposes a mechanism by which emotional processes can guide
(or bias) decision making. It is proposed that individuals form associations between emotions and
behaviour during their experience of the environment. These associations are stored as somatic markers,
possibly in the ventromedial prefrontal cortex. When these or similar situations are encountered again,
the somatic marker associations are re-experienced physiologically and bias cognitive processing to
direct attention away from the negative options. For instance, if we leave a pot on the stove and get
burnt when we try to remove it, we not only create a cognitive representation of the pot but also the
bodily experience of fear in response to getting burnt (i.e., we create a somatic marker). Next time we
are faced with a choice of picking up a pot with our bare hands, we access the information that helps us
identify the object as a pot and the internal bodily information of the emotion of fear that is associated
with that object. Anticipation of a bad outcome before the bad choice is made prevents the bad choice
(e.g., getting burnt) and leads, instead, to a better choice (e.g., using an oven mitt to pick up the pot). The
disturbance of this somatic marker system leads to an insensitivity to potentially negative consequences
due to problems in accessing knowledge of associations between emotions and behaviour.
A major source of evidence for this theory comes from experiments using the Iowa gambling
task—a psychological task thought to simulate real-life decision making. In the Iowa gambling task,
a participant is asked to gamble a hypothetical sum of money in order to finish with more money
at the end of the task. In each trial, the participant has a choice of four different options that offer
different probabilities of gains and losses. Two of the four options provide occasional large gains,
but these gains are offset by frequent or large losses. The other two options provide smaller gains
but less frequent or smaller losses. Optimal decision making during the task requires that a person
avoid occasional large gains in order to secure more frequent small gains that are more profitable in
the long run. Studies employing the Iowa gambling task have found that individuals scoring high on
psychopathy demonstrate gambling behaviour similar to patients with lesions of the orbitofrontal cortex orbitofrontal
by continually selecting the options that provide occasional, large, short-term gains but ultimately lead cortex
to long-term losses (Bechara, Tranel, & Damasio, 2000; van Honk, Hermans, Putman, Montagne, & Part of the
Schutter, 2002). In other words, they continue to make bad choices based on short-term consequences, cortex that lies
next to the
because they have no emotional biasing signals that steer them away from the negative options.
cavity containing
The violence inhibition mechanism model put forward by Blair (1995) assumes that a violence the eye.
inhibition mechanism is activated whenever distress cues (e.g., fearful or sad facial features) are
present to inhibit aggressive behaviour. Blair (1995) has suggested that psychopaths lack a functional
violence inhibition mechanism, due perhaps to dysfunction in the amygdala as this is the brain structure amygdala
involved in the processing of distress cues. The violence inhibition mechanism model is supported by Part of the brain’s
research showing selective impairment in the processing of information relating to fear that prevents limbic system
that is thought
psychopaths from experiencing fear themselves and from recognising fear in the facial expressions of
to regulate
others. This is despite being capable of experiencing and recognising other emotions, such as happiness emotions.
(Lorenz & Newman, 2002). For example, a participant with a psychopathic personality in a research
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study said that he did not really understand what others meant by ‘fear’ (Hare, 1993). However, ‘When
I rob a bank,’ he said, ‘I notice that the teller shakes or becomes tongue tied. One barfed all over the
money. She must have been pretty messed up inside, but I don’t know why. If someone pointed a gun
at me I guess I’d be afraid, but I wouldn’t throw up.’ When asked to describe how he would feel in
such a situation, his reply contained no reference to bodily sensations. He said things such as, ‘I’d give
you the money’, ‘I’d think of ways to get the drop on you’ or ‘I’d try and get my arse out of there’.
When asked how he would feel, not what he would think or do, he seemed perplexed. Asked if he ever
felt his heart pound or his stomach churn, he replied, ‘Of course! I’m not a robot. I really get pumped
up when I have sex or when I get into a fight.’
Research into the underlying aspects of antisocial personality disorder and the related construct of
psychopathy raises important questions. For instance, given research indicating that such behaviours
have biological and environmental determinants, to what degree should individuals with psychopathic
traits and antisocial personality disorder be seen as responsible for their actions? In addition, is there
any potential role for neuroscience (e.g., brain scanning of known offenders) in crime prevention?
These issues will no doubt continue to be a focus of vigorous debate (Adams, 2013; Fox, Kvaran, &
Fontaine, 2013).
TREATMENT OF THE CLUSTER B PERSONALITY DISORDERS: ANTISOCIAL

PERSONALITY DISORDER
Few individuals seek treatment specifically for antisocial personality disorder and many service
providers are reluctant to attempt to treat these individuals. Those who seek help often do so for other
problems, such as marital discord, substance use disorders or suicidal thoughts. Family members or the
courts may send people with antisocial personality disorder for assessment and treatment. Beck and
Freeman (1990) noted that the development of a truly collaborative therapeutic relationship between
the patient and therapist might not be possible. Individuals with antisocial personality disorder often
have poor insight and may reject the diagnosis or deny their symptoms or attribute the problems
that they are experiencing to the actions of others. It is important to also acknowledge the patient’s
capacity to misuse therapy. For example, people with antisocial personality disorder might misuse
therapy by lying to the therapist or by trying to manipulate the therapist into writing a favourable court
report asserting mitigating circumstances for their crimes. They might also attempt to directly threaten
the therapist with violence. The treatment environment should therefore take safety considerations
into account. In addition to difficulty establishing a therapeutic alliance, individuals with antisocial
personality disorder often have poor compliance with treatment and the presence of co-occurring
psychopathology (e.g., substance use) is likely to further hinder treatment progress.
It is therefore not surprising that there is a lack of high-quality clinical trials on the treatment of
antisocial personality disorder. The National Institute for Clinical Excellence (NICE, 2009; 2013)
guidelines for antisocial personality disorder emphasise prevention and intervention at an early age,
where the treatment is focused on conduct disorder or the related diagnosis of oppositional defiant
disorder. There is a limited body of evidence regarding treatment of adult antisocial personality
disorder. The majority of treatment is focused on comorbid disorders (e.g., substance use) and risk
management. No single treatment approach has been found to have demonstrated effectiveness for
antisocial personality disorder (Davidson et al., 2008), although mixed results have been reported for
social skills a range of interventions targeting specific symptoms, such as behaviour therapy incorporating social
training skills training and anger management (Cooke, 1997; Hare, Clark, Grann, & Thornton, 2000; Kraus &
Behavioural Reynolds, 2001).
technique that Treatments successfully used for other personality disorders are now being trialled for antisocial
aims to help
personality disorder. One such form of treatment is mentalisation-based treatment (Bateman &
clients with
problems in Fonagy, 2006). While originally developed for individuals with borderline personality disorder,
interacting and preliminary evidence suggests that this treatment may be effective in reducing self-reported aggressive
communicating behaviour in individuals with antisocial personality disorder with moderate levels of psychopathic
with others. traits (McGauley, Yakeley, Williams, & Bateman, 2011).
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Pharmacological treatment using lithium and antipsychotic medication has been utilised to
help manage impulsive and aggressive behaviours. There is some debate about the value of SSRI
antidepressants to treat symptoms such as irritability and hostility in this group of patients (Millon &
Grossman, 2007).
AETIOLOGY OF THE CLUSTER B PERSONALITY DISORDERS:

BORDERLINE PERSONALITY DISORDER
Similar to antisocial personality disorder, a complex array of biological and psychosocial factors has
been suggested to explain the aetiology of borderline personality disorder. Because so many risk factors
are involved, the causal pathways for this disorder are thought to vary considerably for each individual.
Of the possible biological contributors, genetic findings are limited, so the relative importance
of genetic factors remains unclear. The first methodologically sound twin study based on DSM twin study
criteria found concordance rates for borderline personality disorder of 35 per cent and 7 per cent Study of the
in monozygotic and dizygotic twin pairs respectively, thus supporting a genetic contribution to the heritability of
a disorder by
disorder (Torgersen et al., 2000). Borderline personality disorder features evident between the ages
comparing
of 14 and 24 years may be more heritable than those evident at other ages (Bornovalova, Hicks, concordance
Iacono, & McGue, 2009). Also suggestive of a genetic link is the fact that borderline personality rates for the
disorder is associated with a family history of psychological disturbance (Zanarini et al., 1997). Other disorder between
research suggests abnormalities in the serotonin neurotransmitter system that have been associated monozygotic and
with problems with impulse control (Heinz et al., 2005; Paris, 2005). dizygotic twins.
The genetic vulnerability for borderline personality disorder includes the trait dimension of concordance rate
neuroticism (Livesley, 2008). The component facets of neuroticism in the five factor model include Probability that
anxiety, self-consciousness, vulnerability, impulsivity, hostility and depression. These facets of both members
neuroticism are closely related to two of the major behavioural dimensions of borderline personality of a twin pair will
disorder, that is, emotional dysregulation and impulsivity. However, neuroticism has been found to develop the same
underpin most personality disorders, thereby indicating that it does not aid in determining the specific disorder.
pathway to borderline personality disorder. Determining the precise causes of borderline personality
disorder as opposed to other disorders is also not achieved by combining multiple personality traits.
For instance, Morey and colleagues (2002) point out that a five factor model profile including high
neuroticism, low agreeableness and high conscientiousness characterises schizotypal, avoidant and
obsessive-compulsive personality disorders, as well as borderline personality disorder.

The core elements of the psychopathology of borderline personality disorder—for instance,
impulsivity, emotional instability and impulsive aggression—have been linked to neurobiological
impairments, such as pre-frontal deficits, leading to a failure to control negative emotions (top-down
process) and heightened activity in the limbic system leading to disordered emotional behaviour
(bottom-up process) (Le Doux, 1992). Studies of adolescent patients with borderline personality
disorder have demonstrated that there may be a weakening of the pre-frontal inhibitory control system
(Stoffers, Zanarini, Schmahl, Linehan, & Bohus, 2004), which may be implicated in the high incidence
of impulsive behaviours, including suicide and self-harm, evident in this population.
Similar to the biological factors, psychosocial factors such as the experience of childhood trauma,
while strongly associated with borderline personality disorder, are predictive of a range of DSM-5
mental disorders (e.g., eating disorders, posttraumatic stress disorder, depression and substance use
disorders) (Battle et al., 2004). Of the various forms of childhood trauma, the occurrence of sexual
abuse is particularly linked with borderline personality disorder (Battle et al., 2004). In addition to the
type of abuse, the severity of the abuse is also important, with research demonstrating a link between
a greater severity of abuse and more severe borderline personality symptoms (Zanarini et al., 2002).
However, research has also found that the impact of abuse can be reduced in environments where
families function well (Infurna et al., 2016). Therefore, it appears that abuse is neither a necessary nor
sufficient determinant of borderline personality disorder.
In addition to abuse, it has also been suggested that inconsistent, neglectful or perhaps overly
intensive parenting lead to individuals developing insecure attachment styles that, in extreme cases,
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manifest as the maladaptive interpersonal behaviours seen in those with borderline personality
disorder (Bateman & Fonagy, 2004). However, these patterns are not reported by all individuals with
borderline personality disorder, indicating that there are likely to be a number of different pathways
leading to the development of this disorder.
A complex interaction between biological and psychosocial factors is likely to be important in the
aetiology of borderline personality disorder. For example, the enduring effects of the experience of
trauma in childhood can be understood to be partly due to the detrimental impact of such experiences
hypothalamic- on the structure and functioning of the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus
pituitary-adrenal and pituitary gland form the central part of the HPA axis. During prolonged stress, these glands produce
(HPA) axis hormones that are responsible for the production of adrenaline while also increasing cortisol production.
Three Cortisol is responsible for protecting the body from the effects of stress (e.g., tissue inflammation and
components damage). Excess cortisol, however, suppresses the immune system and increases the risk of infections
of the
and allergies. In addition to weakening the immune system, long-term exposure to cortisol is associated
neuroendocrine
system that work with damage to cells in the hippocampus, resulting in impaired learning. It may be that prolonged
together in a activation of the HPA axis for those experiencing acute stress actually leads to under-responsiveness,
feedback system whereby the HPA axis feedback loop compensates by switching off the stress response and thus
interconnected preventing the negative effects of continually high levels of stress hormones. This theory would explain
with the brain’s the inconsistency of results that exists between studies that have examined the HPA axis response in
limbic system and adults and in younger people with borderline personality disorder (Chanen & Kaess, 2012). Adults with
cerebral cortex.
borderline personality disorder have demonstrated suppressed or delayed cortisol responses (indicating
cortisol an under-responsive HPA axis) when shown stressful images (Carrasco et al., 2007), while young
Hormone patients who are earlier in the course of borderline personality disorder have a more normal cortisol
produced by the stress response (indicating a more active HPA axis) when shown stressful images (Jovev et al., 2008).
adrenal cortex
that helps the
body respond TREATMENT OF THE CLUSTER B PERSONALITY DISORDERS: BORDERLINE
to stressors, PERSONALITY DISORDER
inducing the fight Individuals with borderline personality disorder often seek help. The finding that one in five outpatients
or flight response. has borderline personality disorder indicates that it is common in clinical practice (Zimmerman,
Chelminsky, & Young, 2008). Clinicians can find these patients particularly challenging to treat
because of the interpersonal difficulties, unstable mood (lability), impulsivity and tendency of
individuals with the disorder to engage in risk-taking behaviours, particularly recurrent patterns of
self-harm (such as suicidal acts and self-cutting).
Borderline personality disorder is a very expensive psychiatric disorder (costing society a similar
amount as schizophrenia), with costs including treatment in emergency departments, psychiatric
inpatient hospitals and primary care, plus social welfare, unemployment and disability support
payments (van Asselt, Dirksen, Arntz, & Severens, 2007).
Unfortunately, this patient group also endures significant
stigma and discrimination, and is often treated by healthcare
professionals as though less deserving of care and attention
than those with other severe mental disorders (Avrim et al.,
2006; Chartonas, Kyratsous, Dracass, Lee & Bhui, 2017) .
DR P. MARAZZI/SPL/PHOTOLIBRARY
While still modest compared to other mental disorders,

the research base into the treatment of borderline personality
disorder is more extensive than for any other personality
disorder. With around 30 randomised controlled trials of
treatment for borderline personality disorder, there is clearly a
wide range of specialised treatments, all of which show modest
positive results without any evidence for one form of therapy
being clearly superior over others (Bateman, Gunderson, &
Self-harm in the form of superficial cutting is commonly Mulder, 2015; Stoffers et al., 2012). In addition, most
seen in individuals with borderline personality disorder. treatments have been shown to reduce serious risk-taking and
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other behavioural features (e.g., self-harm and suicidal behaviour, substance abuse, anger outbursts and
misuse of services). However, there is still little evidence that treatment can change the core aspects of
the disorder, particularly impaired interpersonal relationships and identity problems, which appear to
be the most difficult to change. Therefore, even if some of the extreme behaviours have settled and the
diagnosis of borderline personality disorder no longer applies, many individuals continue to experience
miserable and difficult lives, and to have poor social and vocational functioning (Bateman et al., 2015).
Over the years there have been a number of reviews of the evidence for the treatment of
borderline personality disorder. The Cochrane group have recently published a systematic review
of psychological therapies (Stoffers et al., 2012) and another on pharmacotherapy for the disorder
(Stoffers et al., 2010). Their conclusions were that psychological interventions should be the first
line of treatment for borderline personality disorder, and that there was little evidence supporting the
use of pharmacotherapy for the disorder itself, although there was evidence for the use of medication
for co-occurring problems individuals might be experiencing (such as the use of antidepressants to
treat major depressive episodes). These findings have been incorporated into the Australian Clinical
Practice Guideline for the Management of Borderline Personality Disorder (National Health and
Medical Research Council, 2013).
The range of psychotherapies that have been investigated using a randomised controlled design, the
strictest form of evaluating treatments, is very broad. Psychodynamic treatments include transference-
focused psychotherapy (Clarkin, Yoemans, & Kernberg, 2006) and mentalisation-based therapy
(Bateman & Fonagy, 2009). Cognitive behaviour therapy (Davidson et al., 2006) and dialectical
behavioural therapy (Linehan, 1993) are at the other end of the continuum, being more behavioural,
with a range of treatments falling somewhere in between, including schema therapy (Young, 1990)
and integrative models such as cognitive analytic therapy (Ryle, 1997). Although the studies varied
significantly in terms of the sample sizes, methods used and the outcomes examined, all of these
specialised treatments have demonstrated significant improvements when compared to treatment as
usual (Bateman, Gunderson, & Mulder, 2015).
While this might seem cause for optimism, most of the specialised treatments developed for
borderline personality disorder tend to be long term (one to four years) and often comprise a range
of different modalities such as individual therapy, group therapy, family work, psychiatric care and
psychosocial interventions. Thus, such programs are very costly and can take only a small number of
patients, resulting in long waiting lists (often several years long). Therefore the majority of patients
are not able to access these treatments, even if they want to. This has led to a call to develop simpler,
briefer interventions, with a greater emphasis on psychosocial functioning (Bateman, Gunderson, &
Mulder, 2015; Chanen, 2015).
There is also a small but growing literature supporting early intervention for borderline personality
disorder (Chanen et al., 2008a; Chanen et al., 2009; Mehlum et al., 2014; Rossouw & Fonogy, 2012).
These studies also demonstrated that the adult forms of cognitive analytic therapy, dialectical behaviour
therapy and mentalisation-based therapy can be modified for younger patients and shortened.
AETIOLOGY OF THE CLUSTER B PERSONALITY DISORDERS: NARCISSISTIC

There are limited empirical data regarding the origins of narcissistic personality disorder, so
theoretical accounts remain largely speculative. These accounts locate the aetiology of the disorder
in the early developmental period, generally conceptualising it as a consequence of non-empathic,
invalidating and/or inconsistent early childhood experiences (Millon & Grossman, 2007). It is
theorised that the child’s needs for nurturance and affection were not met, with the result that the
fulfilment of these needs is played out in the adult arena. The major contributors to understanding
the causes of this disorder have been psychoanalytic theorists (Kernberg, 1975; Kohut, 1972).
For instance, Kernberg’s (1975) model emphasises the role of cold caregivers displaying either
indifference or aggression towards the child. Kohut (1971; 1977) proposed that non-empathic
responses from caretakers in infancy and childhood lead to the use of narcissism to avoid feelings
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of inadequacy. From a cognitive perspective, Stone (1993) also highlights the role that neglectful
parenting might play in the development of narcissism, suggesting that compensatory beliefs about
personal superiority can arise when a child is exposed to parental indifference. Some authors have
noted a distinction between grandiose narcissism (characterised by self-centeredness, an inflated
self-confidence, a sense of one’s specialness and entitlement, limited capacity for empathy towards
others and a willingness to take advantage of others) and vulnerable narcissism (involving an
external presentation of low self-esteem and anxiety, together with an inner core of inflated self-
beliefs and expectations) (Horton, Bleau, & Drwecki, 2006). These authors have suggested that
permissive caregiving influences the development of the former, while cold, over-controlled
caregiving influences the latter. Despite their theoretical appeal, these aetiological models, with
their emphasis on early child–parent relationships, remain untested. Moreover, these models often
focus on narcissism as a personality dimension in healthy individuals rather than focusing on those
with narcissistic personality disorder specifically.
Livesley, Jang, Jackson, and Vernon (1993) reported that narcissistic personality disorder has the
highest heritability of any personality disorder, a result given further support from a methodologically
sound twin study (Kendler et al., 2008). This genetic contribution may entail an inherited temperament,
with the five factor model profile of high extroversion and low agreeableness being linked to narcissistic
tendencies. However, Morf and Rhodewalt (2001) point out that not all ‘disagreeable extroverts’ are
people with high levels of narcissism.
TREATMENT OF THE CLUSTER B PERSONALITY DISORDERS: NARCISSISTIC

Individuals with narcissistic personality disorder tend to seek treatment only when they are depressed
or experiencing high levels of distress related to relationship difficulties (indeed, prevalence
rates of narcissistic personality disorder may appear lower than they in fact are, as people with
narcissistic features may deny traits that seem to them to be socially undesirable). Middle age may
be a particularly challenging time for those with narcissistic features as they increasingly realise their
grandiose fantasies are unlikely to be realised over the course of their lifetime (a process referred to
as ‘corrective disillusionment’ by Ronningstam and colleagues, 1995). Similar to individuals with
antisocial personality disorder, those with narcissistic personality disorder may consider changing
their interpersonal behaviour only if they are sure of the likely benefits to themselves, rather than being
concerned about the negative impact their behaviour has on others (Benjamin, 1996). Otherwise, they
are generally unlikely to seek treatment voluntarily, tending to believe they do not need treatment and
to see other people as the cause of their problems (again similar to those with antisocial personality
disorder). This lack of insight (into their own personal failings and the effect of their behaviour on
others), together with poor motivation for change (because this would imply that they have a problem),
difficulties incorporating feedback from others, a superior attitude and limited capacity for empathy,
constitute obstacles to seeking treatment and engaging in an effective therapeutic relationship.
A final challenge relates to the almost entirely absent research base on treatment for narcissistic
personality disorder. On a theoretical level, Beck and Freeman (1990) note that the goals for cognitive
therapy with such individuals might include adjustment of grandiose views of the self, better management
of emotional responses to rejection or negative evaluation from others, improving awareness of the
needs and feelings of others and a reduction of exploitative behaviour. However, the effectiveness of
cognitive therapy for people with narcissistic personality disorder has not been investigated.
AETIOLOGY OF THE CLUSTER B PERSONALITY DISORDERS: HISTRIONIC

Approaches regarding the aetiology of histrionic personality disorder closely resemble those for
narcissistic personality disorder. As with narcissistic personality disorder, in the absence of almost
any empirical evidence, aetiological accounts of histrionic personality disorder come predominantly
from psychoanalytic theorists drawing on clinical experience. These models tend to emphasise the
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role of inconsistent, intense and non-empathic parent–child interactions. As a consequence of these

unmet needs for care and attention, it is suggested that the child engages in increasingly dramatic
attempts to be seen and noticed. Alternatively, particularly intense or overwhelming relationships
with parents may leave children feeling as though ‘normal’ relatedness is insufficient, so that they
engage in significant attempts to experience the same early intensity of relationship in adulthood
(Wexler, 1991). Whereas dependent personality disorder is described by Millon and Davis (1996) as
‘passive-dependent’, histrionic personality disorder is described as ‘active-dependent’. That is, people
with histrionic personality disorder go out of their way to attract others to them, using seduction,
attention-seeking and their natural gregariousness. They need this attention in order to feel good
about themselves. Although this may suggest a level of extroversion (which may in part be genetically
determined) (Widiger & Costa, 1994), there is limited empirical support for a genetic basis in histrionic
personality disorder, apart from one study suggesting a higher prevalence of Cluster B personality
disorders among the relatives of individuals with histrionic personality disorder (Dahl, 1993).
TREATMENT OF THE CLUSTER B PERSONALITY DISORDERS: HISTRIONIC
As with narcissistic personality disorder, there is a dearth of empirical findings regarding the
treatment of histrionic personality disorder. Given their dependency issues, individuals with histrionic
personality disorder may be more likely to seek help and become engaged in ongoing therapy than
those with either antisocial or narcissistic personality disorder.
Particular issues to be aware of in treating individuals with histrionic personality disorder include
awareness that people with this condition may present with a range of vague anxiety, depressive and
somatic symptoms that are secondary to their personality disorder. Such symptoms typically arise
following failure or disappointment related to unrealistic expectations of the self and others. As such,
these symptoms are unlikely to respond to treatment in the absence of a focus on their histrionic basis
(Millon, 1996). Another clinical challenge is that the therapeutic relationship can be complicated by
the interpersonal features typical of this disorder, particularly seductiveness, both physical (including
sexualising the therapeutic relationship) and psychological (through ‘presenting’ symptoms to
stimulate interest from the clinician rather than as a genuine reflection of the individual’s difficulties)
(Kraus & Reynolds, 2001).
Cognitive therapy has been suggested as helpful in assisting the identification and challenging of
assumptions about dependency on others (Beck & Freeman, 1990). In the following dialogue between
a therapist and a patient with histrionic personality disorder, the therapist helps the patient to become
aware of her intense difficulty with being alone and how this fear drives her seductive behaviours:
Therapist: So you felt that things were going pretty well with this man at the party?
Patient: Yes, I felt we were getting along really well but then this other woman came along and
he went off and talked to her. He never returned.
Therapist: So how did you feel?
Patient: Devastated!
Therapist: And what happened then?
Patient: I had to call a taxi and go home . . . alone.
Therapist: How did you feel about that?
Patient: Hopeless. I got all dressed up. I went to all this trouble to look my best.
Therapist: I know from what you’ve told me that this has happened before. You go to these parties
and you usually go home with someone and occasionally you don’t.
Patient: Yes.
Therapist: But even when you do take someone home, what happens?
Patient: Well then they just seem to want to have sex but not much else.
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Therapist: And how do you feel afterwards?

Sometimes I feel really flat for days. I feel worthless and so alone and I hate feeling
Patient:
alone!
Okay. So let’s start to look at why it is so bad being alone. This seems to be a very
Therapist:
common experience for you.
AETIOLOGY OF THE CLUSTER C PERSONALITY DISORDERS: AVOIDANT

The personality disorders making up the third cluster (i.e., avoidant, dependent and obsessive-
compulsive personality disorder) are characterised by a predominantly anxious presentation,
underpinned by high levels of the five factor model traits of neuroticism and introversion (low
extroversion). For each of these personality disorders, aetiological and treatment data are limited.
In terms of avoidant personality disorder, Kendler and colleagues (2008) presented evidence for a
family study modest genetic contribution. Family studies indicate a relatively higher incidence of the disorder in the
Study of the first-degree relatives of people with avoidant personality disorder (Johnson et al., 1995). The available
heritability of a evidence points to the role of temperament in the genetic transmission of this disorder. For example, a
disorder involving
study found that 2-year-old children who had high levels of restraint (i.e., a tendency to withdraw and
identifying people
with a particular
avoid social contact) or spontaneity (i.e., a tendency to engage and interact with others) in unfamiliar
disorder and situations demonstrated the same characteristics five years later (Kagan, Rennick, & Snidman, 1987).
people without Millon and Davis (1996) propose that the turning away from others, seen in those with the disorder,
the disorder might have its beginning in the very early developmental period as a response to the pain associated
and then with cold, rejecting and scornful responses from caregivers. In turn, such patterns of social withdrawal
determining elicit negative reactions from others (e.g., teasing and rejection) that are thought to strengthen over
the disorder’s time. Consistent with a role of adverse early experiences, Lobbestael, Arntz, and Bernstein (2010)
frequency within
found a relationship between avoidant personality disorder and the experience of sexual and emotional
each person’s
family. abuse in children. The finding of a significant association between the report of childhood neglect
and avoidant personality disorder in several studies provides further evidence for this view (Cohen,
Crawford, Johnson, & Kasen, 2005; Joyce et al., 2003).
Cognitive models also relate avoidant tendencies to early rejection experiences in the family, which
are seen to contribute to the development of beliefs about the self as inherently deficient, worthless
and unlovable (Beck & Freeman, 1990). This view was supported by a Melbourne-based study of
early maladaptive schemas in people with DSM-defined personality disorders (Jovev & Jackson,
2004). In this study, avoidant personality disorder was linked to schemas relating to defectiveness and
abandonment. Some have suggested that avoidant personality disorder is an extreme manifestation
of social anxiety (Tillfors, Furmark, Ekselius, & Fredrikson, 2004; van Velzen, Emmelkamp, &
Scholing, 2000). In support of this link between the two disorders, most people with social anxiety
(63%) report avoidant traits, while a smaller proportion of those with avoidant personality disorder
achieve a diagnosis of social phobia (48%) (Hummelen, Wilberg, Pedersen, & Karterud, 2007).
Thus, aetiological accounts of social phobia may be relevant for understanding the development and
maintenance of avoidant personality disorder.
TREATMENT OF THE CLUSTER C PERSONALITY DISORDERS: AVOIDANT

Individuals with Cluster C personality disorders, including avoidant personality disorder, tend to be
more likely than those with other personality disorders to seek treatment, often for comorbid disorders
meta-analysis such as depression and anxiety. As such, pharmacological interventions for Cluster C patients typically
Statistical
technique for
involve antidepressant and anxiolytic medications.
summarising Although relatively few studies have investigated the effectiveness of various psychological
results across interventions, the results are encouraging (Weinbrecht, Schulze, Boettcher & Renneberg, 2016).
several studies. A meta-analysis of treatment studies (Bartak et al., 2010) showed that Cluster C patients in all
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treatment conditions (including CBT, interpersonal social skills training and psychodynamic
therapies) made significant gains compared to controls (Karterud et al., 2003; Pretzer, 2004; Strauss et
al., 2006; Stravynski, Marks, & Yule, 1982; Witold, 2009). Importantly, improvement continued after
completion of treatment regardless of treatment type or personality disorder diagnosis.
Focusing specifically on avoidant personality disorder, these patients have been found to benefit
from a range of behavioural techniques aimed at countering social avoidance, including in vivo (real-
life rather than imaginal) exposure to feared social situations and training in assertiveness and other
social skills (Stravynski et al., 1994). In a randomised controlled trial, Emmelkamp and colleagues
(2006) compared brief dynamic and cognitive behaviour therapies for individuals with avoidant
personality disorder. In this study, 62 patients with avoidant personality disorder were randomly
assigned to 20 weekly sessions of CBT or brief dynamic therapy or to a wait-list control condition.
Results indicated that patients in the CBT group showed significantly more improvements at
post-treatment and at follow-up. This suggests that CBT may be the more effective treatment for
avoidant personality disorder, with the results of brief psychodynamic therapy not being significantly
different from those obtained by the wait-list control group.
AETIOLOGY OF THE CLUSTER C PERSONALITY DISORDERS: DEPENDENT separation

PERSONALITY DISORDER anxiety disorder
Disorder of
The fact that it is reasonably common to find a number of members of the same family exhibiting
childhood
dependent personality disorder or suffering from related problems (including separation anxiety characterised
disorder) suggests there may be a genetic predisposition or vulnerability to the development of this by abnormal
personality disorder (Dahl, 1993; Mroczkowski et al., 2016). This genetic vulnerability may entail fear or worry
certain temperamental factors, as suggested by the five factor model account of dependent personality over becoming
disorder as an extreme variant of neuroticism and low extroversion (Costa & Widiger, 2002). separated
Evidence of a psychosocial contribution comes from research linking official records of early from one’s
physical abuse and dependent personality disorder in adulthood (Cohen et al., 2005). In the relative caregivers as
well as clinging
absence of empirical data, cognitive theorists have speculated that dependent personality disorder
behaviour in
is an attachment-based disorder, with early experiences encouraging in the child the view that the the presence of
world is an unsafe place and that s/he is essentially caregivers.
incompetent and unlikely to survive without the
direct involvement of significant others (Beck &

Freeman, 1990). The child then opts to give up
responsibility for the self and to subordinate his/her
own needs and desires to others in order to ensure
that s/he will be taken care of. This view is supported
by evidence showing significant associations
between the dependency schema, as assessed by the
Young Schema Questionnaire (Young & Brown,
1994), and the experience of emotional and sexual
abuse in childhood (Lumley & Harkness, 2007).
TREATMENT OF THE CLUSTER C

PERSONALITY DISORDERS:
DEPENDENT PERSONALITY DISORDER
The available data for dependent personality
disorder is even more limited than for the other
Cluster C disorders (Witold, 2009), though the
DAL
results from schema therapy and dialectical

behaviour therapy trials show promise (Arntz, Genetic predisposition to the development of dependent personality
2012; Haro, Palacios, Moliner, Guillen, & Botella, disorder is suggested by more frequent occurrences of the disorder
2013). As part of a cognitive-behavioural approach, among family members.
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behavioural strategies for anxiety management have been used, along with graded homework tasks
aimed at gradually increasing independent and assertive behaviours (Karterud et al., 2003). Cognitive
techniques are used to challenge dysfunctional beliefs related to personal incompetence and extreme
reliance on others (Renner et al., 2013). Unlike those with other personality disorders, people with
dependent personality disorder may be very willing to engage in therapy, which may be a challenge in
itself. Given that patients with dependent personality disorder commonly hold dysfunctional beliefs
regarding the need to be taken care of by others, it is important for therapists working with such
patients to encourage independence and minimise any tendency for the patient to become overly
dependent on the therapist for emotional support and advice (Millon & Davis, 1996; Millon, Davis,
Millon, Escovar, & Meagher, 2000). For example, a patient with dependent personality disorder may
report the following dysfunctional thinking:
I really want to go out to my team dinner to farewell Tara. But Sarah won’t be there and I don’t
feel safe without her there. I will say I am going but I can call in sick on the day.
Through cognitive restructuring, in which the patient is encouraged to evaluate the evidence for
and against this belief, the patient is helped to develop the following realistic thoughts:
I can do this. I want to be part of things. I have gone out by myself and it went okay—after a while
I had a good time. I am going to give this a shot.
AETIOLOGY OF THE CLUSTER C PERSONALITY DISORDERS:

OBSESSIVE-COMPULSIVE PERSONALITY DISORDER
The limited evidence from twin studies suggests a moderate genetic contribution to the development
heritability of obsessive-compulsive personality disorder, with a heritability estimate of .78 (Kendler et al.,
Percentage 2008; Torgersen, Kringlen, & Cramer, 2001). Research based on the five factor model suggests that
indicating the temperament contributes to this finding, with the profile for the disorder comprising high neuroticism
degree to
and conscientiousness and low levels of agreeableness. However, this profile is not unique to
which genes
contribute to the
obsessive-compulsive personality disorder, having also been found for schizotypal, borderline and
development of a avoidant personality disorders (Morey et al., 2002).
disorder. Emphasising psychosocial factors, Millon and Davis (1996) argue that the features of the disorder
comprise coping responses that the child develops in order to manage negative interpersonal
experiences. For instance, the child may learn to suppress feelings and perform approved
behavioural routines (e.g., excessive tidiness) in order to avoid punishment by parental figures.
Broad support for this contention comes from data indicating a predictive association between
childhood experiences of verbal (Cohen et al., 2005) and emotional abuse (Lobbestael et al., 2010)
and being diagnosed with obsessive-compulsive personality disorder in early adulthood. According
to cognitive theory, the core beliefs of individuals with obsessive-compulsive personality disorder
relate to perfectionistic strivings and the intolerable nature of any perceived faults or personal flaws
(Beck & Freeman, 1990).
TREATMENT OF THE CLUSTER C PERSONALITY DISORDERS:

OBSESSIVE-COMPULSIVE PERSONALITY DISORDER
Individuals with obsessive-compulsive personality disorder typically seek treatment for comorbid
anxiety or depressive conditions. The greater part of the treatment research for this disorder focuses
on cognitive-behavioural approaches. This approach for obsessive-compulsive personality disorder
typically includes challenging dysfunctional beliefs, in vivo exposure to feared situations, and graded
homework tasks aimed at, for example, gradually altering overly rigid routines (Karterud et al., 2003;
Strauss et al., 2006). For example, a patient might be challenged to change his/her daily routines
around showering, dressing and tackling household chores in a particular sequence. In this case,
graded task assignments would be systematically varied by changing the time and sequencing of tasks,
working up to leaving some tasks for a day or so.
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A non-randomised trial by Strauss and colleagues (2006) was conducted to examine the effects
of cognitive therapy on depressive and personality disorder symptoms in patients with avoidant and
obsessive-compulsive personality disorder. They reported that 67 per cent of patients with avoidant
personality disorder and 83 per cent of patients with obsessive-compulsive personality disorder
experienced a clinically significant reduction in personality disorder symptoms and depressive
symptoms from pre- to post-treatment, including no longer meeting criteria for the personality disorder.
Unfortunately, since the study was not randomised and did not include a control group, it is not clear
if these improvements were due to cognitive therapy itself or to some other aspect of the intervention
(such as receiving regular support from a therapist). Also, there was no follow-up assessment
conducted, so it remains unknown whether patients were able to maintain their improvements over
time once treatment had ended. Randomised controlled trials suggest that dialectical behaviour
therapy and schema therapy may be effective for those with this disorder (Arntz, 2012; Haro et al.,
2013). These findings from methodologically sound research provide much encouragement for those
with Cluster C disorders, including obsessive-compulsive personality disorder.
SUMMARY
Personality refers to patterns of thinking, feeling and behaving that are relatively consistent across situations and enduring over
time. In personality disorders, these patterns differ markedly from the expectations of the individual’s cultural group and cause
significant personal distress and impaired functioning.
The DSM-5 identifies ten personality disorders that are further categorised into three clusters. The Cluster A grouping includes
paranoid, schizoid and schizotypal personality disorders, which are characterised by odd or eccentric traits and behaviours. Cluster
B comprises antisocial, borderline, histrionic and narcissistic personality disorders, which are defined by dramatic, emotional or
erratic traits and behaviours. Cluster C includes avoidant, dependent and obsessive-compulsive personality disorders, which
entail anxious traits and behaviours. Epidemiological data reveal a relatively high level of personality disorders in the community,
with conservative estimates of around 13 per cent of the general population having a personality disorder. The prevalence of
personality disorder increases dramatically to 25–40 per cent of individuals in mental health settings.
Among the contemporary models for understanding personality disorders are various factor models (e.g., the five factor
model), Beck’s cognitive model, Young’s schema therapy, Linehan’s biosocial model and dialectical behaviour therapy, Ryle’s
cognitive analytic therapy and mentalisation-based treatment. Common to most of these approaches is the view that a complex
interaction occurs between the genetic predispositions (e.g., for certain personality traits) and aversive psychosocial factors during
childhood (particularly disrupted attachment experiences with primary caregivers and trauma) resulting in the development of
personality disturbance. However, research on the aetiology and treatment of specific personality disorders is generally lacking
(with borderline personality disorder being one exception). Thus, although the field of personality disorders has developed quite
rapidly over the past few decades, it is clearly at a much less mature stage of development compared to work in other fields of
psychological disorder. Further research is required to provide an empirically based assessment approach, greater understanding
of the factors contributing to the development and maintenance of personality disorders and identification of the key components
of effective treatments for those with personality disorders.
KEY TERMS
adoption study. . . . . . . . . . . . . . . . . . . 424 cognitive analytic therapy. . . . . . . . . . 417 five factor model. . . . . . . . . . . . . . . . . . 401
amygdala. . . . . . . . . . . . . . . . . . . . . . . . 425 concordance rate. . . . . . . . . . . . . . . . . 427 heritability . . . . . . . . . . . . . . . . . . . . . . . 434
antipsychotic medications . . . . . . . . . 423 cortisol. . . . . . . . . . . . . . . . . . . . . . . . . . 428 histrionic personality disorder. . . . . . 405
antisocial personality disorder. . . . . . 406 dependent personality disorder . . . . 407 hypothalamic-pituitary-adrenal
avoidant personality disorder. . . . . . . 407 dialectical behaviour therapy (DBT). . . 416 (HPA) axis. . . . . . . . . . . . . . . . . . . . . . . . 428
borderline personality disorder. . . . . 406 epigenetic. . . . . . . . . . . . . . . . . . . . . . . 412 mentalisation. . . . . . . . . . . . . . . . . . . . . 421
Cochrane review . . . . . . . . . . . . . . . . . 416 family study. . . . . . . . . . . . . . . . . . . . . . 432 meta-analysis . . . . . . . . . . . . . . . . . . . . 432
continued
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narcissistic personality disorder . . . . 405 schema. . . . . . . . . . . . . . . . . . . . . . . . . . 413 separation anxiety disorder. . . . . . . . 433
obsessive-compulsive personality schema therapy. . . . . . . . . . . . . . . . . . 415 social skills training . . . . . . . . . . . . . . . 426
disorder. . . . . . . . . . . . . . . . . . . . . . . . . 408 schizoid personality disorder. . . . . . . 404 testosterone. . . . . . . . . . . . . . . . . . . . . 424
orbitofrontal cortex . . . . . . . . . . . . . . . 425 schizotypal personality disorder. . . . 404 twin study . . . . . . . . . . . . . . . . . . . . . . . 427
paranoid personality disorder . . . . . . 404 selective serotonin reuptake
psychopathy. . . . . . . . . . . . . . . . . . . . . 407 inhibitors (SSRIs). . . . . . . . . . . . . . . . . . 424
REVIEW QUESTIONS
LO 13.1
13.1 What are the three domains of personality dysfunction described by Millon (1981) and how might these relate
to the five factors of personality in the five factor model?
LO 13.2
13.2 Describe the three clusters comprising the personality disorders in the DSM-5.
13.3 What role might culture play in the detection and diagnosis of personality disorder?
LO 13.3
13.4 Describe the concerns about and arguments in support of early intervention for borderline personality disorder.
LO 13.4
13.5 Young’s schema therapy model emphasises the role of early maladaptive schema in the development of
personality disorder. When and how do early maladaptive schema develop?
13.6 How does dialectical behaviour therapy explain the development of borderline personality disorder?
13.6 Cognitive analytic therapy focuses on the individual’s ‘reciprocal roles’. What does this construct refer to?
LO 13.5
13.8 How might cognitive behaviour therapy assist you to treat an individual with a paranoid personality disorder?
13.9 A wide range of therapies (behavioural, cognitive, psychodynamic and integrative) have been demonstrated
to be effective at improving outcomes for individuals with borderline personality disorder. Why might this be
the case?
13.10 How might cognitive behaviour therapy (CBT) help you to work with an individual with dependent personality
disorder?
REFERENCES
Adams, T. (2013). How to spot a murderer’s brain. The Guardian Aviram, R. B., Brodsky, B. S., Stanley, B. (2006). Borderline
(May 13). Retrieved from www.theguardian.com/science/2013/ personality disorder, stigma, and treatment implications. Harvard
may/12/how-to-spot-a-murderers-brain. Review of Psychiatry, 14, 249–256.
American Psychiatric Association (1980). Diagnostic and statistical Bamelis, L. L., Evers, S. M., Spinhoven, P., & Arntz A. (2014).
manual of mental disorders (3rd ed.). Washington, DC: Author. Results of a multicenter randomized controlled trial of the clinical
American Psychiatric Association (2010). DSM-5 development. effectiveness of schema therapy for personality disorders. American
Retrieved from www.dsm5.org. Journal of Psychiatry, 171, 305–322.
American Psychiatric Association (2013). Diagnostic and statistical Bartak, A., Spreeuwenberg, M. D., Andrea, H., Holleman, L.,
manual of mental disorders (5th ed.). Arlington: Author. Rijnierse, P., Rossum, B.V., . . . Emmelkamp, P. M. G. (2010).
Arntz, A. (2012). Schema therapy for cluster C personality disorders. Effectiveness of different modalities of psychotherapeutic treatment
In M. van Vreeswihk, J. Broerson, & M. Madort (Eds.), The Wiley- for patients with Cluster C personality disorders: Results of a large
Blackwell handbook of schema therapy: Theory, research, and prospective multicentre study. Psychotherapy and Psychosomatics,
practice (pp. 397–414). London: John Wiley & Sons. 79, 20–30.
rie66620_ch13_399-442.indd 436 07/31/17 09:39 AM

Bateman, A., & Fonagy, P. (2004). Mentalisation based treatment: Caspi, A., McClay, J., Moffit, T. E., Mill, J., Martin, J., Craig,
Psychotherapy for borderline personality disorder. Oxford: Oxford I. W., . . . Poulton, R. (2002). Role of genotype in the cycle of
University Press. violence in maltreated children. Science, 297, 851–854.
Bateman, A. W., & Fonagy, P. (2006). The structure of mentalization Castaneda, R., & Franco, H. (1985). Sex and ethnic distribution of
based treatment. In A. W. Bateman & P. Fonagy (Eds.), borderline personality disorder in an inpatient sample. American
Mentalization-based treatment for borderline personality disorder Journal of Psychiatry, 142, 1202–1203.
(pp. 37–59). Oxford: Oxford University Press. Chanen, A. M. (2015). Borderline personality disorder in young
Bateman, A., & Fonagy, P. (2009). Randomized controlled trial of people: Are we there yet? Journal of Clinical Psychology, 71,
outpatient mentalization based treatment versus structured clinical 778–791.
management for borderline personality disorder. American Journal Chanen, A. M., Jackson, H. J., McCutcheon, L. K., Jovev, M.,
of Psychiatry, 166, 1355–1364. Dudgeon, P., Yuen, H. P., . . . McGorry, P. D. (2008a). Early
Bateman, A., Gunderson, J., & Mulder, R. (2015). Treatment of intervention for adolescents with borderline personality disorder
personality disorder. The Lancet, 385, 735–743. using cognitive analytic therapy: Randomised controlled trial.
Bateman, A., O’Connell, J., Lorenzini, N., Gardner, T., & Fonogy, British Journal of Psychiatry, 193, 477–484.
P. (2016). A randomised controlled trial of mentalization-based Chanen, A. M., Jackson, H. J., McCutcheon, L. K., Jovev, M.,
treatment versus structured clinical management for patients with Dudgeon, P., Yuen, H. P., . . . McGorry, P. D. (2009). Early
comorbid borderline personality disorder and antisocial personality intervention for adolescents with borderline personality disorder: A
disorder. BMC Psychiatry, 16, 304–315. quasi-experimental comparison with treatment as usual. Australian
Battle, C. L., Shea, M. T., Johnson, D. M., Yen, S., Zlotnick, C., and New Zealand Journal of Psychiatry, 43, 397–408.
Zanarini, M. C., . . . Morey, L. C. (2004). Childhood maltreatment Chanen, A. M., Jovev, M., & Jackson, H. J. (2007). Adaptive
associated with adult personality disorders: Findings from the functioning and psychiatric symptoms in adolescents with
Collaborative Longitudinal Personality Disorders Study. Journal of borderline personality disorder. Journal of Clinical Psychiatry, 68,
Personality Disorders, 18, 193–211. 297–306.
Bechara, A., Tranel, D., & Damasio, H. (2000). Characterization Chanen, A. M., & Kaess, M. (2012). Developmental pathways to
of the decision-making deficit of patients with ventromedial borderline personality disorder. Current Psychiatry Reports, 14,
prefrontal cortex lesions. Brain, 123, 2189–2202. 45–53.
Chanen, A. M., & McCutcheon, L. (2013). Prevention and early
Beck, A. T., & Freeman, A. (1990). Cognitive therapy of personality
intervention for borderline personality disorder: Current status and
disorders. New York: Guilford Press.
recent evidence. British Journal of Psychiatry, 202, s24–s29.
Benjamin, L. S. (1996). Interpersonal diagnosis and treatment of
Chanen, A. M., Velakoulis, D., Carison, K., Gaunson, K., Wood,
personality disorders (2nd ed.). New York: Guilford Press.
S. J., Yücel, M., . . . Pantelis, C. (2008b). Orbitofrontal,
Blackburn, R. (2007). Personality disorder and psychopathy:
amygdala and hippocampal volumes in teenagers with first-
Conceptual and empirical investigation. Psychology, Crime and
presentation borderline personality disorder. Psychiatry Research
Law, 13, 7–18.
Neuroimaging, 163, 116–125.
Blair, R. J. R. (1995). A cognitive developmental approach to Chartonas, D., Kyratsous M., Dracass, S., Lee, T., Bhui, K. (2017).
morality: Investigating the psychopath. Cognition & Emotion, 57, Personality disorder: Still the patients psychiatrists dislike? British
1–29. Journal of Psychiatry Bulletin, 41, 12–17.
Bleuler, E. (1924). Textbook of psychiatry. New York: Macmillan. Clarke, S., Thomas, P., & James, K., (2013). Cognitive analytic
Bornovalova, M. A., Hicks, B. M. Iacono, W. G., & McGue, M. therapy for personality disorder: Randomised controlled trial.
(2009). Stability, change, and heritability of borderline personality British Journal of Psychiatry, 202, 129–134.
disorder traits from adolescence to adulthood: A longitudinal twin Clarkin, J. F., Yeomans, F., & Kernberg, O. F. (2006). Psychotherapy
study. Development and Psychopathology, 21, 1335–1353. for borderline personality: Focusing on object relations. New
Bowlby, J., Fry, M., & Ainsworth, M. D. S. (1983). Child Care and York: Wiley.
the Growth of Love. London: Penguin Books. Cleckley, H. M. (1982). The mask of sanity (6th ed.). St Louis: Mosby.
Cadoret, R. J., Yates, W. R., Troughton, E., Woodworth, G., & Cohen, P., Crawford, T. N., Johnson, J. G., & Kasen, S. (2005).
Stewart, M. A. (1995). Genetic-environmental interaction in the The Children in the Community Study of developmental course
genesis of aggressivity and conduct disorders. Archives of General of personality disorders. Journal of Personality Disorders, 19,
Psychiatry, 52, 916–924. 466–486.
Carr, S. N., & Francis, A. J. P. (2010). Early maladaptive schemas Coid, J., Yang, M., Bebbington, P., Moran, P., Brugha, T., Jenkins,
and personality disorder symptoms: An examination in a non- R., . . . Ullrich, S. (2009). Borderline personality disorder: Health
clinical sample. Psychology and Psychotherapy: Theory, Research service use and social functioning among a national household
and Practice, 83, 333–349. population. Psychological Medicine, 39, 1721–1731.
Carrasco, J. L., Diaz-Marsa, M., Pastrana, J. I., Molina, R., Brotons, Connolly, A., Cobb-Richardson, P., & Ball, S. A. (2008). Personality
L., López-Ibor, M. I., & López-Ibor, J. J. (2007). Hypothalamic- disorders in homeless drop-in centre clients. Journal of Personality
pituitary-adrenal axis response in borderline personality disorder Disorders, 22, 573–588.
without post-traumatic features. British Journal of Psychiatry, 190, Cooke, D. J. (1997). The Barlinnie special unit: The rise and fall of
357–358. a therapeutic experiment. In E. Cullen, L. Jones, & R. Woodward
rie66620_ch13_399-442.indd 437 07/31/17 09:39 AM

(Eds.), Therapeutic communities for offenders (pp. 101–120). borderline personality disorder: Psychopathology and function
Chichester: Wiley. from the Collaborative Longitudinal Personality Disorders study.
Costa, P. T., & Widiger, T. A. (Eds.) (2002). Personality disorders Archives of General Psychiatry, 68, 827–837.
and the Five-Factor Model of personality (2nd ed.). Washington, Hare, R. D. (1991). The Hare Psychopathy Checklist—Revised.
DC: American Psychological Association. Toronto: Multi-Health Systems.
Crawford, T. N., Cohen, P., First, M. B., Skodol, A. E., Johnson, Hare, R. D. (1993). Without conscience: The disturbing world of the
J. G., & Kasen, S. (2008). Comorbid Axis I and Axis II disorders psychopaths among us. New York: Simon & Schuster.
in early adolescence: Prognosis 20 years later. Archives of General Hare, R. D. (2006). Psychopathy: A clinical and forensic overview.
Psychiatry, 65, 641–648. Psychiatric Clinics of North America, 29, 709–724.
Dahl, A. A. (1993). The personality disorders: A critical review Hare, R. D., Clark, D., Grann, M., & Thornton, D. (2000). Psychopathy
of family, twin, and adoption studies. Journal of Personality and the predictive validity of the PCL-R: An international
Disorders, 7 (Supp. 1), 86–89. perspective. Behavioural Sciences and the Law, 18, 623–645.
Damasio, A. R. (1994). Descartes’ error: Emotion, reason, and the Hare, R. D., Hart, S. D., & Harpur, T. J. (1991). Psychopathy and
human brain. New York: Putnam. the DSM-IV criteria for antisocial personality disorder. Journal of
Davidson, K., Tyrer, P., Gumley, A., Tata, P., Norrie, J., Palmer, Abnormal Psychology, 100, 391–398.
S., . . . Macaulay, F. (2006). A randomized controlled trial of Haro, V. N., Palacios, A. G., Moliner, R., Guillen, V., & Botella, C.
cognitive behaviour therapy for borderline personality disorder: (2013) Dialectical behavior therapy for the treatment of cluster C
Rationale for trial, method, and description of sample. Journal of personality disorders. Behavioral Psychology, 21, 321–340.
Personality Disorders, 20, 431–449. Hartevelt, J. (2009). Own evidence seals fate. Retrieved from http://
Davidson, K. M., Tyrer, P., Tata, P., Cooke, D., Gumley, A., Ford, www.stuff.co.nz/national/crime/2665587/Own-evidence-seals-
I., . . . Crawford, M. J. (2008). Cognitive behaviour therapy for fate.
violent men with antisocial personality disorder in the community: Heinz, A., Braus, D. F., Smolka, M. N., Wrase, J., Puls, I.,
An exploratory randomized controlled trial. Psychological Hermann, D. (2005). Amygdala-prefrontal coupling depends on a
Medicine, 39, 569–577. genetic variation of the serotonin transporter. Nature Neuroscience,
DeWall, C. N., Pond, R. S., Campbell, W. K., & Twenge, J. 8, 20–21.
(2011). Tuning into psychological change: Linguistic markers of Hoch, A. (1910). Constitutional factors in the dementia praecox
psychological traits and emotions over time in popular US song group. Review of Neurology and Psychiatry, 8, 463–474.
lyrics. Psychology of Aesthetics, Creativity, and the Arts, 5, 200–207. Horton, R. S., Bleau, G., & Drwecki, B. (2006). Parenting narcissus:
Eikenaes I., Egeland J., Hummelen B., & Wilberg, T. (2015). Avoidant What are the links between parenting and narcissism? Journal of
personality disorder versus social phobia: The significance of Personality, 74, 345–376.
childhood neglect. PLoS One, 10, e0122846.3. Huang, Y., Kotov, R., de Girolamo, G., Preti, A., Angermeyr, M.,
Emmelkamp, P. M., Benner, A., Kuipers, A., Feiertag, G. A., Koster, Benjet, C.,  . 
. 
. Kessler, R. C. (2009). DSM-IV personality
H. C., & van Apeldoorn, F. J. (2006). Comparison of brief dynamic disorders in the WHO World Mental Health Surveys. British
and cognitive-behavioural therapies in avoidant personality Journal of Psychiatry, 195, 46–53.
disorder. British Journal of Psychiatry, 189, 60–64. Hummelen, B., Wilberg, T., Pedersen, G., & Karterud, S. (2007).
Eysenck, H. J. (1994). The biology of morality. In B. Puka (Ed.), The relationship between avoidant personality disorder and social
Defining perspectives in moral development (pp. 212–229). New phobia. Comprehensive Psychiatry, 48, 348–356.
York: Garland Publishing. Jackson, H. J., & Burgess, P. M. (2000). Personality disorders in
Fox, A. R., Kvaran, T. H., & Fontaine, R. G. (2013). Psychopathy the community: A report from the Australian National Survey of
and culpability: How responsible is the psychopath for criminal Mental Health and Wellbeing. Social Psychiatry and Psychiatric
wrongdoing? Law and Social Inquiry, 38, 1–26. Epidemiology, 35, 531–538.
Giesen-Bloo, J., van Dyck, R., Spinhoven, P., van Tilburg, W., Jackson, H. J., & Burgess, P. M. (2004). Personality disorders in
Dirksen, C., van Asselt, T., . . . Arntz, A. (2006). Outpatient the community: Results from the Australian National Survey of
psychotherapy for borderline personality disorder: Randomized Mental Health and Wellbeing. Part III: Relationships between
trial of schema-focused therapy versus transference-focused specific type of personality disorder, Axis I mental disorders and
psychotherapy. Archives of General Psychiatry, 63, 649–658. physical conditions with disability and health consultations. Social
Glenn, A. L., Johnson, A. K., & Raine, A. (2013). Antisocial Psychiatry and Psychiatric Epidemiology, 39, 765–776.
personality disorder: A current review. Current Psychiatry Reports, Jacob, G. A., & Arnoud, A. (2013). Schema therapy for personality
15, 427. disorders: A review. International Journal of Cognitive Therapy,
Grant, B. F., Goldstein, R. B., Chou, S. P., Huang, B., Stinson, F. S., 6, 171–185.
Dawson, D. A., . . . Compton, W. M. (2009). Sociodemographic Johnson, B. A., Brent, D. A., Connolly, J., Bridge, J., Matta, J.,
and psychopathologic predictors of first incidence of DSM- Constantine, D., . . . White, T. (1995). Familial aggregation of
IV substance use, mood and anxiety disorders: Results from the adolescent personality disorders. Journal of the American Academy
Wave 2 National Epidemiologic Survey on Alcohol and Related of Child and Adolescent Psychiatry, 34, 798–804.
Conditions. Molecular Psychiatry, 14, 1051–1066. Jovev, M., Garner, B., Phillips, L., Velakoulis, D., Wood, S. J.,
Gunderson, J. G., Stout, R. L., McGlashan, T. H., Shea, M. T., Morey, Jackson, H. J., . . . Chanen, A. M. (2008). An MRI study of
L. C., Grilo, C. M., . . . Sanislow, C. (2011). Ten-year course of pituitary volume and parasuicidal behavior in teenagers with
rie66620_ch13_399-442.indd 438 07/31/17 09:39 AM

first-presentation borderline personality disorder. Psychiatry within an individual growth curve framework. Development and
Research: Neuroimaging, 162, 273–277. Psychopathology, 17, 1207–1237.
Jovev, M., & Jackson, H. J. (2004). Early maladaptive schemas Lenzenweger, M. F., Loranger, A. W., Korfine, L., & Neff, C.
in personality disordered individuals. Journal of Personality (1997). Detecting personality disorders in a nonclinical population:
Disorders, 18, 467–478. Application of a 2-stage procedure for case identification. Archives
Jovev, M., & Jackson, H. J. (2006). The relationship of borderline of General Psychiatry, 54, 345–351.
personality disorder, life events and functioning in an Australian Linehan, M. M. (1993). Cognitive-behavioral treatment of borderline
psychiatric sample. Journal of Personality Disorders, 20, personality disorder. New York: Guilford Press.
205–217. Linehan, M. (2012). Emotion regulation and dialectical behaviour
Joyce, P. R., McKenzie, S. E., Luty, R. T., Mulder, R. D., Sullivan, therapy. Paper presented at the Second International Congress
P. F., & Cloninger, R. C. (2003). Temperament, childhood on Borderline Personality Disorder and Allied Disorders, 27–29
environment and psychopathology as risk factors for avoidant and September, Amsterdam, the Netherlands.
borderline personality disorders. Australian and New Zealand Livesley, J. (2008). Towards a genetically-informed model of
Journal of Psychiatry, 37, 756–764. borderline personality disorder. Journal of Personality Disorders,
Kagan, J., Rennick, J. S., & Snidman, M, (1987). The physiology 22, 42–71.
and psychology of behavioral inhibition in children. Child Livesley, W. J. (2012). Disorder in the proposed DSM-5 classification
Development, 50, 1459–1473. of personality disorders. Clinical Psychology & Psychotherapy, 19,
Karterud, S., Pedersen, G., Bjordal, E., Brabrand, J., Friis, S., 364–368.
Haaseth, O., . . . Urnes, O. (2003). Day treatment of patients with Livesley, W. J., Jang, K. L., Jackson, D. N., & Vernon, P. A. (1993).
personality disorders: Experiences from a Norwegian treatment Genetic and environmental contributors to dimensions of personality
research network. Journal of Personality Disorders, 17, 243–262. disorder. American Journal of Psychiatry, 160, 1826–1831.
Kendler, K. S., Aggen, S. H., Czajkowski, N., Roysamb, E., Tambs, Lobbestael, J., Arntz, A., & Bernstein, A. P. (2010). Disentangling
K., Torgersen, S.,  . . 
. Reichborn-Kjennerud, T. (2008). The the relationship between different types of childhood maltreatment
structure of genetic and environmental risk factors for DSM- and personality disorders. Journal of Personality Disorders, 24,
IV personality disorders: A multivariate twin study. Archives of 285–295.
General Psychiatry, 65, 1438–1446. Lorenz, A. R., & Newman, J. P. (2002). Deficient response
Kendler, K. S., Myers, J., Torgersen, S., Neale, M. C., & Reichborn- modulation and emotion processing in low-anxious Caucasian
Kjennerud, T. (2007). The heritability of cluster A personality psychopathic offenders: Results from a lexical decision task.
disorders assessed by both personality interview and questionnaire. Emotion, 2, 91–104.
Psychological Medicine, 37, 655–665. Lumley, M. N., & Harkness, K. L. (2007). Specificity in the relations
Kernberg, O. (1975). Borderline conditions and pathological among childhood adversity, early maladaptive schemas, and
narcissism. New York: Jason Aronson. symptom profiles in adolescent depression. Cognitive Therapy and
Kessler, R. C. (1994). The National Comorbidity Survey of the Research, 31, 639–657.
United States. International Review of Psychiatry, 6, 365–376. Maier, W., Lichtermann, D., Minges, J., & Heun, R. (1994).
Koehne, K., Hamilton, B., Sands, N., & Humphries, C. (2012). Personality disorders among the relatives of schizophrenia patients.
Working around a contested diagnosis: Borderline personality Schizophrenia Bulletin, 20, 481–493.
disorder in adolescence, Health, 17, 37–56. McCrae, R. R., & Costa, P. T. Jnr. (1984). Emerging lives, enduring
Kohut, H. (1971). The analysis of the self. New York: International dispositions: Personality in adulthood. Boston: Little Brown.
Universities Press. McGauley, G., Yakeley, J., Williams, A., & Bateman A. (2011).
Kohut, H. (1972). Thoughts on narcissism and narcissistic rage. Attachment, mentalization and antisocial personality disorder: The
Psychoanalytic Study of the Child, 27, 360–400. possible contribution of mentalization-based treatment. European
Kohut, H. (1977). The restoration of the self. New York: International Journal of Psychotherapy and Counselling, 13, 371–393.
Universities Press. Meehl, P. E. (1989). Schizotaxia revisited. Archives of General
Krakowski, M. (2003). Violence and serotonin: Influence of impulse Psychiatry, 46, 935–944.
control, affect regulation, and social functioning. Journal of Mehlum, L., Tormoen, A. J., Ramberg, M., Haga, E., Diep, L. M.,
Neuropsychiatry and Clinical Neurosciences, 15, 294–305. Laberg, S., . . . Groholt, B. (2014). Dialectical behavior therapy for
Kraus, G., & Reynolds, D. J. (2001). The ‘A-B-Cs’ of the Cluster adolescents with repeated suicidal and self-harming behavior: A
Bs: Identifying, understanding and treating Cluster B personality randomized trial. Journal of the American Academy of Child and
disorders. Clinical Psychology Review, 21, 345–373. Adolescent Psychiatry, 53, 1082–1091.
Lahti, J., Raikkonen, K., Sovio, U., Miettunen, J., Hartikainen, A. L., Millon, T. (1981). Disorders of personality: DSM-III, Axis II. New
Pouta, A., . . . Veijola, J. (2009). Early-life origins of schizotypal York: Wiley-Interscience.
traits in adulthood. British Journal of Psychiatry, 195, 132–137. Millon, T. (1996). Personality and psychopathology: Building a
Le Doux, J. E. (1992). Emotion in the amygdala. In J. P. Aggleton clinical science. New York: Wiley.
(Ed.), The amygdala: Neurobiological aspects of emotion, memory, Millon, T. (with Davis, R. D.) (1996). Disorders of personality:
and mental dysfunction (pp. 339–351). New York: Wiley-Liss. DSM-IV and beyond (2nd ed.). New York: Wiley.
Lenzenweger, M. F., & Castro, D. D. (2005). Predicting change in Millon, T., Davis R. D., Millon, C., Escovar, L., & Meagher, S.
borderline personality: Using neurobehavioral systems indicators (2000). Personality disorders in modern life. New York: Wiley.
rie66620_ch13_399-442.indd 439 07/31/17 09:39 AM

Millon, T., & Grossman, S. (2007). Moderating severe personality Pretzer, J. (2004). Cognitive therapy of personality disorders. In
disorders: A personalized psychotherapy. Hoboken: Wiley. G. G. Magnavita (Ed.), Handbook of personality disorders: Theory
Morey, L. C., Gunderson, J. G., Quigley, B. D., Shea, T., Skodol, A. E., and practice (pp. 169–193). New York: Wiley.
McGlashan, T. H., . . . Zanarini, M. C. (2002). The representation Quirk, S. E., El-Gabalawy, R., Brenan, S. L., Bolton, J. M., Sareen,
of borderline, avoidant, obsessive-compulsive, and schizotypal J., Berk, M., . . . Williams, L. (2014). Personality disorders and
personality disorders by the Five-Factor Model. Journal of physical comorbidities in adults from the United States: Data
Personality Disorders, 16, 215–234. from the National Epidemiologic Survey on Alcohol and Related
Morf, C. C., & Rhodewalt, F. (2001). Expanding the dynamic self Conditions. Social Psychiatry and Psychiatric Epidemiology, 50,
regulatory processes mode of narcissism: Research directions for 807–820.
the future. Psychological Inquiry, 12, 243–351. Raine, A. (1997). Antisocial behavior and psychophysiology: A
Mroczkowski, M. M., Goes, F. S., Riddle, M. A., Grados, M. A., biological perspective. In D. M. Stoff, J. Breiling, & J. D. Maser
Bienvenu, O. J., Greenberg, B. D.,  . 
. . 
Samuels, J. (2016). (Eds.), Handbook of antisocial personality disorder (pp. 289–304).
Dependent personality, separation anxiety disorder and other New York: Wiley.
anxiety disorders in OCD. Personality and Mental Health, 10, Raine, A. (2002). Biosocial studies of antisocial and violent behavior
22–28. in children and adults: A review. Journal of Abnormal Child
Mulder, R. T., Joyce, P. R., Frampton, C. M., Luty, S. E., & Sullivan, Psychology, 30, 311–326.
P. F. (2006). Six months of treatment for depression: Outcome and Renner, F., van Goora, M., Huibers, M., Arntz, A., Butz, B., &
predictors of the course of illness. American Journal of Psychiatry, Bernstein, D. (2013). Short-term group schema cognitive-
163, 95–100. behavioral therapy for young adults with personality disorders
National Collaborating Centre for Mental Health (2009). Borderline and personality disorder features: Associations with changes in
personality disorder: Treatment and management. National clinical symptomatic distress, schemas, schema modes and coping styles.
practice guideline number 78. Leicester: The British Psychological Behaviour Research and Therapy, 51, 487–492.
Society and The Royal College of Psychiatrists. Ronningstam, E., Gunderson, J., & Lyons, M. (1995). Changes in
National Health and Medical Research Council (2013). Clinical pathological narcissism. American Journal of Psychiatry, 152,
practice guideline for the management of borderline personality 253–257.
disorder. Melbourne: Author. Rossouw, T. I., & Fonagy, P. (2012). Mentalization-based treatment
National Institute for Clinical Excellence (2009). Antisocial for self-harm in adolescents: A randomized controlled trial. Journal
personality disorder: Treatment, management and prevention. of the American Academy of Child and Adolescent Psychiatry, 51,
Retrieved from nice.org.uk/cg77. 1304–1313.
National Institute for Clinical Excellence (2013). Antisocial Ryder, A. G., Surohara, M., & Kirmayer, L. J. (2015). Culture and
behaviour and conduct disorders in children and young people: personality disorder: From a fragmented literature to a contextually
Recognition, intervention and management. Retrieved from nice grounded alternative. Current Opinion in Psychiatry, 28, 40–45.
.org.uk/cg158. Ryle, A. (1997). Cognitive analytic therapy for borderline personality
Newton-Howes, G., Clark, L. A., & Chanen, A. M. (2015). Personality disorder. Chichester: John Wiley & Sons.
disorder across the life course. The Lancet, 385, 727–734. Ryle, A. (2004). The contribution of cognitive analytic therapy to the
Newton-Howes, G., Tyrer, P., Anagnostakis, K., Cooper, S., Bowden- treatment of borderline personality disorder. Journal of Personality
Jones, O., & Weaver, T. (2010). The prevalence of personality Disorders, 18, 3–35.
disorder, its comorbidity with mental state disorders, and its Ryle, A., & Kerr, I. B. (2002). Introducing cognitive analytic therapy.
clinical significance in community mental health teams. Social Chichester: John Wiley & Sons.
Psychiatry & Psychiatric Epidemiology, 45, 453–460. Samuels, J., Eaton, W. W., Bienvenu, O. J., Brown, C. H., Costa, P. T.
Paris, J. (1998). Personality disorders in sociocultural perspective. Jr., & Nestadt, G. (2002). Prevalence and correlates of personality
Journal of Personality Disorders, 12, 289–301. disorders in a community sample. British Journal of Psychiatry,
Paris, J. (2005). Neurobiological dimensional models of personality: 180, 536–542.
A review of the models of Cloninger, Depue, and Siever. Journal of Sansone, R. A., & Sansone, L. A. (2011). Personality disorders: A
Personality Disorders, 19, 156–170. nation-based perspective on prevalence. Innovations in Clinical
Paris, J. (2013). Personality disorders begin in adolescence. Journal Neuroscience, 8, 13–18.
of the Canadian Academy of Child and Adolescent Psychiatry, 22, Schuppert, H. M., Giesen-Bloo, J., van Gemert, T. G., Wiersema,
195–196. H. M., Minderaa, R. B., Emmelkamp, P. M. G., & Nauta, M. H.
Parker, G. (1997). Special feature: The aetiology of personality (2009). Effectiveness of an emotion regulation group training
disorders: A review and consideration of research models. Journal for adolescents: A randomized controlled pilot study. Clinical
of Personality Disorders, 11, 345–369. Psychology and Psychotherapy, 16, 467–478.
Persons, J. B. (2008). The case formulation approach to cognitive- Sharp, C., & Fonogy, P. (2016). Practitioner review: Borderline
behaviour therapy. New York: Guilford. personality disorder in adolescence—recent conceptualization,
Pompili, M., Girardi, P., Ruberto, A., & Tatarelli, R. (2005). Suicide intervention, and implications for clinical practice. Journal of
in borderline personality disorder: A meta-analysis. Nordic Journal Child Psychology and Psychiatry, 56, 1266–1288.
of Psychiatry, 59, 319–324.
rie66620_ch13_399-442.indd 440 07/31/17 09:39 AM

Siever, L. J., & Davis, K. L. (2004). The pathophysiology of Ullrich, S., & Coid, J. (2009). The age distribution of self-reported
schizophrenia disorders: Perspectives from the spectrum. American personality disorder traits in a household population. Journal of
Journal of Psychiatry, 161, 398–413. Personality Disorders, 23, 187–200.
Skodol, A. E., Gunderson, J. G., McGlashan, T. H., Dyck, I. R., van Asselt, A. D., Dirksen, C. D., Arntz, A., & Severens, J. L. (2007).
Stout, R. L., Bender, D. S., . . . Oldham, J. M. (2002a). Functional The cost of borderline personality disorder: societal cost of illness
impairment in patients with schizotypal, borderline, avoidant, or in BPD-patients. European Psychiatry, 22, 354–361.
obsessive-compulsive personality disorder. American Journal of van Honk, J., Hermans, E. J., Putman, P., Montagne, B., & Schutter,
Psychiatry, 159, 276–283. D. J. (2002). Defective somatic markers in sub-clinical psychopathy.
Skodol, A. E., Gunderson, J. G., Pfohl, B., Widiger, T. A., Livesley, Neuroreport, 13, 1025–1027.
W. J., & Siever, L. J. (2002b). The borderline diagnosis I: van Velzen, C. J. M., Emmelkamp, P. M. G., & Scholing, A. (2000).
Psychopathology, comorbidity, and personality structure. Biological Generalized social phobia versus avoidant personality disorder:
Psychiatry, 51, 936–950. Differences in psychopathology, personality traits, and social
Stoffers, J. M., & Lieb, K. (2015). Pharmacotherapy for borderline and occupational functioning. Journal of Anxiety Disorders, 14,
personality disorder: Current evidence and recent trends. Current 395–411.
Psychiatry Reports, 17, 534.
Weinbrecht, S., Schulze, L., Boettcher, B., & Renneberg, B. (2016).
Stoffers, J. M., Völlm, B. A., Rücker, G., Timmer, A., Huband, N.,
Avoidant personality disorder: A current review. Current Psychiatry
& Lieb, K. (2010). Pharmacological interventions for borderline
Reports, 18, 29.
personality disorder. Cochrane Database of Systematic Reviews,
Wexler, D. B. (1991). The adolescent self: Strategies for self-
Issue 6. Art. No. CD005653.
management, self-soothing, and self-esteem in adolescents. New
Stoffers, J. M., Völlm, B. A., Rücker, G., Timmer, A., Huband, N., &
York: Norton.
Lieb, K. (2012). Psychological therapies for people with borderline
personality disorders. Cochrane Database of Systematic Reviews, Widiger, T. A., & Costa, P. T. (1994). Personality and personality
15, 8. disorders. Journal of Abnormal Psychology, 103, 79–91.
Stoffers, K., Zanarini, M., Schmahl, C., Linehan, M., & Bohus, M. Winograd, G., Cohen, P., & Chen, H. (2008). Adolescent borderline
(2004). Borderline personality disorder. Lancet, 364, 453–461. symptoms in the community: Prognosis for functioning over
Stone, M. H. (1993). Abnormalities of personality: Within and 20 years. Journal of Child Psychology and Psychiatry, 49,
beyond the realm of treatment. New York: W. W. Norton & Co. 933–941.
Strauss, J. L., Hayes, A. M., Johnson, S. L., Newman, C. F., Brown, Witold, S. (2009). Follow-up psychotherapy outcome of patients
G. K., Barber, J. P., . . . Beck, A. T. (2006). Early alliance, alliance with dependent, avoidant and obsessive-compulsive personality
ruptures, and symptom change in a nonrandomized trial of cognitive disorders: A meta-analytic review. International Journal of
therapy for avoidant and obsessive-compulsive personality disorders. Psychiatry in Clinical Practice, 13, 153–165.
Journal of Consulting and Clinical Psychology, 74, 337–345. Woods, S. W., Addington, J., Cadenhead, K. S., Cannon, T. D.,
Stravynski, A., Belisle, M., Marcouiller, M., Lavellee, Y. J., & Elie, Cornblatt, B. A., Heinssen, R., . . . McGlashan, T. H. (2009).
R. (1994). The treatment of avoidant personality disorder by social Validity of the prodromal risk syndrome for first psychosis:
skills training in the clinic or real-life settings. Canadian Journal Findings from the North American Prodrome Longitudinal Study.
of Psychiatry, 39, 377–383. Schizophrenia Bulletin, 35, 894–908.
Stravynski, A., Marks, I., & Yule, W. (1982). Social skills problems World Health Organization (1992). The ICD-10 classification of
in neurotic disorders. Archives of General Psychiatry, 39, mental and behavioural disorders: Clinical descriptions and
1378–1385. diagnostic categories. Geneva: Author.
Tillfors, M., Furmark, T., Ekselius, L., & Fredrikson, M. (2004). Yang, M., Ulrich, S., Roberts, A., & Coid, J. (2007) Childhood
Social phobia and avoidant personality disorder: One spectrum institutional care and personality disorder traits in adulthood:
disorder? Nordic Journal of Psychiatry, 58, 147–152. Findings from the British national surveys of psychiatric morbidity.
Torgersen, S., Kringlen, E., & Cramer, V. (2001). The prevalence of American Journal of Orthopsychiatry, 77, 67–75.
personality disorders in a community sample. Archives of General Yildirim, B., & Derksen, J. (2013). Systematic review, structural
Psychiatry, 58, 590–596. analysis, and new theoretical perspectives on the role of serotonin
Torgersen, S., Lygren, S., Oien, P. A., Skre, I., Onstad, S., Edvardsen, and associated genes in the etiology of psychopathy and sociopathy.
J., . . . Kringlen, E. (2000). A twin study of personality disorders. Neuroscience and Biobehavioral Reviews, 37, 1254–1296.
Comprehensive Psychiatry, 41, 416–425. Young, J. E. (1990). Cognitive therapy for personality disorders:
Twenge, J. M., & Campbell, W. K. (2009). The narcissism epidemic: A schema-focused approach. Sarasota: Professional Resource
Living in the age of entitlement. New York: Simon & Schuster. Exchange.
Tyrer, P., Mulder, R., Crawford, M., Newton-Howes, G., Simonsen, Young, J. E., & Brown, G. (1994). Young Schema Questionnaire.
E., Ndetei, D., . . . Barrett, B. (2010). Personality disorders: A new In J. E. Young (Ed.), Cognitive therapy for personality disorder:
global perspective. World Psychiatry, 9, 56–60. A schema-focused approach (rev. ed., pp. 63–76). Sarasota:
Tyrer, P., Reed, G., & Crawford, M. (2015). Classification, Professional Resources Press.
assessment, prevalence, and effect of personality disorder. The Young, J. E., Klosko, J. S., & Weishaar, M. E. (2003). Schema
Lancet, 385, 717–726. therapy: A practitioner’s guide. New York: Guilford Press.
rie66620_ch13_399-442.indd 441 07/31/17 09:39 AM

Zanarini, M. C., Frankenburg, F. R., Reich, D. B., & Fitzmaurice, G. Zanarini, M. C., Yong, L., Frankenburg, F. R., Hennen, J., Reich,
(2010). Time to attainment of recovery from borderline personality D. B., Marino, M. F., & Vujanovic, A. A. (2002). Severity of
disorder and stability of recovery: A 10-year prospective follow-up reported childhood sexual abuse and its relationship to severity of
study. American Journal of Psychiatry, 167, 663–667. borderline psychopathology and psychosocial impairment among
Zanarini, M. C., Williams, A. A., Lewis, R. E., Reich, R. B., Vera, S. C., borderline patients. Journal of Nervous and Mental Disease, 190,
Martino, M. F., . . . Frankenberg, F. (1997). Reported pathological 381–387.
childhood experiences associated with the development of Zimmerman, M. E., Chelminski, I., & Young, D. (2008). The
borderline personality disorder. American Journal of Psychiatry, frequency of personality disorders in psychiatric patients.
154, 1101–1106. Psychiatric Clinics of North America, 31, 405–420.
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CHAPTER 14
Disorders of childhood
Alina Morawska
Matthew Sanders
CHAPTER OUTLINE
● Psychological and behavioural disorders in children
● Historical and current approaches to the understanding and classification of childhood disorders
● Neurodevelopmental disorders
● Externalising disorders
● Internalising disorders
● Elimination disorders
● Summary

14.1 Describe the key behavioural and emotional problems of children that are identified by parents and identify the
main challenges in examining the mental health problems of children.
14.2 Describe key themes in the classification of childhood psychological disorders.
14.3 Describe the main characteristics of the neurodevelopmental disorders.
14.4 Describe the key features and factors that contribute to the development and maintenance of externalising
disorders and the evidence-based approaches to the treatment of these disorders.
14.5 Describe the key characteristics and treatment of separation anxiety disorder and selective mutism.
14.6 Describe the various elimination disorders and their treatments.
DISORDERS OF CHILDHOOD: AN AUSTRALASIAN FOCUS

Mental health problems during childhood and adolescence cause considerable suffering for affected individuals, their
families and communities, and can impair the child’s educational and social development as well as mental health in
later life. Recognition of the far-reaching effects of mental health problems in young people has resulted in considerable
attention in Australia from various organisations and governments to develop initiatives to promote the wellbeing of
children and adolescents. In particular, more attention is being paid to prevention and early intervention efforts to
decrease the likelihood that children will develop severe mental health problems. Nevertheless, child and adolescent
mental health in Australia receives only a small fraction of the overall health budget, despite the fundamental importance
of childhood and adolescence on future functioning.
Adequate access to prevention and intervention services is especially difficult for vulnerable groups of children,
and the plight of refugee children in particular has gained considerable attention in Australia and worldwide. Refugee
children have often experienced significant trauma, displacement and instability in their lives, and the effects of these
experiences on children’s subsequent mental health have been well-documented. Australia’s system of detaining
children in onshore or offshore detention centres has been widely condemned because it continues to add to the trauma
experienced by these children.
continued
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The Australian Human Rights Commission produced

a report in 2014 (The Forgotten Children: National Inquiry
into Children in Immigration Detention), which stated that
‘Prolonged detention is having profoundly negative impacts
on the mental and emotional health and development of
children’ (p. 29). It also found that the rates of mental health
problems experienced by children in detention were much
higher than those of the community in general.
SHUTTERSTOCK.COM
Children from refugee backgrounds are at higher risk
of developing mental health problems and their parents
experience more barriers to accessing effective mental health
services. There is the added challenge, too, of ensuring that
the assessment and treatment of mental health needs in
these children is provided in a culturally sensitive manner. The Forgotten Children report, produced by the
This chapter aims to provide an overview of current Australian Human Rights Commission, found higher
understandings regarding psychological disorders in rates of mental health problems in children in
childhood. The chapter will discuss the diagnosis, detention than in the general community.
epidemiology (prevalence, age of onset and course),
aetiology, treatment and prevention of a range of childhood
disorders, including neurodevelopmental disorders (attention-deficit/hyperactivity disorder, specific learning disorder,
autism spectrum disorder and intellectual disability), externalising disorders (oppositional defiant disorder and conduct
disorder), internalising disorders (separation anxiety disorder and selective mutism) and elimination disorders (enuresis
and encopresis). Before providing information on these various disorders, however, the chapter will begin by exposing
the myths and highlighting the research challenges that feature in the field of childhood psychological disorders.
LO 14.1 Psychological and behavioural disorders

in children
Myths, realities and research challenges

Childhood is often considered a carefree, joyful time, with few responsibilities and problems. Many
parents and professionals assume that any difficulties that are encountered during childhood will
simply disappear as the child grows out of them. However, neither of these assumptions is supported
by the research.
The reality is that psychological and behavioural problems in children are very common and
many parents, teachers and other caregivers are concerned about children’s adjustment. Although
epidemiological data on child and adolescent mental health is lacking (Erskine et al., 2016), worldwide
rates suggest that approximately 13 per cent of children and adolescents are affected by some form of
mental disorder (Polanczyk, Salum, Sugaya, Caye, & Rohde, 2015). The Australian National Survey
of Mental Health and Wellbeing indicated that approximately one in seven 4–17-year-olds met criteria
for a mental disorder (Lawrence et al., 2015). The percentage of children who had various mental
disorders during a 12-month period as identified in the survey are displayed in Table 14.1. It was found
that almost a third of children had more than one disorder and that more boys than girls had mental
disorders. However, not all mental disorders are more common in boys than in girls. For example,
among New Zealand secondary school students, 16 per cent of girls and 9 per cent of boys reported
clinical levels of depression and 21 per cent of girls and 10 per cent of boys reported having seriously
thought about suicide in the past 12 months (Clark et al., 2013).
Despite these high rates of reported behavioural and emotional problems, not all children receive
help. Approximately half of the children with a mental disorder identified in the Australian National
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Chapter 14 Disorders of childhood 445
TABLE 14.1 Prevalence (%) of mental disorders among 4–17-year-olds by type of disorder and severity
DISORDER MILD (%) MODERATE (%) SEVERE (%) TOTAL (%)
Any anxiety disorder 3.7 1.9 1.3 6.9
Major depressive disorder 0.6 1.0 1.2 2.8
ADHD* 4.9 1.8 0.8 7.4
Conduct disorder 1.2 0.5 0.4 2.1
Any mental disorder 8.3 3.5 2.1 13.9

*ADHD: attention-deficit/hyperactivity disorder
Source: Second Australian Child and Adolescent Survey of Mental Health and Wellbeing (2015)
Survey of Mental Health and Wellbeing had accessed services for emotional and behavioural problems
in the previous 12 months (Lawrence et al., 2015), and only 3 per cent had used specialist child and
adolescent mental health services. Queensland surveys indicate that only about 14 per cent of parents
participate in parenting education to assist in promoting children’s development and managing any
difficulties (Sanders, Markie-Dadds, Rinaldis, Firman, & Baig, 2007).
While a proportion of children will outgrow their difficulties, there is substantial evidence that
early problems have considerable persistence over time (Bayer, Hiscock, Ukoumunne, Price, & Wake,
2008). Problem behaviours in toddlers and preschool-aged children typically continue into the primary
school years (Basten et al., 2016) and into adolescence (Keenan, Shaw, Delliquardi, Giovannelli, &
Walsh, 1998). Indeed, Greenberg, Speltz, and DeKlyen (1993) maintain that ‘for a substantial number
of children, factors occurring during infancy and the preschool years appear to set a developmental
trajectory that leads transactionally to school-age conduct disorders, adolescent violence and serious
offending, and adult psychiatric disorder’ (p. 191). There is also growing evidence that inhibited
and withdrawn behaviour in young children is fairly stable over time (Weems, 2008). In general, the
literature suggests that once children’s behaviour is established in a maladaptive pattern it does not
readily change in the absence of intervention.
It is also important to recognise that children live within families and that the child’s mental health
affects not only the individual child but also siblings, parents and other family members. Parents of
children with a mental disorder report higher levels of stress, mental health problems, marital conflict
and difficulties with work functioning, which may not only result from the child’s disorder but also
potentially contribute to the child’s difficulties. Siblings often experience stress, confusion and anxiety
but may also feel left out and miss out on parental attention.
A number of factors complicate research on psychological disorders in children. Traditionally,
most work done in the area has been a downward extension of adult research, with adult models of
psychological problems and intervention approaches applied to children. Yet it cannot be assumed that
models and interventions developed for adults will be appropriate for children. In addition, most studies
have focused on a single developmental time-point, making it difficult to examine the developmental
progression of both normal and pathological processes. Another problem relates to the substantial
comorbidity among childhood disorders, which makes it difficult to tease apart factors affecting
the different disorders. This comorbidity may be a result of limited potential for the expression of
difficulties, especially in younger children (e.g., a tantrum might mean ‘I’m angry’ or ‘I’m scared’),
true overlap between disorders, or an artefact of the considerable overlap in the diagnostic criteria
for different disorders. There is also the challenge of distinguishing between normal and abnormal
behaviour in children (e.g., children differ in the ages at which they meet certain developmental
milestones). Finally, there is even debate about whether children should in fact be diagnosed with
specific mental health conditions due to the stigma associated with labels, and concerns about the
overdiagnosis and overmedicalisation of certain conditions.
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As with adult psychological disorders, it is essential when examining behavioural and emotional
problems in children to consider both risk and protective factors, with research traditionally focusing
on the former and neglecting the latter. Risk factors are characteristics or hazards that increase
the possibility of occurrence, severity, duration or frequency of later psychological disorders,
while protective factors are variables that increase resilience under conditions of adversity and
increase resistance to later disturbance (Beckwith, 2000). The focus on risk factors while neglecting
protective factors is problematic, since it appears that it is the balance of risk versus protective
factors that is most important in affecting development (Beckwith, 2000; Sameroff & Fiese, 2000).
In particular, the critical role of nurturing environments for healthy child development is increasingly
being recognised (Biglan, Flay, Embry, & Sandler, 2012). According to Biglan and colleagues,
such environments minimise toxic events; teach, promote and reinforce the skills needed to become
productive adult members of society; monitor and limit opportunities for problem behaviour; and
foster psychological flexibility.
Risk and protective factors may be genetic or environmental. While the nature–nurture debate
has moved beyond debating whether nature or nurture determines developmental outcomes, there is
ongoing research examining the relative contributions of each of these influences. Within the family
environment, adverse childhood experiences (see www.cdc.gov/violenceprevention/acestudy/) are
common, and include all forms of abuse and neglect, domestic violence, parental criminal history
and substance abuse, parental separation or divorce, or mental illness in the household. Exposure to
adverse childhood experiences shows a ‘dose–response’ relationship with functioning in adulthood,
meaning that the greater the ‘dose’ or number of adverse experiences as a child, the worse the
‘response’ in terms of the individual’s health, mental health and general wellbeing as an adult. Broader
environment-related risks can include poor neighbourhoods, schools and basic services, and greater
environmental health risks, which contribute to parental stress and may have a negative impact on the
parent–child relationship (Sameroff & Fiese, 2000). From an intervention perspective, it is important
to note that many of the identified risk factors (such as poverty) cannot be changed, and the only
ones that can be altered relatively easily are parenting factors and aspects of parent–child interaction.
These factors also serve as important protective factors; the child who has a good relationship with
his/her parent may be more resilient in the face of other adversity in their environment. The need to
focus on the parent–child dynamic in treatment is underscored by the fact that, in general, risk factors
in the environment are transmitted to the child through their negative impact on the child’s primary
caregiving relationship (Conger & Donnellan, 2007).
Indigenous youth, in particular, are at greater risk of emotional and behavioural problems than non-
Indigenous youth. There is substantial evidence that parenting programs can improve family relationships
and improve child outcomes; however, little research has focused on Indigenous communities. Parenting
programs need to be sensitive to the political and cultural context in which parenting takes place, flexibly
incorporate cultural practices and expectations, and develop an evidence base of outcomes for families
in diverse communities. As research is needed to evaluate the acceptability and effectiveness of these
programs, culturally sensitive research practices are also necessary, and the value of program evaluation
and its benefit to the community must be clear. Community acceptance of the research process and
the intervention itself is vital and may be influenced by community perceptions, current priorities and
local issues.
More broadly, research supports the notion that some children are more affected by both positive
and negative environmental factors as a result of their genetic makeup (Belsky & Pluess, 2009).
Specifically, the differential susceptibility hypothesis proposes that genes previously seen to increase
the risk for developing mental health problems have been found to operate more like ‘plasticity genes’
than ‘vulnerability genes’, thus making individuals more susceptible to positive as well as negative
environmental effects (Belsky & Pluess, 2009). The literature on gene–environment interactions is
burgeoning as researchers across disciplines work together to establish the critical factors contributing
to child and adult emotional and behavioural outcomes (Frigerio et al., 2009; Kochanska, Philibert,
& Barry, 2009; Ellis, Boyce, Belsky, Bakermans-Kranenburg, & van Ijzendoorn, 2011). While this
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is a relatively novel area of research, it holds promise in terms of assisting in determining the most
appropriate interventions for those children showing early signs of behavioural or emotional problems
(Tremblay, 2010).
Overall, most children are inherently resilient and can deal with some adversity. Generally speaking,
children exposed to just one risk factor are no more likely to have a mental disorder than children not
exposed to risk factors. However, as Rutter (2000) suggests, it is ‘distinctly unusual for risks to occur
truly in isolation’ (p. 657). It is also important to remember that the presence of protective factors,
such as a close relationship with parents or parental supervision of adolescents, can ameliorate the
presence of risk factors.

to the understanding and classification
of childhood disorders
Prior to the twentieth century, there was almost no recognition of psychological disorders in children.
Similar to early views about mentally ill adults, childhood mental illness or behavioural disorders
were attributed to negative spiritual influences, and children with problems were often mistreated,
caged or killed (Mash & Dozois, 2003). During the nineteenth century, children were seen either as
miniature adults not necessitating specific diagnostic and intervention considerations, or were seen as
being immune to mental disorders. At the beginning
of the twentieth century, interest in children began
to emerge, although to date less attention has been
paid to child compared to adult mental health (Silk,
Nath, Siegel, & Kendall, 2000).
The early twentieth century witnessed increased
interest in child psychopathology, with the work
of Alfred Binet, Sigmund Freud and Jean Piaget,
among others. There was greater recognition that

children were vulnerable to mental illness, and
that special considerations needed to be taken into
account when diagnosing and treating psychological
problems in children (Silk et al., 2000). Despite
this increasing interest in childhood psychological
disorders, children were neglected in the early
versions of the Diagnostic and Statistical Manual
of Mental Disorders (DSM) and specific childhood
diagnoses were not included until as recently as the
BILDARCHIV MONHEIM GMBH/ALAMY
DSM-III (American Psychiatric Association [APA],

1980). There was considerable modification to the
childhood diagnoses in the DSM-III-R (APA, 1986)
and fine-tuning in the DSM-IV and its text revision
DSM-IV-TR (APA, 1994; 2000).
The latest edition, the DSM-5, has resulted in
the fine-tuning of diagnostic criteria for childhood
disorders and several new diagnostic categories
(APA, 2013). However, the main change from Researchers such as Jean Piaget helped to
the perspective of diagnosing conditions during increase interest in child psychopathology in the
childhood is a major restructure of condition early twentieth century.
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categories. In previous editions of the DSM, childhood conditions were listed under the category of
‘Disorders Usually First Diagnosed in Infancy, Childhood or Adolescence’. However, in the DSM-5
this category is no longer included. Thus, while many of the disorders from previous editions of the
DSM have been retained in the DSM-5, childhood disorders now appear throughout the manual. This
reorganisation, in which no clear distinction is made between disorders in children versus adults, may
fail to sufficiently take into account childhood manifestations of psychological disturbance. However,
this concern is somewhat alleviated by the fact that the new structure does follow a developmental
lifespan approach, which may assist in conceptualising the placement of childhood disorders.
Specifically, this approach focuses on how development affects the diagnosis and symptoms of
mental disorders, including factors such as the age at which disorders first occur, how symptoms
and diagnoses change across the lifespan and how disorders might evolve into new disorders over the
course of the lifespan.
Another diagnostic tool in the field of mental health problems in children is the Diagnostic
Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood
(DC:0–3R) (Zero to Three, 1994; 2005). This was the first developmentally based system for
diagnosing mental health and developmental disorders in infants and toddlers, thus comprising
a downward extension of the DSM to this young age group. Its diagnostic categories reflect the
consensus of a multidisciplinary group of experts in early childhood development and mental health.
While it has many of the same problems as the DSM, and currently has limited empirical support, it
provides a framework for examining very early difficulties, has an important focus on parent–infant
relationships, and highlights the potential continuity of childhood psychological problems from the
early to later years of childhood and beyond.
In contemporary diagnostic approaches, the most common forms of psychological disorders in
children can be categorised as either externalising (under-controlled; behaviours directed at others)
or internalising (over-controlled; feelings and states that are inner-directed) (Reynolds, 1992).
Unlike the externalising disorders, the diagnostic criteria for many of the internalising disorders
in children are the same as those for adults, with only minor modifications. Table 14.2 provides a
list of the DSM-5 diagnostic categories for disorders usually first diagnosed in infancy, childhood
or adolescence. While many children who experience considerable problems may not meet the
diagnostic criteria for a disorder, such children and their families nevertheless need assistance and
support, and efforts should be made to prevent the chances of problems worsening over time. In
fact, one of the main criticisms of the DSM-5 is that it does not take into account the dimensional
nature of many childhood conditions, thus potentially reducing access to services for those who are
experiencing problems but which are not yet of sufficient severity to meet the diagnostic criteria
(e.g., British Psychological Society, 2012).
The field of developmental psychopathology emerged in the mid-1980s, focusing on a lifespan
approach and combining data and research from normal and clinical samples (Cicchetti, 1993;
Sroufe, 1990). This approach emphasises the need to examine child behaviour and adjustment across
TABLE 14.2 The diagnostic categories relevant to infancy, childhood or adolescence in the DSM-5
Neurodevelopmental disorders Intellectual disability (intellectual Intellectual disability (intellectual

developmental disorder) developmental
disorder)
Mild
Moderate
Severe
Profound
Global developmental delay
Unspecified intellectual disability (intellectual
developmental disorder)
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Communication disorders Language disorder

Speech sound disorder
Childhood-onset fluency disorder (stuttering)
Social (pragmatic) communication disorder
Unspecified communication disorder
Attention-deficit/hyperactivity disorder Attention-deficit/hyperactivity disorder

Combined presentation
Predominantly inattentive presentation
Predominantly hyperactive/
impulsive presentation
Other specified attention-deficit/hyperactivity
disorder
Unspecified attention-deficit/hyperactivity
disorder
Specific learning disorder With impairment in reading

With impairment in written expression
With impairment in mathematics
Autism spectrum disorder
Tic disorders Tourette’s disorder

Persistent (chronic) motor or vocal tic disorder
Provisional tic disorder
Other specified tic disorder
Unspecified tic disorder
Motor disorders Developmental coordination disorder

Stereotypic movement disorder
Other neurodevelopmental disorders Other specified neurodevelopmental

disorder
Unspecified neurodevelopmental disorder
Anxiety disorders Separation anxiety disorder

Selective mutism
Depressive disorders Disruptive mood

Dysregulation disorder
Trauma- and stressor-related Reactive attachment disorder

disorders Disinhibited social engagement disorder
Feeding and eating disorders Pica

Rumination disorder
Avoidant/restrictive food intake disorder
Elimination disorders Enuresis

Encopresis
Other specified elimination disorder
Unspecified elimination disorder
Gender dysphoria Gender dysphoria in children
Disruptive, impulse-control and Oppositional defiant disorder

conduct disorders Conduct disorder
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development and to examine both normal and abnormal development to gain a clear picture of the
precursors and course of psychological difficulties. It also focuses on understanding development in
context, nestled within multiple environmental influences (Bronfenbrenner, 1979).
Intervention approaches for managing childhood disorders have also come to the forefront in recent
meta-analysis decades, with a seminal meta-analysis by Weisz, Weiss, Alicke, and Klotz (1987) providing evidence
Statistical
for the effectiveness of psychological treatments with children. There is now considerable support
technique for
summarising for childhood interventions, particularly for behavioural family interventions (Chorpita et al., 2011;
results across Comer et al., 2013; Fossum, Handegård, Adolfsen, Vis, & Wynn, 2016; Weisz, Doss, & Hawley,
several studies. 2005; Weisz & Gray, 2008).
LO 14.3 Neurodevelopmental disorders

The DSM-5 includes a category of conditions referred to as the ‘neurodevelopmental disorders’. These
conditions are characterised by their emergence in the early developmental period, often before the
child commences school. Such disorders cover a broad array of developmental deficits that affect
the individual’s personal, social, academic and/or occupational functioning. In this section, the
neurodevelopmental disorders of attention-deficit/hyperactivity disorder, specific learning disorder,
autism spectrum disorder and intellectual disability will be dealt with in turn.
The diagnosis and epidemiology of attention-deficit/

hyperactivity disorder
attention-deficit/ Attention-deficit/hyperactivity disorder (ADHD) is defined by symptoms of (a) inattention and/or
hyperactivity (b) hyperactivity and impulsivity (APA, 2013). Inattention includes symptoms such as not paying
disorder (ADHD) attention to task details or making careless mistakes, having difficulty sustaining attention over time,
Disorder marked being easily distracted and being forgetful. Hyperactivity symptoms include fidgeting, moving about
by deficits excessively and not being able to stay seated. Impulsivity includes difficulties with waiting in turn,
in attention,
blurting out answers or interrupting. While most children diagnosed with ADHD show symptoms
controlling
impulses and of both inattention and hyperactivity/impulsivity, some show a pattern of predominantly one type of
regulating activity symptom (Ford, Goodman, & Meltzer, 2003). Thus, ADHD can be diagnosed as combined presentation,
levels. predominantly inattentive presentation or predominantly hyperactive/impulsive presentation.
When making a diagnosis of ADHD, it is necessary to conduct a comprehensive assessment
to ensure that the symptoms occur across settings (e.g., both at home and at school). The child’s
developmental stage also needs to be taken into account when making a diagnosis. For example, the
abilities to stay focused for longer periods of time and to restrain oneself from acting on an impulse
develop with age. A certain level of distractibility and impulsivity is evident in all children and it
is important to be aware of developmental norms when making a diagnosis. Indeed, the fact that
distractibility and impulsivity are normal for all children, particularly at certain ages, is one factor that
fuels media reports challenging the validity of the ADHD construct. This challenge and the response
of the scientific community are shown in Table 14.3.
In addition, there are gender differences in ADHD symptomatology. Girls show less hyperactivity,
inattention, impulsivity and externalising problems than boys (Gershon & Gershon, 2002; Hasson &
Fine, 2012) but show more intellectual impairments and internalising problems (Gershon & Gershon,
2002) compared to boys.
A meta-analysis of studies investigating the prevalence of ADHD found a pooled prevalence
estimate of 7.2 per cent across populations (Thomas, Sanders, Doust, Beller, & Glasziou, 2015).
Another meta-analysis indicated that variability in prevalence rates across studies is largely due to
methodological features of the studies, and that there has been no increase in ADHD rates over time
(Polanczyk et al., 2014). ADHD usually begins in early childhood, although it can also develop during
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TABLE 14.3 The conflicting positions of media reports and an international consensus statement on ADHD
(signed by more than 80 scientists) regarding the validity of the ADHD construct
Media reports
ADHD is frequently explored in the media and there is a wide array of often inaccurate information presented, leading many
to question whether ADHD really exists and whether children are being overmedicated. Some suggest that the symptoms of
ADHD are simply normal child behaviours that are, however, annoying to parents and teachers, and are therefore categorised
as a disorder.
International consensus statement on ADHD

We, the undersigned consortium of international scientists, are deeply concerned about the periodic inaccurate portrayal
of attention deficit hyperactivity disorder (ADHD) in media reports. This is a disorder with which we are all very familiar and
toward which many of us have dedicated scientific studies if not entire careers. We fear that inaccurate stories rendering
ADHD as a myth, fraud, or benign condition may cause thousands of sufferers not to seek treatment for their disorder. It also
leaves the public with a general sense that this disorder is not valid or real or consists of a rather trivial affliction . . . We cannot
overemphasise the point that, as a matter of science, the notion that ADHD does not exist is simply wrong. All of the major
medical associations and government health agencies recognise ADHD as a genuine disorder because the scientific evidence
indicating it is so overwhelming.
Source: From Consortium of International Scientists (2002). International consensus statement on ADHD. Clinical Child and Family Psychology Review, 5, 89–111. With
permission of Springer.
adolescence. In general, ADHD appears to diminish with increasing age, but in some cases there is
a continuation of symptoms into adulthood (Willoughby, 2003). While the pattern of symptoms in
adults with ADHD is similar to that of children, there are some differences. For instance, symptoms of
ADHD in adults may include having difficulty completing mundane tasks and procrastination. There
is a high level of comorbidity between ADHD and oppositional defiant disorder (Petty et al., 2009).
The aetiology of attention-deficit/hyperactivity disorder

Factors contributing to the development of attention-deficit/hyperactivity disorder include genetics,
and family and parenting variables. Controversially, some parents and professionals point to diet as a
contributing factor.
GENETIC CONTRIBUTION
There is a considerable genetic contribution to the development of ADHD (Levy, Hay, & Bennett,
2006). This inherited vulnerability may entail some form of neuropsychological impairment, which
has been posited as the key factor underlying ADHD (Nigg, 2005). executive
In terms of neuropsychological deficits, a large body of research has found deficits in executive functions
functions among children with ADHD relative to both healthy children and children with conduct Functions of the
disorder (suggesting that these deficits are specific to ADHD rather than to externalising disorders brain that involve
the ability to
generally) (Nigg, 2005; Wåhlstedt, Thorell, & Bohlin, 2009). Executive functions include the skills of
sustain attention;
goal-setting, planning how to achieve goals, and monitoring one’s behaviour while pursuing the goal use abstract
(e.g., being able to maintain, switch and stop behaviours as required to achieve the goal). Examples reasoning;
of common cognitive tests used to assess executive functions in children with ADHD are shown in plan, initiate
Table 14.4. Brown (2006) suggests that while executive function problems underpin ADHD, different and monitor
aspects may be a problem in different individuals. Furthermore, he proposes that the problems lie with goal-directed
the switching on and off of these executive functions (such as beginning to focus attention) rather than behaviours;
and shift from
with the function itself (such as not being able to focus attention at all). This is consistent with the fact
maladaptive
that individuals with ADHD often report that they are able to attend to a task as long as it is something patterns of
that interests them. In other words, the deficit is not in the function itself but whether it is appropriately behaviour to
activated or inhibited. In addition to impaired executive functions, autonomic under-arousal (similar more adaptive
to adolescents and adults with externalising disorders) has been seen in ADHD preschoolers (Crowell ones.
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et al., 2006). Also, children with ADHD appear to have a lower response to reinforcement, meaning
that they may need stronger motivators to alter their behaviour (Luman, Oosterlaan, & Sergeant, 2005).
TABLE 14.4 Common cognitive tests used to assess executive functions in children with ADHD
TASK DESCRIPTION
Stop task Two stimuli (e.g., an ‘X’ and an ‘O’) are presented with equal probability via a computer. The child is required
to press an appropriate key as quickly as possible when the stimulus is detected. However, on approximately
one-quarter of the trials, a signal (such as a tone) is given indicating that the child should not respond. The
timing of the signal is varied to measure how much warning a child needs to inhibit the key-pressing response.
Trailmaking There are two versions: Trails A and B. In Trails A the child draws a line to connect a series of letters (A-B-C-D
etc.) scattered randomly on the page. Trails A provides a baseline measure of the child’s speed of processing. In
Trails B, the child must alternate between letters and number sequences (A-1-B-2-C-3 etc.). The difference in the
time taken to complete Trails A and B is used to measure the child’s ability to shift between different tasks (i.e.,
alternating between following a letter sequence and following a number sequence).
Mazes The child is asked to draw a line demonstrating the way out of a maze on a sheet of paper while attempting
to avoid entering any blind alleys. The task is designed to assess the child’s planning ability (i.e., the use of
foresight to choose appropriate options and reject inappropriate ones).
Source: Adapted from Nigg, J. T. (2005). Neuropsychologic theory and findings in attention-deficit/hyperactivity disorder: The state of the field and salient challenges
for the coming decade. Biological Psychiatry, 57, 1424–1435.
FAMILY AND PARENTING VARIABLES

Many of the underlying family and parenting variables contributing to oppositional defiant disorder and
conduct disorder are also present for children with ADHD. While there appears to be a stronger biological
contribution to ADHD compared to these other conditions, children’s behaviour is nevertheless influenced
by their environment, and interventions for ADHD targeting both biological and parenting factors tend
to be more effective than those targeting biological factors alone. In particular, parental inconsistency
and lack of involvement have been associated with ADHD symptomatology (Ellis & Nigg, 2009).
DIET
There has been much controversy surrounding the possible impact of diet on behaviour problems
in children, and ADHD in particular. Many parents and professionals believe that diet—particularly
artificial additives—have a causal influence on ADHD. It has been argued that the consumption of
artificial sweeteners, colours and preservatives contributes to children becoming more hyperactive.
In response to this view, many parents have tried a variety of diets, called elimination diets, whereby
certain foods or substances are first eliminated and then gradually reintroduced into the child’s diet
to determine their role in producing symptoms. For instance, the Feingold diet is a food-elimination
program developed by the paediatrician Benjamin Feingold to treat symptoms of hyperactivity.
The diet consists of eliminating a number of artificial colours and flavours, aspartame (an artificial
sweetener), some preservatives and certain salicylates (found in a wide range of foods and beverages).
While there is evidence that for some children certain dietary constituents may contribute to
symptoms of ADHD (Pelsser et al., 2009; 2011), in general the evidence points to other causal factors.
The results of a randomised controlled trial found no specific effect of food colourings and preservatives
on ADHD symptoms on objective clinic assessments of symptoms (Bateman et al., 2004). However,
despite this finding, some parents still reported differences in their child’s behaviour with alterations
in diet. A recent meta-analysis found some support for artificial food colour exclusion diets as well as
for fatty acid supplementation but noted that the effects were small and that particularly for trials of
exclusion diets, children were selected on the basis of pre-existing food sensitivities (Sonuga-Barke et
al., 2013). This is a relatively new field of research and it is likely that as more data becomes available,
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better guidelines for individual children will enable

tailoring of individual treatment plans.
Drug therapy is a common approach to the
management of children with externalising disorder
and ADHD; however, research has primarily focused
on children with a diagnosis of ADHD where
psychostimulant medications (e.g., Ritalin) have
been extensively used and shown to be effective
with at least some children. For decades, stimulant
medications such as methylphenidate (Ritalin) and
dextroamphetamine sulfate (Dexedrine) have been
the most common drugs used in the treatment of
ADHD. These stimulants increase the availability
DAL
of dopamine and have been found to reduce the
overactivity, impulsivity and inattention characteristic It has been argued that the consumption of artificial sweeteners,
of individuals with ADHD as well as improving colours and preservatives contributes to ADHD, although more
associated behaviours such as academic performance research is needed to evaluate this hypothesis.
and social functioning. However, the use of
pharmacological approaches calls for caution due to the long-term outcomes of medication trials, such
as the Multimodal Treatment of ADHD (MTA) trial (Molina et al., 2009). The prevailing opinion for
the use of medication for children with ADHD recommends a conservative approach whereby drugs
are used only in combination with some form of psychosocial treatment. Drug therapy provided in
the absence of any psychosocial intervention is rarely considered an adequate treatment. Behavioural
parenting intervention, behavioural classroom management and behavioural peer interventions are well-
established treatments for ADHD (Evans, Owens, & Bunford, 2014).
Specific learning disorder

A specific learning disorder is diagnosed when a child’s academic achievement is below what is specific learning
expected given his/her chronological age and is not accounted for by intellectual disability. Academic disorder
achievement is usually assessed through standardised testing in areas such as reading, mathematics or Disorder
written language. Learning disorders include subtypes of reading, mathematics and written expression. of learning
characterised
The reading subtype is the most common learning disorder and will be described in this section.
by lower than
expected
THE DIAGNOSIS AND EPIDEMIOLOGY OF READING DISORDER performance in a
Reading disorder is characterised by difficulties in reading accuracy, fluency and comprehension that particular area of
are unexpected in relation to the child’s chronological age. To be diagnosed with the disorder, these learning relative
reading problems must not be the result of general developmental disability, intellectual disability, to the child’s
sensory impairment (e.g., vision problems) or lack of access to appropriate education or sociocultural chronological age
opportunities (Breier et al., 2001). and intellectual
Reading disorder is one of the most common childhood disorders, with a prevalence rate of ability.
4–7 per cent (Snowling, 1998). Once established, the condition has a considerable degree of stability, reading disorder
with a study by Smart, Sanson, and Prior (1996) finding little evidence of spontaneous recovery over Learning disorder
a two-year period in 7–8-year-old children with the disorder. In addition, the evidence suggests that involving deficits
persistent reading disorder results in poor school grades, early school leaving and limited employment in reading ability.
opportunities (McGee, Share, Moffitt, Williams, & Silva, 1998). Without intervention, there are costly
and long-ranging negative outcomes for both individuals and society (Smart et al., 1996).
There is a high degree of overlap between reading disorder and behaviour problems, with the literature
focusing on a possible aetiological connection between reading disorder and ADHD in particular. The
comorbidity between reading disorder and ADHD is between 15 and 45 per cent, depending on the
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study (Purvis & Tannock, 2000). In general, the results of studies are consistent with the hypothesis that
the ADHD-type behavioural problems of most children with reading disorder arise as a consequence of
failure to learn rather than ADHD contributing to the development of reading problems.
THE AETIOLOGY AND TREATMENT OF READING DISORDER
heritability There is some evidence for the heritability of reading disorder (Wadsworth, Olson, Pennington, &
Percentage DeFries, 2000). For example, there is a 50 per cent probability of a boy having a reading disability if
indicating the his father had a reading disability (Snowling, 1998).
degree to
There is little evidence for the idea that low general cognitive ability accounts for the development
which genes
contribute to the
of reading disorder. Similarly, while low language ability may account for some children’s reading
development of a difficulties, it may also be a consequence of poor reading ability (McGee, Williams, Moffitt, &
disorder. Anderson, 1989). In contrast to general cognitive and language skills, research suggests that deficits
in phonological awareness, working memory and the speed of processing written language may
contribute to the development of reading disorder (Purvis & Tannock, 2000), each of which will be
considered in turn.
Phonological awareness entails understanding the
sound structure of one’s oral language (Malicky &
Norman, 1999). Phonological limitations may lead
to inefficiencies in working memory, with working
memory defined as a processing resource of limited
capacity involved in the preservation of information
while simultaneously processing the same or
other information (Swanson & Berninger, 1995).
Specifically, difficulties in phonological decoding
may simply take up too much of the available
working memory, and hence lead to inefficient
processing of other components of reading (such as
comprehending the words) (Brady, 1991).
Deficits in working memory may themselves be
a possible cause of reading disorder. For example, in
order to read an unfamiliar word, the child needs to

DAL
sound out the word and, holding all the individual

The treatment of reading disorder is effective for most children of early
primary school age.
sounds in working memory, put them together to
read the entire word as one. If the child’s working
memory is deficient, the process of holding all the parts of the word and then putting it together
becomes much more difficult. In support of the role of working memory deficits in reading disorder,
impairments in verbal working memory have been found to be significantly higher in children with
reading disorder (Willcutt et al., 2001).
In addition to phonological awareness and working memory, limitations in the speed of processing
written language may be a third component in the aetiology of reading disorder. Written language
processing speed refers to the time taken to read aloud words presented in the form of lists (Simon,
Joshi, & Williams, 1999). A review by Compton and Carlisle (1994) identified word reading speed,
particularly in non-word reading (e.g., ‘bim’ or ‘sluck’), as an important factor in differentiating
problem readers from non-problem readers. Slow word recognition creates a bottleneck in the
information-processing system, where the reader’s attention is largely devoted to the identification,
rather than the understanding, of words.
A meta-analysis of interventions for children and adolescents with reading disorder found that
only phonological (i.e., sounding out words) approaches led to significantly improved outcomes
(Galuschka, Ise, Krick, & Schulte-Körne, 2014). It has been found that reading skills continue to
improve well into adolescence if students with a reading disorder pursue opportunities that promote
further development of basic literacy skills (Gillon & Dodd, 1997). In a review of intervention studies,
Torgesen (2000) found that more than 50 per cent of children most at risk for reading failure can be
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helped to learn at approximately normative rates in early primary school, and that only 3–6 per cent
do not respond at all.
Autism spectrum disorder

A major change in the DSM-5 is the consolidation of four previously separate disorders (autistic
disorder, Asperger’s syndrome, childhood disintegrative disorder and pervasive developmental
disorder not otherwise specified) into a single disorder, labelled autism spectrum disorder. This change
reflects a consensus in the literature that the previous categories were often difficult to distinguish.
Autism spectrum disorder is characterised by marked impairments in social communication and social autism spectrum
interaction as well as repetitive behaviours, interests and activities. disorder
Characterised
THE DIAGNOSIS AND EPIDEMIOLOGY OF AUTISM SPECTRUM DISORDER by impairments
Symptoms characteristic of autism spectrum disorder include qualitative impairments in social in social
interaction and social communication such as deficits in social-emotional reciprocity (i.e., the ability communication
to engage with others and share thoughts and feelings), abnormalities in eye contact or an absence of and interaction,
interest in peers. As well as impairments in social interaction and communication, the disorder is also and repetitive
behaviours,
characterised by repetitive and restricted patterns of behaviour. These may entail preoccupation with
interests and
a specific activity such as collecting football statistics, an insistence on sameness in routines, or motor activities.
mannerisms such as body-rocking. Severity levels are also defined (as shown in Table 14.5), which are
designed to assist in making decisions about the level of support required for children.
TABLE 14.5 Autism spectrum disorder severity levels
SEVERITY LEVEL SOCIAL COMMUNICATION RESTRICTED, REPETITIVE BEHAVIOURS
Level 3 Severe deficits in verbal and non-verbal social Inflexibility of behaviour, extreme difficulty
‘Requiring very communication skills cause severe impairments in coping with change, or other restricted/
substantial support’ functioning, very limited initiation of social interactions repetitive behaviours that markedly
and minimal response to social overtures from others. For interfere with functioning in all spheres.
example, a person with few words of intelligible speech Great distress/difficulty changing focus or
who rarely initiates interaction and, when s/he does, action.

makes unusual approaches to meet his/her needs only
and responds to only very direct social approaches.
Level 2 Marked deficits in verbal and non-verbal social Inflexibility of behaviour, difficulty coping
‘Requiring substantial communication skills; social impairments apparent with change or other restricted/repetitive
support’ even with supports in place; limited initiation of social behaviours appear frequently enough to
interactions; and reduced or abnormal responses to be obvious to the casual observer and
social overtures from others. For example, a person who interfere with functioning in a variety
speaks simple sentences, whose interaction is limited to of contexts. Distress and/or difficulty
narrow special interests and who has markedly odd non- changing focus or action.
verbal communication.
Level 1 Without supports in place, deficits in social communication Inflexibility of behaviour causes
‘Requiring support’ cause noticeable impairments. Difficulty initiating social significant interference with functioning
interactions and clear examples of atypical or unsuccessful in one or more contexts. Difficulty
responses to the social overtures of others. May appear switching between activities. Problems
to have decreased interest in social interactions. For of organisation and planning hamper
example, a person who is able to speak in full sentences independence.
and engages in communication but whose to-and-fro
conversation with others fails and whose attempts to make
friends are odd and typically unsuccessful.
Source: Adapted from the Diagnostic and Statistical Manual of Mental Disorders (5th ed.,). Copyright 2013, American Psychiatric Association.
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Children with autism spectrum disorder are defined by two essential core deficits. First, these
children have social communication problems in the form of deficits in social-emotional reciprocity
and difficulty comprehending non-verbal communication (Tanguay, 2000). Second, children with
this disorder demonstrate deficits in ‘theory of mind’, which is the understanding that others have a
perspective that differs from their own (Baron-Cohen, 1995). These core deficits in communication
and theory of mind lead to difficulties in social interaction. For example, infants and young children
with autism spectrum disorder fail to engage in non-verbal social interactions such as joint attention,
which entails the coordination of attention between the infant, another person and an object
(McArthur & Adamson, 1996). They also often have great difficulty in entering play situations and
engaging in cooperative play (Paul, 2003). These children are often withdrawn and do not engage in
social interactions with others.
The prevalence of autism spectrum disorder appears to be about 1 per cent (Baron-Cohen et al.,
2009). Boys outnumber girls by approximately 2:1 (Szatmari, Jones, Zwaigenbaum, & MacLean, 1998).
An alarming rise in the prevalence of autism has been reported in the media, and questions have been
raised about what has led to this ‘epidemic’ of autism. Everything from food additives to vaccines to
various toxins in the environment has been suggested, but none has shown any links to the development
of autism. International data do indeed suggest a rise in prevalence. For example, between 2002 and
2006 the Centers for Disease Control and Prevention in the United States found a 57 per cent rise in the
prevalence of autistic spectrum disorders (Centers for Disease Control and Prevention, 2009). This rise in
prevalence is most likely due to changes in the diagnostic criteria, more consistency in how diagnoses are
made and increased awareness of autism spectrum disorder rather than an actual increase in the disorder’s
occurrence (Bishop, Whitehouse, Watt, & Line, 2008; Fombonne, 2003; Williams et al., 2005).
Approximately 75 per cent of children with autism spectrum disorder have a poor outcome
(including a lack of independent living and unemployment), while the remainder have a good outcome
(Tidmarsh & Volkmar, 2003). Predictors of good outcome include the acquisition of language skills
before age 6, IQ levels above 50 and having an area of greater strength (e.g., some level of skill in
mathematics or music).
THE AETIOLOGY OF AUTISM SPECTRUM DISORDER

There is evidence of a genetic vulnerability for autism and there is about a 60 per cent concordance
concordance rate
Probability that rate for autism in monozygotic twins, meaning that in more than half of cases if one twin is affected the
both members other is also likely to show symptoms of autism (Bailey, Le Couteur, Gottesman, & Bolton, 1995). No
of a twin pair will
specific genes have been identified to date and it is thought that a number of genes act in combination
develop the same
disorder.
to raise vulnerability for autism spectrum disorder.
A range of other biological factors have been proposed as contributing to autism spectrum disorder.
prenatal Prenatal and perinatal insults (such as maternal ill-health during pregnancy) can increase the risk of
The period the disorder. However, the involvement of dietary explanations (e.g., the recommended use of wheat-
occurring before or milk-free diets to prevent autism spectrum disorder) has not been supported (Volkmar, Cook,
birth.
Pomeroy, Realmuto, & Tanguay, 1999). Nor is there support for the idea that the disorder is caused by
perinatal vaccination (Immunization Safety Review Committee, 2004). A small study published in 1998 raised
The period the question of a causal role for the measles-mumps-rubella combination vaccine in the development
occurring around of autism (Wakefield et al., 1998). However, this paper was later retracted by The Lancet, and other
the time of birth. studies have consistently found no support for the link between vaccination and autism. There has
been a recent explosion in studies looking at various physiological explanations for autism spectrum
disorder, such as mitochondrial dysfunction (i.e., the inability to effectively produce the energy our
cells need to function) and inflammation (i.e., part of the body’s response to injury), but outcomes to
date are not conclusive (Rossignol & Frye, 2012).
Another possible causal factor for autism spectrum disorder, including the social and emotional
problems that characterise the disorder, is extremely severe social deprivation. For instance, a study of
Romanian orphans who had been adopted in the United Kingdom, conducted by O’Connor, Bredenkamp,
and Rutter (1999), found a higher than expected prevalence rate of autism spectrum disorder. These
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children had been exposed to severely deprived conditions, both physically and psychologically,
including very limited contact with other children and adults, and minimal emotional support from carers.
This deprivation is thought to have led to the occurrence of autism spectrum disorder in some of these
children. Such extreme circumstances, however, cannot account for the majority of cases of the disorder.
THE TREATMENT OF AUTISM SPECTRUM DISORDER

Early intervention for children with autism spectrum disorder is very important to ensure the highest
level of adaptation and functioning possible (Rogers, 1996). The aim of interventions is to help the
child develop better social and emotional relationships, learn better communication skills, and to
decrease stereotypic behaviours such as head banging.
Behaviour modification programs used either alone or in combination have been found to be
effective in improving the functioning of children with autism spectrum disorder (Wong, et al.,
2015). These begin with an analysis of the child’s environment to assess the environmental conditions
and contingencies that can be used to help the child acquire skills. As just one example, positive
reinforcement such as praise or tangible rewards is used to encourage desirable behaviour. Such
interventions can significantly improve communication and social skills, reduce challenging behaviour
and enhance independent living skills (Wong et al., 2015). Pharmacotherapy may also be combined
with behavioural treatment, although the research on medication for the treatment of autism is limited.
Pharmacotherapy may be used to target specific problems such as aggression towards the self or
others, irritability, hyperactivity and repetitive behaviour (Masi, 2004).
Intellectual disability
Intellectual disability comprises a heterogeneous group of disorders with multiple causes, all of which intellectual
involve deficits in intellectual functioning and adaptive functioning. disability
Group of
THE DIAGNOSIS AND EPIDEMIOLOGY OF INTELLECTUAL DISABILITY disorders
The previous edition of the DSM referred to intellectual disability as mental retardation (APA, 2000). characterised
In the DSM-5 (APA, 2013), intellectual disability comprises: by deficits in
intellectual
∙ deficits in intellectual functioning such as reasoning, problem solving, planning, abstract thinking, and adaptive
judgment, academic learning and learning from experience. These deficits are determined in part functioning.
by the individual’s performance on an intelligence test, with scores below 65–75 falling within the
intellectually disabled range
∙ deficits in adaptive functioning that result in a failure to meet developmental and sociocultural
standards for personal independence and social responsibility. Table 14.6 provides information on
the different severity levels of intellectual disability based on impaired adaptive functioning
∙ the onset of these deficits in intellectual and adaptive functioning in childhood.
The adaptive functioning skills are assessed by structured tests, most commonly the Vineland
Adaptive Behaviour Scale. This instrument assesses the age-appropriate personal and social skills
necessary for everyday living. It includes the domains of communication (e.g., how well the child
can express his/her needs), daily-living skills (e.g., hygiene), socialisation (e.g., coping skills) and
motor skills. pervasive
The estimated prevalence of intellectual impairment is approximately 1 per cent (Szymanski & developmental
King, 1999). Approximately 85 per cent of those with the condition have an IQ within the mild range disorders
of intellectual impairment. More boys are diagnosed with intellectual impairment than girls (Murphy, Disorders
characterised
Yeargin-Allsopp, Decoufle, & Drews, 1995). Intellectual impairment co-occurs with a wide range of
by severe
disorders including epilepsy, cerebral palsy, sensory deficits and pervasive developmental disorders and persisting
(Murphy, Boyle, Schendel, Decoufle, & Yeargin-Allsopp, 1998). Intellectually impaired children are impairment in
also at significantly increased risk of various types of psychological disorders, including anxiety and several areas of
depression, with up to 70 per cent of these children thus affected (Dykens, 2000). development.
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TABLE 14.6 The DSM-5 categories of intellectual disability
SEVERITY
LEVEL CONCEPTUAL DOMAIN SOCIAL DOMAIN PRACTICAL DOMAIN
Mild For preschool children, there Compared with typically The individual may function age-
may be no obvious conceptual developing age-matched peers, appropriately in personal care. Individuals
differences. For school-age children the individual is immature in social need some support with complex daily
and adults, there are difficulties in interactions. For example, there living tasks in comparison to peers. In
learning academic skills involving may be difficulty in accurately adulthood, supports typically involve
reading, writing, arithmetic, time or perceiving peers’ social cues. grocery shopping, transportation, home
money, with support needed in one Communication, conversation and childcare organising, nutritious
or more areas to meet age-related and language are more concrete food preparation, and banking and
expectations. In adults, abstract or immature than expected for money management. Recreational
thinking, executive function (i.e., age. There may be difficulties skills resemble those of age-matched
planning, strategising, priority regulating emotion and behaviour peers, although judgment related to
setting and cognitive flexibility) in age-appropriate fashion; these wellbeing and organisation around
and short-term memory, as well as difficulties are noticed by peers in recreation requires support. In adulthood,
functional use of academic skills social situations. There is limited competitive employment is often seen in
(e.g., reading, money management), understanding of risk in social jobs that do not emphasise conceptual
are impaired. There is a somewhat situations; social judgment is skills. Individuals generally need support
concrete approach to problems immature for age and the person to make healthcare decisions and legal
and solutions compared with age- is at risk of being manipulated by decisions, and to learn to perform a
matched peers. others (gullibility). skilled vocation competently. Support is
typically needed to raise a family.
Moderate All through development, the The individual shows marked The individual can care for personal
individual’s conceptual skills lag differences from peers in social needs involving eating, dressing,
markedly behind those of peers. and communicative behaviour elimination and hygiene as an adult,
For preschoolers, language and across development. Spoken although an extended period of teaching
pre-academic skills develop language is typically a primary and time is needed for the individual
slowly. For school-age children, tool for social communication but to become independent in these areas
progress in reading, writing, is much less complex than that of and reminders may be needed. Similarly,
mathematics and understanding peers. Capacity for relationships participation in all household tasks can
of time and money occurs slowly is evident in ties to family and be achieved by adulthood, although an
across the school years and is friends and the individual may extended period of teaching is needed
markedly limited compared with have successful friendships and ongoing supports will typically occur
that of peers. For adults, academic across life and sometimes for adult-level performance. Independent
skill development is typically at romantic relations in adulthood. employment in jobs that require limited
an elementary level and support However, individuals may not conceptual and communication skills can
is required for all use of academic perceive or interpret social cues be achieved but considerable support
skills in work and personal life. accurately. Social judgment from co-workers, supervisors and others
Ongoing assistance on a daily and decision-making abilities is needed to manage social expectations,
basis is needed to complete are limited and caretakers job complexities and ancillary
conceptual tasks of day-to-day must assist the person with responsibilities such as scheduling,
life, and others may take over life decisions. Friendships with transportation, health benefits and
these responsibilities fully for the typically developing peers are money management. A variety of
individual. often affected by communication recreational skills can be developed.
or social limitations. Significant These typically require additional
social and communicative support supports and learning opportunities over
is needed in work settings for an extended period of time. Maladaptive
success. behaviour is present in a significant
minority and causes social problems.
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SEVERITY
LEVEL CONCEPTUAL DOMAIN SOCIAL DOMAIN PRACTICAL DOMAIN
Severe Attainment of conceptual skills is Spoken language is quite The individual requires support for
limited. The individual generally limited in terms of vocabulary all activities of daily living, including
has little understanding of and grammar. Speech may be meals, dressing, bathing and
written language or of concepts single words or phrases and elimination. The individual requires
involving numbers, quantity, time may be supplemented through supervision at all times. The individual
and money. Caretakers provide augmentative means. Speech and cannot make responsible decisions
extensive supports for problem communication are focused on regarding wellbeing of self or others.
solving throughout life. the here and now within everyday In adulthood, participation in tasks at
events. Language is used for home, recreation and work requires
social communication more ongoing support and assistance. Skill
than for explication. Individuals acquisition in all domains involves long-
understand simple speech term teaching and ongoing support.
and gestural communication. Maladaptive behaviour, including
Relationships with family self-injury, is present in a significant
members and familiar others are minority.
a source of pleasure and help.
Profound Conceptual skills generally The individual has very limited The individual is dependent on others
involve the physical world rather understanding of symbolic for all aspects of daily physical care,
than symbolic processes. The communication in speech health and safety, although he/she may
individual may use objects in or gesture. He or she may be able to participate in some of these
goal-directed fashion for self- understand some simple activities as well. Individuals without
care, work and recreation. instructions or gestures. The severe physical impairments may assist
Certain visuospatial skills, such as individual expresses his/her with some daily work tasks at home,
matching and sorting based on own desires and emotions like carrying dishes to the table. Simple
physical characteristics, may be largely through non-verbal, non- actions with objects may be the basis of
acquired. However, co-occurring symbolic communication. The participation in some vocational activities
motor and sensory impairments individual enjoys relationships with high levels of ongoing support.
may prevent functional use of with well-known family members, Recreational activities may involve,
objects. caretakers and familiar others, for example, enjoyment in listening

and initiates and responds to music, watching movies, going
to social interactions through out for walks or participating in water
gestural and emotional cues. Co- activities, all with the support of others.
occurring sensory and physical Co-occurring physical and sensory
impairments may prevent many impairments are frequent barriers to
social activities. participation (beyond watching) in home,
recreational and vocational activities.
Maladaptive behaviour is present in a
significant minority.
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders (5th ed.,). Copyright © 2013, American Psychiatric Association.
All Rights Reserved.
According to the DSM-5 diagnostic criteria for intellectual disability, the onset must occur in the
developmental period, meaning that the intellectual and adaptive deficits are present during childhood
or adolescence. The age of onset depends somewhat on the causes of intellectual impairment (e.g.,
some biological causes take time to develop and have an adverse impact on intellectual functioning).
The course is heterogeneous and depends on the presence of biomedical factors (e.g., metabolic
disorders) and psychosocial factors (e.g., access to therapy) (Szymanski & King, 1999). For example,
if a metabolic disorder is present it may shorten the individual’s lifespan, while access to therapy may
improve quality of life and reduce mortality.
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THE AETIOLOGY OF INTELLECTUAL DISABILITY

There is a wide range of causes for intellectual disability and, generally, the more severe the
impairment the more likely it is that a cause can be determined. In approximately 60 per cent of cases
of severe intellectual impairment there is a known cause, versus 20–24 per cent for children with mild
intellectual disability (Flint & Wilike, 1996). A thorough assessment in an attempt to identify the
cause of intellectual disability is essential, since the condition may be treatable or it may be associated
with a heightened risk for medical conditions (e.g., the intellectual impairment in Down syndrome is
associated with cardiovascular problems) (Szymanski & King, 1999).
More than 500 genetic conditions (e.g.,
Down syndrome) are associated with intellectual
disability and contribute the largest proportion
of known causes (Flint & Wilike, 1996; Yeargin-
Allsopp, Murphy, Cordero, & Decoufle, 1997).
Exposure to toxic agents such as cigarette
smoke and alcohol during pregnancy can also
cause intellectual disability (Drews, Murphy, &
Yeargin-Allsopp, 1996; Streissguth, Barr, &
Sampson, 1990). Similarly, perinatal conditions
such as maternal infection and low birth weight,
as well as postnatal causes, including exposure
to environmental contaminants such as lead, are
known to contribute to intellectual disability
(Murphy et al., 1998). Finally, traumatic injury
DAL
to the head is a factor leading to impairment

Down syndrome is a common cause of intellectual disability, which occurs (Szymanski & King, 1999).
when a third copy of chromosome 21 is present in the genome.
postnatal THE TREATMENT OF INTELLECTUAL DISABILITY

The period Interventions for those with an intellectual disability involve a number of components. Following
occurring after assessment and diagnosis, it is important to treat any underlying condition. For example, phenylketonuria
birth.
(which is a metabolic disorder where the body lacks the enzyme necessary to metabolise or break
down certain amino acids) requires early intervention to reduce the impact on the infant. Secondly,
early intervention including physical therapy (e.g., motor coordination skills), occupational therapy
(e.g., toileting skills) and speech therapy, as well as family support, are important to assist in
improving the individual’s quality of life and reducing the stress for families. It is also important to
identify any associated or co-occurring physical conditions, such as epilepsy, which require treatment
in their own right. Finally, any mental health problems need to be identified and treated appropriately
(Szymanski & King, 1999). This includes ongoing assessment and support for the child to monitor for
externalising any emerging symptoms or mental health problems that develop as the child matures.
disorders
Broad
categorisation
of childhood LO 14.4 Externalising disorders
disorders
that includes Externalising disorders are described as problems of under-control, where behaviours are directed at
disorders others (Reynolds, 1992). These types of behaviours are seen by others as oppositional, non-compliant,
characterised attention seeking and disruptive. While impairing the child’s functioning, these disorders also
by problems of
impact significantly on parents and siblings, on teachers and classrooms, as well as on the broader
under-control,
where behaviours neighbourhood and community setting. For example, if a child refuses to do what s/he is asked and
are directed at becomes angry and loud when not getting his/her own way in a classroom context, this is likely to have
others (such as a negative effect not only on that child’s learning capacity but also on the amount of time and attention
conduct disorder). the teacher can devote to other children and the extent to which other children are able to stay on task
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and continue learning while the disruptions are occurring. The disorders falling under the category of oppositional
externalising disorders include oppositional defiant disorder and conduct disorder and are classified in defiant disorder
the DSM-5 under the heading ‘Disruptive, Impulse-Control and Conduct Disorders’. Disorder
of chronic
misbehaviour in
children marked
The diagnosis and epidemiology of oppositional defiant disorder by belligerence,
Oppositional defiant disorder is characterised by a persistent pattern of angry/irritable mood irritability and
(e.g., often losing their temper), argumentative/defiant behaviour (e.g., not following instructions, defiance.
actively defying rules or deliberately annoying others) and vindictiveness (e.g., being spiteful) conduct disorder
(APA, 2013). It involves difficulty regulating emotion (e.g., controlling one’s temper) and Disorder marked
a negative affective style (e.g., blaming others and being easily annoyed by others) (Baving, by chronic
Laucht, & Schmidt, 2000). disregard for the
While the DSM-5 provides some guidance on expected levels of such behaviours in typically rights of others,
developing children, when making a diagnosis of oppositional defiant disorder it is critical to take including specific
behaviours such
into account the child’s developmental stage and gender, and the environment in which the child is as stealing, lying
growing up. Some behaviour is normative at different ages, such as temper tantrums in very young and engaging in
children (Egger & Angold, 2006). In addition, the same type of disturbed behaviour may look different acts of violence.
in children of varying age. For example, a preschooler is likely to steal lollies or toys, whereas an older
child might steal video games or money (Keenan & Wakschlag, 2004). In terms of gender, defiance
in boys may be more active (e.g., arguing), while in girls it may be more passive (e.g., ignoring)
(Ohan & Johnston, 2005). In addition, in order to meet criteria for oppositional defiant disorder, the
behaviours must occur across different settings and situations (i.e., home, school and the community).
Thus, all of these factors point to the need for using multiple forms of assessment (e.g., interviews,
questionnaires and direct observations of the child’s behaviour) and multiple sources of information
(e.g., child, parent and teacher) in order to gain the most complete picture of the child’s difficulties
(Owens & Hoza, 2003), as significant differences between sources have been demonstrated in the
literature (Munkvold, Lundervold, Lie, & Manger, 2009).
Oppositional defiant disorder is one of the most common childhood diagnoses, affecting up to
approximately 3 per cent of all children (Canino, Polanczyk, Bauermeister, Rohde, & Frick, 2010) and up
to 8 per cent of preschoolers (Lavigne, LeBailly, Hopkins, Gouze,
& Binns, 2009). In an extensive review, Boylan, Vaillancourt,

Boyle, and Szatmari (2007) found that the prevalence of
oppositional defiant disorder reported in community samples
ranged from 2.6–15.6 per cent, and in clinical samples from
28–65 per cent. The wide range in prevalence rates is due to
differences across studies in the methods used to assess the
disorder, such as differences in the source of information used
(e.g., parent interview versus clinical diagnostic interview).
Oppositional defiant disorder is more common in boys, with a
ratio of boys to girls of approximately 1.6:1 (Demmer, Hooley,
Sheen, McGillivray, & Lum, 2017). The disorder can occur
during any stage of childhood but is most commonly diagnosed
during middle childhood.
Despite popular myths that children simply grow out of
‘naughty’ behaviour, research has demonstrated the stability of
oppositional defiant disorder over time in the preschool period
(Speltz, McClellan, DeKlyen, & Jones, 1999) as well as into the
iSTOCK
primary school years (Maughan, Rowe, Messer, Goodman, &

Meltzer, 2004) and even into adulthood (Burke, Rowe, & Oppositional defiant disorder is characterised by a
Boylan, 2014). Research has suggested that there is a slight persistent pattern of negativistic, spiteful, irritable and non-
increase in the prevalence of oppositional defiant disorder in compliant behaviour.
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adolescence (Maughan et al., 2004). The longer the disorder persists, the more likely that the child will
also develop other conditions, including attention-deficit/hyperactivity disorder, anxiety disorders,
depressive disorders and early substance use (King, Iacono, & McGue, 2004; Lavigne et al., 2001). In
longitudinal studies, oppositional defiant disorder appears to be part of the developmental history of a
wide range of disorders in adulthood (Copeland, Shanahan, Costello, & Angold, 2009).
The aetiology of oppositional defiant disorder

A broad array of risk factors for oppositional defiant disorder have been identified, including
biological, psychological and social factors (Bradley & Mandell, 2005).
BIOLOGICAL AND PSYCHOLOGICAL FACTORS

androgen Biologically, there is some evidence of alterations in androgen (a hormone related to aggressiveness) in
Substance (such children with the disorder (van Goozen et al., 2000). Differences in patterns of frontal brain activation
as testosterone) posited to be the biological basis of a negative affective style have also been demonstrated in children
producing male
with oppositional defiant disorder compared to healthy controls (Baving et al., 2000). There is some
characteristics.
evidence of autonomic under-arousal in preschoolers with the disorder (similar to adolescents and
adults with externalising disorders), which may contribute to children seeking to increase their arousal
through problem behaviours (Crowell et al., 2006). Finally, traumatic brain injury has been associated
with the development of oppositional defiant disorder symptomatology (Max et al., 1998). In terms
of psychological factors, difficult temperament (e.g., a child who is irritable or difficult to settle) as
well as problems with understanding social cues (e.g., whether a facial expression indicates anger or
surprise) have been found to be important risk factors for oppositional defiant disorder (Bradley &
Mandell, 2005).
PARENTING PRACTICES
Most emphasis in understanding the aetiology of oppositional defiant disorder has been placed on
parenting practices. In particular, it has been suggested that parent behaviours, along with other
aspects of the family environment, may account for some of the differences in the timing, development
and course of child behaviour problems (Patterson & Bank, 1989). There is a strong and consistent
line of evidence suggesting that environmental influences within the family environment play a role
in the development of oppositional defiant disorder, and externalising disorders more broadly (Burt,
2009; Petitclerc, Boivin, Dionne, Zoccolillo, & Tremblay, 2009). Parents of non-compliant, aggressive
children are characterised as being highly punitive and critical of their children and more likely to
attribute their children’s misbehaviour to more dispositional, intentional and stable characteristics of
the child (e.g., ‘He’s always doing hurtful things to me because he’s mean and that’s never going
to change’) compared to parents of non-problem children (Rubin, Stewart, & Chen, 1995). Another
parental behaviour correlated with externalising behaviour problems is the use of restrictive control
(Weiss, Dodge, Bates, & Pettit, 1992). Restrictive control entails behaviours intended to stop or
punish the child such as giving negative instructions (i.e., telling the child what not to do rather than
the desired behaviour), removing objects from the child, scolding and smacking. Restrictive control
can be contrasted with authoritative parenting, where parents use assertive discipline in the context of
a warm, loving family environment.
INTERACTION BETWEEN PARENT AND CHILD

Rather than focusing solely on the behaviour of the parent, other approaches focus on the interactions
between the parent and child. The dominant model in this regard is Patterson’s (1982) coercive
processes model. In essence, the model proposes that parents and children engage in progressively
more coercive interactions with each other through learning processes (i.e., patterns of reinforcement)
involved for both parent and child. For example, a child might respond to an instruction from his/her
mother by refusing to follow the instruction and throwing a tantrum. The child’s mother may at this
point, to keep the peace, withdraw the instruction (thereby reinforcing the child’s tantrum behaviour),
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leading to the child settling down (thereby reinforcing the mother’s giving in to the child). Over time,
in response to the child’s increasing defiance, the mother may increase her insistence that the child
comply, which in turn results in the child increasing the volume of his/her protests until the mother
gives in. The parent and child thus become locked into a cycle of increasing conflict and coercion. The
model also incorporates a range of variables that can have a negative impact on parental discipline,
including poor parental problem-solving skills, parental arousal, family stress, illness, poverty,
unemployment, marital conflict and divorce, psychiatric disturbance in the parents, and parental drug
and alcohol abuse. For example, if the mother is depressed she may lack the energy and motivation to
ensure that her child complies with her instructions.
The diagnosis and epidemiology of conduct disorder

Conduct disorder is characterised by a persistent pattern of violation of rules and the rights of others,
thought to develop from earlier oppositional defiant disorder and to be a precursor to adult criminality and
antisocial personality disorder (APA, 2013). Behaviours characteristic of conduct disorder include stealing,
fighting with others, being cruel to people or animals, destroying property or playing truant from school.
Conduct disorder is more common in boys than girls (Maughan et al., 2004). The prevalence rate
of the disorder across childhood is approximately 3 per cent (Canino et al., 2010), but may be as
high as 6 per cent in adolescence (Ford, Goodman, & Meltzer, 2003). Conduct disorder is defined
as having two subtypes: early onset (prior to age 10) and late onset (11 years or older) (Lahey et al.,
1998). However, this pattern is most characteristic of boys. For girls there is some evidence that the
late onset subtype is the only course (Loeber, Burke, Lahey, Winters, & Zera, 2000). In general, there
are low rates of conduct disorder in early childhood, with rates rising slowly for boys into adolescence.
For girls the risk remains low until early adolescence.
Several longitudinal studies have shed light on the development of conduct disorder. These
include the Dunedin Study (dunedinstudy.otago.ac.nz), a seminal longitudinal study recognised for
its immense contributions to the understanding of child and adolescent psychopathology, and the
Australian Temperament Project (www.aifs.gov.au/atp). Both of these studies are ongoing and have
examined various aspects of child development. The findings from these studies demonstrate that
problem behaviours are widespread during the adolescent period (13–18 years). For example, in the
Australian Temperament Project, cigarette and alcohol use were common among 17–18-year-olds,
with 39 per cent and 85 per cent respectively using these substances. However, marijuana use was lower
(19%). Property offences were relatively common, with approximately 10–20 per cent of adolescents
engaging in theft or vandalism. Up to 34 per cent of 12–14-year-olds had been involved in fighting.
Both studies have identified two groups of children on the basis of the frequency and range of
antisocial behaviour. The first group consists of those children who did not exhibit antisocial behaviour
until the early adolescent years (late-starter or experimental group). The second group shows
persistent antisocial and conduct behaviour from early childhood (persistent or early-starter group)
(Moffitt, 1993). What is interesting about the persistent group is that, looking back, these children
could be differentiated from others on the basis of a number of characteristics (e.g., temperamental
characteristics such as negativity, behaviour problems, social competence, parenting practices and
family relationships) by about the age of 5–6 years. Their antisocial behaviour continued to worsen
over time and, while there was some evidence of a levelling off or reduction in these behaviours during
late adolescence, there were continuing high levels of problem behaviour. The majority of adolescents
in the persistent group continued to engage in antisocial behaviour into early adulthood (Smart et al.,
2005). The experimental group could be distinguished from the no/low antisocial behaviour children
only at about the age of 12–13, and during adolescence this group resembled the persistent group
(Vassallo et al., 2002). However, towards the end of adolescence, the experimental group showed a
reduction in antisocial behaviour compared to the persistent group, and this reduction continued into
young adulthood. The differences in problem behaviours between the low/non-antisocial, experimental
and persistent groups over the course of childhood and adolescence are shown in Figure 14.1.
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70
Persistent vs low
60
Proportion of variables on which

Experimental vs low
groups significantly differ (%)

50
40
30
20
10
0
0 –1 1–2 2 –3 3–4 5–6 7– 8 9 –10 11–12 12 –13 13 –14 15 –16 17 –18
Age (years)
FIGURE 14.1 Differences in the proportion of problems between the persistent and low/non-antisocial groups
and between the experimental and low/non-antisocial groups throughout childhood and adolescence
Source: From Smart et al. (2003). Patterns and precursors of adolescent antisocial behaviour: Types, resiliency and environmental
influences. Second report. Melbourne: Australian Institute of Family Studies.
The aetiology of conduct disorder

The presence of oppositional defiant disorder and attention-deficit/hyperactivity disorder during
childhood is often a precursor to conduct disorder, although not all children with these conditions go
on to develop conduct disorder (Mannuzza, Klein, Abikoff, & Moulton, 2004). Clearly, other variables
play a role, some of which are similar to those for oppositional defiant disorder, and some of which
are modifiable by intervention.
BIOLOGICAL AND PSYCHOLOGICAL FACTORS

In terms of biological factors, there does appear to be a common genetic element to conduct disorder,
oppositional defiant disorder and attention-deficit/hyperactivity disorder (Tuvblad, Zheng, Raine, &
Baker, 2009). Another biological factor may be the low cortisol levels that have been found to
characterise boys who show persistent patterns of conduct behaviour, with cortisol levels thought
to underlie aggression (McBurnett, Lahey, Rathouz, & Loeber, 2000). Similarly, higher levels of
androgen hormones have also been associated with conduct disorder (Dorn et al., 2009).
Psychological factors that may be involved in the development of conduct disorder include
temperamental characteristics in young children, such as negativity (e.g., crying and complaining),
volatility (e.g., temper outbursts) and low persistence (e.g., giving up on tasks when they are perceived
as too hard), which are associated with an increased risk of later conduct problems (Vassallo et al.,
2002). Furthermore, callous-unemotional personality traits have also been linked to the development
and severity of conduct disorder. These traits are characterised by manipulative behaviour and a lack
of guilt, remorse and empathy (Dadds, Fraser, Frost, & Hawes, 2005).
SOCIAL FACTORS
In terms of social factors, poor social skills (e.g., endorsing more aggressive/antisocial solutions to
conflict situations and demonstrating lower assertiveness) are common in conduct disordered children
(Dunn, Lochman, & Colder, 1997). Associating with antisocial peers and peer rejection contribute
significantly to the development of conduct disorder (van Lier, Vuijk, & Crijnen, 2005). In fact, it
appears that associating with antisocial peers is one of the most important predictors of conduct
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problems (Vassallo et al., 2002). Family factors including family structure (e.g., single parent), family
relationships (e.g., marital conflict) and certain parenting practices are all associated with conduct
disorder. Concerning the latter, parents of antisocial adolescents tend to monitor and supervise their
teenagers less, demonstrate less warmth and use harsher discipline (Vassallo et al., 2002). Difficulties
in the parent–child relationship and less advantaged family environments are important risk factors
for those children exhibiting antisocial behaviour (particularly violent behaviour) from a young age
(Loeber, Burke, & Pardini, 2009; Smart et al., 2003).
The treatment and prevention of externalising disorders

A substantial literature has developed on the management of externalising problems in children.
However, only a relatively small number of intervention approaches have been shown to be
effective in reducing these problems. Given what is known about the risk factors contributing to the
development of conduct problems, various psychosocial treatments have been developed to target
them. These include:
∙ interventions designed to improve parenting skills and family relationships (including parenting
interventions, attachment-based approaches and family therapy)
∙ interventions designed to improve children’s social relationships with others and their problem-
solving skills
∙ school-based interventions designed to improve classroom and playground behaviour at school
∙ pharmacological approaches.
PARENTING INTERVENTIONS
The family provides the first and most important social, emotional, interpersonal, economic and
cultural context for human development and, as a result, family relationships have a pervasive influence
on the wellbeing of children. Findings from behaviour genetics research, as well as epidemiological
correlational
studies, correlational studies and experimental studies, all support the notion that parenting practices study
have a major influence on children’s development (Collins, Maccoby, Steinberg, Hetherington, & Type of study in
Bornstein, 2000). Thus, it is not surprising that the treatment approach with the strongest support for which researchers
treating problem behaviours in children is parent management training.
assess only the

This approach is derived from social learning theory and cognitive-behavioural therapy principles relationship
(Patterson, 1982). It typically involves training parents to use a variety of positive parenting strategies between two
such as praise and attention for desired behaviour, providing rewards contingent upon the child variables and do
not manipulate
engaging in desired behaviours (e.g., star charts), using clear and calm instructions, and employing
one variable to
fair and age-appropriate rules. In contrast to punitive parenting practices, parents are taught to apply determine its
a number of consistent consequences for problem behaviours, such as response cost (i.e., removing effect on another
privileges for breaking rules), planned ignoring (i.e., not providing attention for minor, attention- variable (as in
seeking behaviour), quiet time (i.e., removal of the child to the edge of an activity following an experimental
inappropriate behaviour) and time out (i.e., removing the child from the situation where the problem study).
has occurred). The intervention can be delivered to parents either on an individual basis or in a group experimental
setting over an 8–12 session period. study
Two of the best known parenting programs are the ‘Incredible Years’ developed by Carolyn Type of study that
Webster-Stratton at the University of Washington (Webster-Stratton, 1990) and the ‘Triple P-Positive can address the
Parenting Program’ developed by Matthew Sanders and colleagues at the University of Queensland issue of causality
(Sanders, 1999). An overview of the session content of the Triple P-Positive Parenting Program given that the
is shown in Table 14.7. Both of these approaches have been subjected to a number of randomised independent
variable is directly
controlled trials with young preschool-aged children and have demonstrated sustained improvements
manipulated so
in children’s behaviour and adjustment compared with control families on a treatment waiting list. that its effect on
There is less evidence concerning the beneficial effects of parent management training with older the dependent
children and teenagers, however, as fewer studies have been conducted with older children, and variable can be
problem behaviours may be more established in them, making change more difficult. examined.
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TABLE 14.7 Overview of the session content for the Triple P-Positive Parenting Program
SESSION NUMBER CONTENT DURATION
1. Intake interview • Nature and history of presenting problem 60 mins

• Associated problems
• Developmental, social and relevant family history
• Parent/s’ perceptions of the problem
• Keeping track of children’s behaviour
2. Observation and sharing of • Completion of intake interview/s 60 mins

assessment findings • Observation of parent–child interaction
• Review of assessment results
• Causes of child behaviour problems
• Goals for change and intervention negotiation
3. Promoting children’s • Principles of positive parenting 60 mins

development • Developing positive relationships with children
• Encouraging desirable behaviour
• Teaching new skills and behaviours
4. Managing misbehaviour • Managing misbehaviour 60 mins

• Developing parenting routines
• Finalising behaviour charts (e.g., reward charts where children earn
stamps, stickers or points for engaging in desired behaviours)
5. Practice session 1 • Practice task 40 mins

• Self-evaluation and feedback
• Goal-setting
• Other issues
• Goals for between-session practice


• Goal-setting
• Other issues

• Goal-setting
• Other issues
8. Planned activities training • Update on progress 60 mins

• High-risk situations
• Planned activities routines (which involves planning how to manage
difficult situations ahead of time to prevent behaviour problems from
occurring in these high-risk situations)
9. Implementing planned • Encouraging independent play 60 mins

activities • Further planning
• Engaging activity (which involves the use of positive parenting
strategies to promote children’s engagement in the activity)
• Getting ready to go out
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SESSION NUMBER CONTENT DURATION
10. Closure session • Family survival tips (e.g., working as a team, with parents avoiding 60 mins
arguments in front of the child)
• Phasing out the program
• Progress review
• Maintenance of change
• Problem solving for the future
• Future goals
• Final assessment
The training of practitioners implementing parenting programs

To ensure the best outcomes from parenting programs, a high standard of training for the practitioners
of these programs is essential. Thus the trainers of practitioners are Masters- or PhD-level professionals
(mainly clinical or educational psychologists). All Triple P training is coordinated by Triple P
International, which has a network of trainers around the world. By having a central body organise
training in this way, practitioners are assured of being trained in the actual content of the program
and being made aware of the latest developments in the program as supported by research. It also
ensures that the same training materials (e.g., DVDs demonstrating core consultation skills) are used
for all practitioners. Maintaining control over the initial training of practitioners in this way, while not
without its challenges (e.g., when the demand for a program occurs in different cultural contexts), is
achievable and helps to promote quality standards.
The training of practitioners is also enhanced if the delivery of the courses is customised to a
certain extent to cater for the special characteristics of the practitioners undergoing training. This can
be accomplished by ensuring trainers are familiar with the local context, including where different
practitioners work, their role in providing parenting support, their professional backgrounds and their
level of experience. Tailoring can involve the selection of relevant (to the audience) case examples
and illustrations, as well as drawing upon the knowledge, experience and expertise of the practitioners
themselves.
In addition to offering some flexibility in the training process, effective training highlights the
need to provide some flexibility when implementing the parenting program. The training process
encourages practitioners to work collaboratively with parents and to be responsive to client needs and
the situational context while preserving the key or essential elements of the program (Mazzucchelli &
Sanders 2010).
Large-scale implementation of parenting programs
Much has been learnt about how to most effectively increase parenting support in communities.
Detailed guidelines for implementing parenting programs on a larger scale have been developed and
are being used in a number of studies around the world. Several criteria need to be met for the approach
to be effective, including:
∙ using parenting programs that work
∙ using cost-effective programs
∙ ensuring the program is culturally relevant to where it is being implemented
∙ establishing achievable rates of participation by community members
∙ having a plan for evaluating the effectiveness of the intervention.
Each of these will be dealt with in turn.
Parents prefer parenting programs that have evidence that they actually work (Sanders, Haslam,
Calam, Southwell, & Stallman, 2011). However, parents vary greatly in the level and type of support
that they require from a parenting program or are prepared to participate in. To ensure that the diverse
needs of parents are addressed, a population-level parenting strategy requires that different evidence-
based interventions are available.
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A public health approach to parenting support can be a cost-effective approach to prevention.

Parenting programs that achieve maximum benefits while minimising costs ensure that families of all
socioeconomic groups and across all cultures have access to the program.
Parenting programs implemented on a large scale need to be acceptable to ethnically and
socioeconomically diverse parents. To ensure that the program is culturally acceptable, it is important
for program developers to communicate with parents directly rather than to rely exclusively on
the views of professionals serving minority populations, who may actually hold views on cultural
acceptability that differ from the parents they serve (Morawska et al., 2011).
Careful attention needs to be given to ensuring that participation targets are set at the outset.
This ensures the training of requisite numbers of practitioners who have the capacity, interest and
organisational support to implement the program effectively. The resources required to implement
the program depend on, for example, the number of sessions required in the program and the type of
practitioner who delivers the program (e.g., nurses, psychologists, social workers, teachers, family
support workers, doctors).
Importantly, parenting programs delivered on a large scale need to be evaluated to ensure they
have had a beneficial impact. Determining reliable ways of assessing the prevalence and incidence
rates of child problems and parenting practices targeted by a parenting program is a major challenge.
Several approaches have been used to assess the widescale effects of parenting programs. These
include accessing data at a local government level to track rates over time of child abuse and neglect
cases, hospitalisations and emergency room visits due to maltreatment, and out-of-home placements
(Prinz & Sanders, 2007). There is a need for a range of brief, reliable, valid and change-sensitive
measures of parenting for use in public health interventions. Such measures need to be low cost; easy
to use, score and interpret; have low literacy demands; and be easy to translate into different languages.
ATTACHMENT-BASED APPROACHES TO PARENTING

Originating with the ideas of John Bowlby (1982), attachment theory emphasises parental attunement
to the child’s emotional cues during early caregiving years as a means to promoting optimal social-
emotional and cognitive development (for an overview, see Karen, 1994). Attachment research over
the past 30 years or so has generally shown that children whose caregivers accurately perceived and
sensitively responded to their emotional cues during early caregiving years have been more likely to
express their emotional distress directly to the caregiver and develop greater capacities for coping in
response to distress. Attachment-based approaches to parenting focus on improving the quality of the
parent’s relationship with the child. These approaches are mostly derived from psychodynamic theories
and emphasise that disturbances in the child’s attachment to parental caregivers (insecure attachment)
are the basis for the child’s conduct problems. At present there is little evidence showing that insecure
attachment is present in the majority of children with conduct problems. Few empirically based
evaluations have been conducted to establish whether attachment-based approaches alone are effective
in changing behaviour. Attachment-based concepts have been most effective when they are integrated
into more behaviourally oriented parenting interventions, such as Incredible Years and Triple P.
FAMILY THERAPY
A range of family therapy approaches target families as a whole and recognise that families are a system
comprising many working parts. Family therapists share a belief that involving families in solutions
often benefits clients, regardless of whether the clients consider a problem an ‘individual’ or ‘family’
issue. Family involvement is commonly accomplished by direct participation in the therapy session.
Functional Family Therapy is a short-term (approximately 30 hours), family-therapy intervention for
delinquent youth at risk for institutionalisation and their families that has good empirical support
(Alexander, 1973). It is designed to improve the attributions family members make about each other’s
behaviours, family communication and supportiveness and to decrease negativity and dysfunctional
patterns of behaviour. A number of outcome studies on functional family therapy with delinquent
adolescents have shown significant improvement in recidivism compared to families in control groups
(Alexander, Barton, Schiavo, & Parsons, 1976).
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CHILD-FOCUSED APPROACHES
Children with conduct problems display specific
difficulties solving social problems and tend to respond
to hypothetical conflict situations by using combative,
aggressive strategies. They also tend to believe that
others have hostile intentions towards them (Dodge,
1993). Based on this type of research, cognitive-
behavioural interventions have been developed to
train children directly in social and problem-solving
skills. Problem-solving skills training is designed to
teach the child the skills associated with each stage
of problem solving: skills for identifying the problem,
generating a range of possible solutions, selecting the
most appropriate solution, and evaluating the success
of the selected solution. The child learns these
DAL
skills through: School-based strategies can be an important component in the
effective treatment of conduct problems as, after the age of 5 or
1. the therapist modelling the desired behaviour
6 years, children spend much of their day at school.
2. the child rehearsing the behaviour
3. the therapist providing feedback to the child
regarding his/her skill in performing the behaviour
4. the child being positively reinforced for engaging in the desired behaviour.
Outcome evaluations have found that a 20-session social problem-solving training approach is
effective in treating children with antisocial behaviour (Kazdin, 1996).
SCHOOL-BASED APPROACHES
School-based strategies may be an important component in the effective treatment of conduct problems
in school-aged children. After the age of 5 or 6 years, children spend up to half their waking hours
at school. It is in this environment that much of their emotional, social and cognitive development
occurs. The school-based management of conduct problems can involve the application of behaviour-
change principles, such as the teacher’s use of attention and reward contingent upon the child engaging
in desirable behaviour and consequences for misbehaviour such as time-out contingencies. These
programs can take a number of forms, including:
∙ individually tailored management programs, administered by teachers, targeting a child’s disruptive
behaviour in the classroom or playground
∙ class-wide behaviour management programs targeting the behaviour of a number of conduct
problem children, or indeed the behaviour of an entire class
∙ school-wide behaviour management programs involving all classes and each grade.
Some programs such as ‘FAST TRACK’ involve the concurrent targeting of home and school,
and include multiple change agents including parents, teachers, peers and the curriculum (Conduct
Problems Prevention Research Group, 2002). Although it is tempting to conclude that school-based
programs such as FAST TRACK that target multiple risk and protective factors will produce better
long-term outcomes, this approach remains to be evaluated.
COMBINED APPROACHES
For longstanding externalising problems, where there are additional complicating family factors, a
combination of approaches is often utilised. For example, the ‘Treatment Foster Care’ program for
delinquent youth combines interventions for the adolescent, the family, the foster parents and teachers,
as relevant (Chamberlain & Reid, 1998). A combination of parenting interventions and child-focused
interventions has also been commonly applied (Kazdin, Esveldt-Dawson, French, & Unis, 1987).
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Similarly, multisystemic therapy aims to treat delinquent youth by changing aspects of the social
environment, both within the family and in the school and broader community (Schoenwald &
Henggeler, 2005).
CASE STUDY: PARENT MANAGEMENT TRAINING FOR OPPOSITIONAL

DEFIANT DISORDER
Presenting problems
Kylie and Mark, parents of Alex, a 6-year-old boy, participated in the Triple P-Positive Parenting Program due to the
difficulties they were having with Alex’s behaviour both at home and at school. Kylie reported a number of disruptive
behaviours that Alex was demonstrating at home, including disobedience, name calling, teasing, swearing, pushing
his sibling and tantrums. Alex also demonstrated the following non-compliant behaviours at school, as reported by his
teacher: not following instructions, disrupting other students, calling out and off-task behaviour. Mark reported that Alex
typically responded to requests by completely ignoring him and Kylie reported that she felt ‘angry and resentful’ over
Alex’s behaviour.
Kylie’s three major concerns were Alex’s non-compliance with instructions, his aggression towards his siblings and
his disruptive behaviour in class. Kylie reported that Alex typically failed to respond to her instructions, particularly in
the late afternoon and early evenings. Kylie described bedtime as the most difficult moments with Alex as he would
typically hit out, kick and scream. Mark and Kylie both reported that they would give up at night-time as they were
exhausted and did not know what to do in order to calm Alex down.
Assessment
The initial assessment involved an interview with Kylie and Mark, an observation of parent–child interaction in their
home and the completion of standardised questionnaires. Interview and observation data revealed a number of factors
that were contributing to the difficulties that Mark and Kylie were experiencing with Alex. Factors contributing to Alex’s
behaviours of non-compliance included his parents not following through with instructions, using inconsistent discipline
strategies and vague instructions, and the accidental rewards Alex would receive when engaging in non-compliance.
For example, Mark would run around and chase Alex when he was not complying with Mark’s instructions. When this
occurred Alex would laugh, thinking it was a game.
Kylie and Mark were given a number of questionnaires to complete both before and after participating in the Triple P
program to gauge the frequency, duration and intensity of Alex’s problems. Moreover, the questionnaire data were
able to indicate whether Alex’s problems were in the clinical or normal range. The results from these questionnaires
are presented in Table 14.8. The questionnaires included the Eyberg Child Behaviour Inventory (ECBI), Parenting Scale,
Parent Problem Checklist, and the Depression, Anxiety and Stress Scales.
On almost all of the measures provided to Kylie and Mark, they scored in the clinical range of severity at the beginning
of treatment. For example, the ECBI scores of parental perceptions of the intensity of disruptive behaviour were extremely
high before the program. Both parents’ scores far exceeded the clinical cut-off of 132 for Intensity and 15 for Problems
used to define cases of clinical severity. Scores of parenting style, as measured by the Parenting Scale, indicated clinical
levels of dysfunctional parenting styles for both Kylie and Mark. In terms of depression, anxiety and stress, Kylie scored
in the mild to moderate range, whereas Mark scored in the normal range on the depressive and anxious scale, but in the
moderate range for stress. On the Parent Problem Checklist, Kylie and Mark reported a high degree of conflict between
them over childrearing and family management, again exceeding the clinical range cut-off score of 5.
The results from the questionnaires provided in combination with the observation and reports from Alex’s parents
indicated that Alex met the criteria for oppositional defiant disorder, according to the DSM-5.
Intervention
To help Alex’s parents change their current parenting practices it was anticipated that learning positive parenting
strategies would be effective. Kylie and Mark completed the 10-session Standard Triple P-Positive Parenting Program,
which was provided by the second author of this chapter. The intervention was an individually administered program
to parents with each session lasting between 40 and 60 minutes. Both parents were encouraged to participate and to
discuss their participation in the program with Alex’s teacher at school.
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TABLE 14.8 Questionnaire scores for Alex and his parents before and after participating in the Standard Triple
P-Positive Parenting Program
SHOWED MOVED OUT

RELIABLE OF CLINICAL
MEASURE BEFORE AFTER CHANGE RANGE
Mother
ECBI intensity 192 112 Yes Yes
ECBI problem 24 7 Yes Yes
Parenting Scale Laxness: 5.6 Laxness: 3.5 Yes Yes

Overreactivity: 4.5 Overreactivity: 2.8
Hostility: 4.0 Hostility: 2.6
Depression 14 6 Yes Yes
Anxiety 9 4 Yes Yes
Stress 24 8 Yes Yes
Parent Problem Checklist Problem score: 11 Problem score: 4 Yes Yes
Father
ECBI intensity 181 114 Yes Yes
ECBI problem 22 10 Yes Yes
Parenting Scale Laxness: 4.2 Laxness: 3.4 Yes Yes

Overreactivity: 4.4 Overreactivity: 3.4
Hostility: 3.8 Hostility: 3.8
Depression 8 5 No No
Anxiety 3 0 No No
Stress 23 7 Yes Yes
Parent Problem Checklist Problem score: 10 Problem score: 6 Yes Yes
The aim of the Triple P program is to provide parents with strategies and techniques to promote positive interactions
with their children. The program also provides effective positive parenting and behaviour-management strategies such
as, giving clear calm instructions and using logical consequences, quiet time and timeout for undesired behaviours.
Treatment outcome
As detailed in Table 14.8, Alex’s parents reported a noticeable difference in Alex’s behaviour after completion of the
program. Furthermore, Kylie and Mark reported feeling more confident in their parenting skills. Kylie indicated that the
strategy’s ‘clear, calm instructions’ were most helpful for her, whereas Mark indicated that spending brief and frequent
amounts of ‘quality time’ with Alex was the key to improvements in Alex’s behaviour. Anecdotal reports taken from an
interview with Kylie following the program indicated the types of improvements experienced by the family:
I feel a huge sense of relief because Alex’s behaviour has really improved and I am nowhere near as stressed and
worried about him. I have learned some really useful techniques that I am confident with and I use them every day at
home. I was trying some of the techniques before but I realised I wasn’t doing them properly. I have a plan now, Alex
continued
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knows it and I stick to it. Before Mark and I would be very stressed about what we should do, and we would argue
and fight over how to handle the situation. After doing Triple P, there is no shouting any more and everything is so
much calmer and quieter. Since we started we have not had any further complaints about his behaviour at school,
which really seems to have settled, thank goodness.
These results indicate that the focus on positive parenting strategies was able to assist Alex and his parents.
LO 14.5 Internalising disorders

In contrast to externalising disorders, internalising disorders such as anxiety or depression are often
described as over-controlled, where feelings and states are inner-directed (Reynolds, 1992). Unlike
the externalising disorders, children suffering from internalising disorders often go unnoticed as their
behaviour does not affect others in the same way. They are likely to withdraw from others, keep quiet
and avoid bringing attention to themselves. The possibility of failing to identify and treat internalising
disorders in children is concerning since these problems involve considerable suffering for the
individual and may even entail suicidal thinking and behaviour. Indeed, as shown in Table 14.9, the
Australian Child and Adolescent Survey of Mental Health and Wellbeing found that suicidal thoughts
and behaviours are not uncommon among Australian adolescents (Lawrence et al., 2015). In addition,
around 1 in 10 adolescents reported self-harming, and the highest rate was in those adolescents with
major depressive disorder.
TABLE 14.9 The percentage of male and female adolescents reporting to have experienced suicidal
thinking and behaviour
RISK BEHAVIOUR MALES FEMALES ALL ADOLESCENTS
Suicidal ideation in past 12 months 4.5 10.7 7.5
Suicide plan in past 12 months 2.9 7.6 5.2

Suicide attempt ever 1.9 4.5 3.2
Suicide attempt in past 12 months 1.5 3.4 2.4

Source: Second Australian Child and Adolescent Survey of Mental Health and Wellbeing (2015)
There are few specific diagnostic categories for childhood internalising disorders, and the adult
criteria for anxiety and depressive disorders are applied to children with only minor modifications.
For example, to meet the DSM-5 criteria for major depressive disorder, the child may display irritable
separation
rather than depressed mood and fail to make expected weight gains rather than lose weight. Children’s
anxiety disorder
responses and behaviour may also be different from that of adults with similar conditions. For
Disorder of
childhood example, anxious children may respond to requests to attend an anxiety-provoking situation with non-
characterised compliance and oppositional behaviour, which is uncommon in adults.
by abnormal In this section, the focus will be on separation anxiety disorder. After this, selective mutism will
fear or worry be described as an example of a disorder that is specific to childhood and, while rare, has a serious
over becoming impact on functioning. A new depressive disorder diagnosis (disruptive mood dysregulation disorder)
separated was introduced for children in the DSM-5. However, this has been criticised as turning ‘temper
from one’s
tantrums into a mental disorder’ (France, 2012). There appears to be relatively little research on the
caregivers as
well as clinging validity of this disorder at this stage (Brotman et al., 2006; Leibenluft, 2011) and its comorbidity
behaviour in with other disorders, including oppositional defiant disorder, is very high, to the point that it cannot
the presence of be distinguished from oppositional defiant disorder (Mayes, Waxmonsky, Calhoun, & Bixler, 2016).
caregivers. Furthermore, there are no identified treatments for this disorder (Leibenluft, 2011).
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The diagnosis and epidemiology of separation

anxiety disorder
Separation anxiety (i.e., protest when separating from a caregiver) is common and normative in
young children, peaking at around 13–18 months (Kearney, Sims, Pursell, & Tillotson, 2003). In
contrast, separation anxiety disorder is characteristic of older children. It is usually expressed through
distress in anticipation of, or on separation from an attachment figure (i.e., a caregiver), the need to
know the whereabouts of the attachment figure, extreme homesickness and preoccupation with harm
coming to the attachment figure (Suveg, Aschenbrand, & Kendall, 2005). The distinguishing feature
of separation anxiety disorder is a fear specifically related to separation experiences, and this fear is
greatly reduced in the presence of the attachment figure. In contrast, other anxiety disorders tend to
be characterised by fears and worries around a range of concerns and are generally not significantly
reduced in the presence of caregivers.
Separation anxiety disorder occurs in approximately 4 per cent of children, although the range
across studies is very large (Cartwright-Hatton, McNicol, & Doubleday, 2006). It is more common
among girls and among pre-adolescent children, occurring most commonly during middle childhood
(7–9 years) (Compton, Nelson, & March, 2000), with very low prevalence in preschoolers (Lavigne,
LeBailly, Hopkins, Gouze, & Binns, 2009).
Most cases of separation anxiety disorder in young children tend to improve over time (Hale,
Raaijmakers, Muris, van Hoof, & Meeus, 2008); however, they may worsen again in adolescence
(Van Oort, Greaves-Lord, Verhulst, Ormel, & Huizink, 2009). For those children who continue to
meet the criteria for the disorder, there is a high level of comorbid diagnoses and therefore a high level
of impairment in functioning (Foley, Pickles, Maes, Silberg, & Eaves, 2004). Comorbid diagnoses
can include other internalising disorders (depression and anxiety), as well as externalising disorders
(e.g., the child may engage in the behaviours of oppositional defiant disorder to reduce the likelihood
of separation). Furthermore, childhood separation anxiety disorder is strongly linked to the later
development of anxiety disorders in adulthood (Klein, 1995). This finding points to the need for
early identification of and intervention in separation anxiety disorder in order to prevent the often
debilitating course of anxiety throughout the lifespan.
The aetiology of separation anxiety disorder

A number of pathways are thought to contribute to the development and maintenance of separation
anxiety disorder, including a genetic component, the modelling of parental anxiety, parenting
behaviours and other environmental factors (such as family conflict).
GENETIC COMPONENT
There is evidence that children inherit a non-specific, genetic vulnerability to separation anxiety
disorder, characterised as a predisposition to anxiety in general (Suveg et al., 2005). This genetic
vulnerability is termed behavioural inhibition and is characterised by a tendency to display anxiety
and to withdraw in unfamiliar situations. There is evidence to suggest that this genetic influence may
be more important for girls than for boys (Feigon, Waldman, Levy, & Hay, 2001).
PARENTING AND PARENTAL ANXIETY

A factor that may have both a genetic and environmental component is that of parental anxiety and
parenting. While there are some inconsistencies in the literature, Rappee (2012) noted that the evidence
for parenting in the aetiology of anxiety is extensive. Many parents of children with separation anxiety
disorder also show symptoms of anxiety, suggesting the familial inheritance of anxiety. In addition,
parents who are anxious themselves tend to model anxious behaviour and poor coping with anxiety-
provoking situations. Children learn how to cope with difficult situations in part by watching others,
and if parents model anxiety in fearful situations, the child is likely to respond in a similar fashion.
Furthermore, parents may provide fewer opportunities for their child to confront and master fearful
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situations. In order to reduce the child’s distress, parents can often inadvertently reinforce their child’s
anxiety by providing too much attention, reassurance and sympathy. In some families, parents do not
give children much attention when they are behaving well, but become very concerned and attentive
when the child becomes ill, stressed or anxious. Parents can therefore accidentally reward their child
for being anxious. Finally, parents of anxious children tend to grant their child less autonomy and are
overprotective. Parents who are too protective (either because of their own anxiety or because of their
concern for their child) may not provide enough opportunities for practising separations and may send
the subtle message that the child cannot cope with the situation.
OTHER FAMILY FACTORS

cognitive Other family factors that play a role in separation anxiety are attachment insecurity and parental
behaviour absence. Children who are securely attached to their primary caregivers tend to be protected from
therapy (CBT) separation anxiety (Dallaire & Weinraub, 2005). That is, these children feel confident to explore their
Type of environment and to experience novel things, secure in the knowledge that their caregiver is there to
psychological protect them. However, there is also evidence that brief, planned separations (e.g., going to school
treatment that
camp) actually protect children from separation anxiety disorder, perhaps because they provide the
combines both
cognitive and child with opportunities to master separations (Poulton, Milne, Craske, & Menzies, 2001).
behavioural In summary, children inherit a predisposition to experience a heightened sense of anxiety and,
concepts and in the presence of a range of family environmental factors, this anxiety can become clinical and
techniques. significantly impair the child’s functioning.
The treatment of separation anxiety disorder

There is limited evidence that medication is an effective treatment
for children with separation anxiety disorder (Suveg et al., 2005). In
general, the intervention of choice for the disorder is cognitive behaviour
therapy (CBT) (Vidair & Gunlicks-Stoessel, 2009), although separation
anxiety disorder has often not been specifically investigated in
intervention studies but instead has been included with other childhood
anxiety disorders. Thus, the intervention strategies recommended for
childhood anxiety tend to be similar, regardless of the type of anxiety
disorder present. Increasingly, the evidence for including parents in

the intervention is being strengthened (Higa-McMillan, Francis, Rith-
Najarian, & Chorpita, 2016).
CBT for separation anxiety disorder includes a number of elements such
as psychoeducation, exposure, coping-skills training and reinforcement
(Jurbergs & Ledley, 2005). Psychoeducation focuses on teaching the
child, as well as his/her parents, about anxiety and how it is maintained.
In particular, parents need to be aware of how their own behaviour
(e.g., modelling anxiety for their child and inadvertently reinforcing their
child’s anxiety) may affect the child’s anxiety, and to be familiar with
strategies to support their child’s successful coping. The next stage of
CBT involves coping-skills training, which aims to teach the child coping
strategies for dealing with anxiety-provoking situations. For example,
children may be taught how to use positive coping statements (e.g., ‘Even
DAL
though I’ll be away from home I’ll be with friends who care about me’)
The experience of separation anxiety is to counter negative, anxiety-provoking thoughts (e.g., ‘I’ll be all alone’).
common and normative among toddlers; this Relaxation skills, including slow, deep breathing and imaginal relaxation
is to be contrasted from the relatively rare (e.g., imagining a pleasant scene), are often taught to children to help
condition of separation anxiety disorder, which reduce the physiological effects of anxiety. Once children are familiar
is most common among older children. with the coping skills, exposure is introduced. Here, a hierarchy of feared
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situations is constructed, listing separation events in order from the least anxiety-provoking (e.g.,
being babysat by Grandma while parents are out during the day) to the most anxiety-provoking
(e.g., going to school camp without the parents). Children then work through the hierarchy, using their
coping skills to assist with managing their anxiety in each of the situations. Reinforcement is used
by the parents to encourage the child to continue with the exposures. Reinforcement can consist of
social reinforcement such as praise, as well as more tangible reinforcement, including special treats or
outings, time with the parent or access to a special activity.
A successful prevention and early intervention school-based program developed in Australia for
the management of childhood anxiety is the ‘Friends Program’ (Barrett, Farrell, Ollendick, & Dadds,
2006). While it is not specifically designed for separation anxiety disorder, it incorporates standard
CBT elements for anxiety and provides a good example of an intervention that can be utilised at a
school-wide level to reach the greatest number of children and thereby reduce the overall prevalence
of childhood anxiety, including separation anxieties.
CASE STUDY: COGNITIVE-BEHAVIOURAL TREATMENT FOR ANXIETY

Presenting problems
Jessica was a 12-year-old girl referred for treatment because of her anxiety and worry about a range of situations
outside of home. She experienced considerable anxiety about attending school, going to school camps, sleeping over at
friends’ places and meeting new people. She felt scared, worried and confused in these situations and often developed
headaches and stomach aches as a result. She also experienced difficulties with falling asleep most nights as a result of
worrying. Jessica reported that her main coping strategy was to talk to her mother when she felt anxious, as her mother
would offer Jessica reassurance and support.
Jessica did not like being outside of the home and felt most comfortable and safe at home. She did not like being
away from her family, because of worries about something bad happening to the people she cared about. She also
experienced worries and concerns about her friends and what they were thinking and doing.
Jessica had a family history of anxiety, as both her older sister and father had previously been diagnosed and treated
for anxiety disorders. Jessica’s anxiety was maintained by a number of factors. The first of these was that through
avoidance of worrying situations, her anxiety went down. In other words, her avoidance was being negatively reinforced
and was therefore likely to keep occurring in the future. Secondly, she had limited coping strategies for dealing with
anxiety in a constructive (i.e., non-avoidant) way. Related to this, she appeared to use other people for support and
reassurance and hence had not developed her own strategies for approaching anxiety-provoking situations.
Assessment and treatment

Assessment consisted of an interview with Jessica and her mother. Following this, Jessica attended 12 sessions of CBT,
which included relaxation training, helping Jessica to identify and challenge the negative thoughts that were driving her
anxiety (e.g., ‘Something terrible will happen to my family when I’m away at school camp’) and problem solving to find
ways for her to effectively manage her anxiety. All sessions included homework tasks so that Jessica could practise her
new skills in between sessions, which she completed diligently.
Outcome
At the end of the treatment, Jessica reported reduced anxiety and worry overall, and showed evidence of generalisation
of improvement to new situations, meaning she was able to apply her newly learned skills to different situations. For
example, even though public speaking was not specifically targeted in her treatment, she was able to give a class
presentation with no anxiety, and achieved her goal of presenting in front of the school as a school leader, also with
limited anxiety. In addition, the frequency and severity of her somatic symptoms (i.e., headaches and stomach aches) had
reduced, as reported by her mother. In terms of sleep, Jessica reported that she had problems falling asleep on no more
than one or two nights a week, which was also an improvement.
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The diagnosis and epidemiology of selective mutism

selective mutism Selective mutism is a psychological disorder characterised by a persistent failure to speak in selected
Disorder settings, for a period of at least one month after the beginning of the school year, even though the
characterised child understands spoken language and has the ability to speak. Generally, these children tend to
by a persistent
speak to their families and a few selected others but do not speak in school or other major social
failure to speak
in certain settings
situations (Black & Udhe, 1994). Children with selective mutism may respond or make their
even though the needs known by nodding their heads, pointing or by remaining emotionless or expressionless until
individual has the someone guesses what they want. It is an understudied disorder, with most of the literature on
ability to speak. selective mutism consisting of single case studies or small case series (Carlson, Mitchell, & Segool,
2008; Tancer, 1992).
Selective mutism occurs in less than 1 per cent of children (Viana, Beidel, & Rabian, 2009). It
has been suggested that this prevalence rate is an underestimate since children with the condition
do not usually disturb anyone and do not attract much attention (Kumpulainen, Rasanen, Raaska, &
Somppi, 1998). In addition, parents may also often not come forward due to their own shyness or
anxiety (Kopp & Gillberg, 1997). It appears that it is more common in girls than boys (Cunningham,
McHolm, Boyle, & Patel, 2004).
The onset of selective mutism is usually gradual (Dow, Sonies, Scheib, Moss, & Leonard, 1995).
Some children experience selective mutism for short periods of time, while others experience the
problem for many years. The rate of remission is not known. Yet even when the disorder does remit,
the individual often continues to have marked discomfort in speaking situations (Remschmidt, Poller,
Herpertz-Dahlmann, Hennigause, & Gutenbunner, 2001).
A wide variety of comorbid psychological problems have been described (Viana et al., 2009),
with one study finding that 98 per cent of children with selective mutism met criteria for another
disorder (Kristensen, 2000). The most common of these comorbid conditions are anxiety disorders,
with up to 75 per cent of children with selective mutism meeting criteria for an anxiety disorder such
as separation anxiety disorder and social phobia. In addition, some studies have found that more than
40 per cent of children with selective mutism meet criteria for an elimination disorder. Speech and
language problems have also been noted in up to 40 per cent of children with the disorder (Black &
Udhe, 1995; Kristensen, 2000). Finally, deficits in academic performance and social communication
are associated with selective mutism (Ford, Kratochwill, Sladeczek, & Carlson, 1998). Often it may
be difficult or impossible to assess a child’s performance and his/her need for additional assistance
given the failure to speak (Porjes, 1992).
The aetiology of selective mutism

An unsupported, yet commonly believed, aetiological explanation for selective mutism is that a history
of early psychological or physical trauma leads to the disorder (MacGregor, Pullar, & Cundall, 1994).
In more recent accounts, however, there has been a shift to biological, temperamental and anxiety
components, and in fact in the DSM-5 this diagnosis has been moved into the ‘anxiety disorders’
category.
Dow and colleagues (1995) suggest that selective mutism may be the manifestation of a shy,
inhibited temperament, and there is some resemblance of these children to adults suffering from
social phobia (e.g., avoidance or fear of public speaking, which is very common in social phobia),
suggesting anxiety as the aetiological basis (Black, 1996; Turk, Heimberg, & Hope, 2001). Several
lines of research suggest that the condition is best viewed as a variant of social phobia. In Black and
Udhe’s (1994) study, 97 per cent of children with selective mutism met diagnostic criteria for social
phobia. Furthermore, when asked whether it was hard to talk due to shyness or nervousness, 73 per
cent replied yes, 3 per cent replied no and 23 per cent did not respond. Finally, up to 70 per cent of
first-degree relatives of the children in the sample had a diagnosis of social phobia, again supporting
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a link between selective mutism and social phobia. In other research, significant correlations have
been found between parent ratings of their children’s mutism severity and anxiety symptoms (Black
& Udhe, 1992). A final source of evidence supporting the conceptualisation of selective mutism as a
variant of social phobia is the fact that treatment with anxiety-based approaches has been successful in
the treatment of selective mutism (Black & Udhe, 1992; 1994).
The treatment of selective mutism

There is very little empirical research available regarding treatment for selective mutism, and what
evidence is available suggests that it is quite resistant to treatment (Anstendig, 1998; Carlson et al.,
2008). There is some evidence that pharmacotherapy, especially in the case of resistant cases, may
have some benefit. However, behavioural interventions have been the most frequently used approaches
to treatment, essentially directed at eliminating all reinforcement for mutism while bolstering self-
confidence and decreasing anxiety (Anstendig, 1998; Dow et al., 1995; Wright, Holmes, Cuccaro, &
Leonhardt, 1994).
The effective treatment of selective mutism consists of a number of steps to address three basic
problems (Schill, Kratochwill, & Gardner, 1996):
∙ the child’s high level of anxiety in social situations
∙ the limited experience the child has had in speaking with people other than family members
∙ the high level of reinforcement that is present for non-verbal communication.
A number of techniques have been described in the literature for the treatment of selective mutism,
although only a limited number of studies have provided support for these. The techniques include
anxiety reduction through graduated exposure to feared situations and reinforcement of the child’s
efforts during graduated exposure. Another technique is self-modelling of appropriate actions, which
refers to a procedure in which a person observes him/herself performing at the most effective level
possible. Auditory and video recordings can be used for self-modelling in settings in which the child is
silent. Specifically, videotapes are constructed in which the child answers a set of questions presented
by the parent or therapist. Another section of videotape is made of the teacher (or another appropriate
person to whom the child has not talked) asking the questions. An edited tape is then made that shows
the teacher asking the questions followed by the child answering them, giving the impression that the
child is having a conversation with the person. enuresis
Elimination
disorder in
children who are
LO 14.6 Elimination disorders at least 5 years of
age and who wet
the bed or their
Enuresis (involuntary emptying of the bladder) and encopresis (repetitive soiling in inappropriate clothes at least
places) are the two types of elimination disorders. twice a week for
three months.
The diagnosis and epidemiology of enuresis encopresis

Elimination
Enuresis entails the involuntary emptying of the bladder in the absence of an organic cause, and can disorder in
occur either at night-time (nocturnal enuresis) or during the day (diurnal enuresis), although the latter children who
is rare. In order to meet the criteria for nocturnal enuresis, the child needs to be aged five years or are at least 4
older, as there are a number of physical developments that need to occur for the child to be capable of years old and
holding on during the course of the night. Sufficient bladder control is usually achieved by the age of who defecate
inappropriately
five years (Bischof & Benson, 2004). Enuresis is divided into two categories: primary enuresis occurs at least once a
when the child has never been dry, while secondary enuresis is when the child has had a period of month for three
dryness for at least six months. months.
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Nocturnal enuresis is relatively common, with rates of about 15–22 per cent in boys and 7–15
per cent in girls at age 7 (Devlin, 1991). Data from the United States suggest that the prevalence
in 8–11-year-old boys is about 6 per cent, and about 2.5 per cent in girls, with high comorbidity
with attention-deficit/hyperactivity disorder (Shreeram, He, Kalaydjian, Brothers, & Merikangas,
2009). There is a spontaneous resolution rate of approximately 15 per cent of cases per year that
continues into adulthood, meaning that most children simply grow out of the disorder and it is very
rare in adulthood (Forsythe & Redmond, 1974). Nevertheless, children with enuresis experience
embarrassment, social isolation, behavioural problems and low self-esteem (Butler & Heron, 2008;
Erdogan et al., 2008) that can lead to ongoing adult difficulties and therefore highlight the need for
early intervention (Dunlop, 2005).
The aetiology of enuresis

There are differences in the aetiological explanations for primary and secondary enuresis. Generally,
psychological factors rarely contribute to the development of primary enuresis, whereas specific
psychosocial events are much more common in secondary enuresis (Fritz et al., 2004). For example,
stressful life events such as parental divorce, the death of a loved one or other trauma can lead to the
development of secondary enuresis.
Inherited factors are thought to play a substantial role in enuresis, with about a 43 per cent
concordance rate among monozygotic twins compared with a 19 per cent concordance rate in dizygotic
twins (Hublin, Kapiro, Partnen, & Koskenvuo, 1998). Also supporting a high level of heritability
is the fact that the chances of a child developing enuresis are greater if a parent was enuretic as a
child (44% of such children will have enuresis) (von Gontard, Heron, & Joinson, 2011), and these
rates increase even further if both parents were affected (77% of these children will develop enuresis)
parasympathetic (Bawkin, 1973).
nervous system The specific factor that is inherited has not been pinpointed, but may be related to general
Part of the
developmental immaturity as well as more specific hormonal and physical factors. In terms of general
autonomic
nervous system factors of delayed development, children with enuresis tend to have lower than average height and later
that is involved development of milestones (such as walking) (Gross & Dornsbusch, 1982; Shaffer, 1985). The possible
in maintaining specific factors include: reduced functional bladder capacity; hyperactivity of the parasympathetic
bodily systems nervous system; abnormal sleep patterns and arousability (i.e., reduced waking from sleep in response to
(such as the sensation of a full bladder); and limited regulation of vasopressin (a specific type of chemical linked
breathing and to bladder regulation) (Bader, Neveus, Kruse, & Sillen, 2002; Rittig, Knudsen, Norgaard, Pedersen, &
digestion) when
Djurhuus, 1989; Yakinci, Mangen, Durmaz, Balbay, & Karabiber, 1997).
the organism
is not active or
aroused.
The treatment of enuresis
bell and pad The most successful treatment of enuresis involves a conditioning approach, with success rates of
method
approximately 66 per cent (with success defined as the child experiencing fewer than one wet night per
Treatment for
enuresis in which
month) (Houts, Berman, & Abramson, 1994). Conditioning interventions appear to be more successful
a pad placed than medication (Houts et al., 1994; Schulman, Colish, von Zuben, & Kodman-Jones, 2000). For
under a sleeping example, desmopressin (an antidiuretic that leads to decreased urine production and increased urine
child to detect concentration) has a good initial response rate (70 per cent), but results in low levels of complete
traces of urine dryness (24.5 per cent) (Moffatt, Harlos, Kirshen, & Burd, 1993).
sets off a bell The bell and pad method, based on conditioning principles, is the most effective intervention for
when urine is nocturnal enuresis (Friman & Jones, 1998). As part of this intervention, a urine-sensitive pad is placed
detected, so as
on the bed and is connected to an alarm. During the night, when the child wets the bed, the alarm
to condition the
child to wake is activated and the child is woken. The child is expected to turn the alarm off. The bell and pad is
up and use the often combined with other interventions, such as having the child participate in changing the sheets at
bathroom before night (cleanliness training), bladder control exercises (retention control training) and rewards for dry
urinating. nights. While these additional techniques are commonly used in treatment, there is little evidence for
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the effectiveness of these components in addition to the alarm (Caldwell, Nankivell, & Sureshkumar,
2013). The bell and pad treatment is thought to work by teaching the child to avoid the aversive
situation of being woken at night by the alarm, and over time the child learns to avoid this through
increased bladder control.
The diagnosis and epidemiology of encopresis

Encopresis is defined as repetitive soiling in inappropriate places at least once a month for three
months, in a child at least four years old. Medical or physical problems need to be ruled out before the
diagnosis can be confirmed. Encopresis can be retentive, where the child tends to hold on for as long
as possible, or non-retentive, where soiling is intermittent and there is no evidence of constipation.
The majority of cases of encopresis are retentive, with only 5–20 per cent of encopretic children
classified as non-retentive (Fritz & Armbrust, 1982).
Encopresis is diagnosed in approximately 1.5–7.5 per cent of children (Doleys, 1983). Prior to the
age of four years, the child may not have physical control over his/her anal functioning, thus precluding
the diagnosis being made in younger children. In many cases of children with encopresis, there is a
history of hard, painful stools at earlier ages and many have not had success with toileting. Encopresis
tends to decline with age and is seen in approximately 0.75 per cent of children by 10–12 years
(Houts & Abramson, 1990). Children with encopresis tend to have more anxiety/depressive symptoms,
more attention difficulties, greater social problems, more disruptive behaviour and poorer school
performance, emphasising the importance of treatment despite the reduced prevalence of the disorder
with age (Cox, Morris, Borowitz, & Sutphen, 2002).
The aetiology of encopresis

An aetiological model of encopresis has been proposed by Cox, Sutphen, Ling, and Quillian (1996).
According to this model, the child initially experiences an episode of constipation (resulting from
physical or psychological factors), which leads to faecal impaction and a large hard stool. The
passage of these stools is difficult and may be painful, and consequently the child may anticipate
future difficulties. Given this painful experience, the child may experience rectal distension cues as
unpleasant and try to ignore them and avoid going to the toilet. This results in chronic constipation with
overflow incontinence. When this occurs, parents may request more toilet usage, which is generally
resisted by the child, and the resistance and continued soiling lead to parent–child conflict. Finally,
shame and rejection can lead the child to hide or lie about dirty underwear.
The treatment of encopresis

Medical management combined with behavioural treatment tends to be more effective than medical
management alone (Borowitz, Cox, Sutphen, & Kovatchev, 2002). Medical intervention involves
cleanout of the bowel with laxatives, dietary recommendations and a toilet-sitting schedule.
Biofeedback can also be used to help children learn the cues of defecation and control their anal
functioning.
Behavioural interventions involve providing psychoeducation for parents and children (including
education about the nature and causes of encopresis), combined with an appropriate reinforcement
schedule for encouraging children to use the toilet. Parents are also trained to respond to soiling in
a matter-of-fact manner, so that attention and hence accidental reinforcement for soiling is reduced.
While treatments can be successful, there is often the need for long-term monitoring. For instance,
a follow-up study of 324 children treated for encopresis indicated that 87 per cent had improved but
42 per cent were still soiling (Rockney, McQuade, Days, & Linn, 1996). Novel approaches utilising
internet-based interventions for children and families also hold some promise (Ritterband et al., 2008).
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SUMMARY
Disorders of childhood are common, although they are often unrecognised and untreated. Many adult disorders can be traced
back to childhood symptoms, highlighting the importance of prevention and early intervention. While externalising problems
receive much attention as a result of their impact on others, it is nevertheless important to continue research into the full range of
childhood disorders since they can all have debilitating outcomes. An important message of this chapter is the extent to which the
family environment can play a role in the development and maintenance of psychological and behavioural problems in children.
Fortunately, effective evidence-based parenting interventions are available to assist parents in changing their child’s behaviour and
improving coping skills.
The primary challenge now is to ensure that such interventions are widely available and easily accessible to parents. This
issue of translating research findings into practice is vitally important since many service providers continue to offer programs with
little or no evidence supporting their effectiveness. Psychologists have been at the forefront of tackling this issue by designing
more flexible interventions that reach more parents. In particular, Kazdin and Blase (2011) provide a model of how flexible service
delivery and the integration of prevention and intervention can assist in reducing the burden of mental illness. For example,
the use of the internet in the delivery of treatment (Spence, Holmes, March, & Lipp, 2006) and self-help approaches (Rapee,
Abbott, & Lyneham, 2006) have been evaluated for childhood anxiety, as well as for child behavioural problems (Sanders, Baker, &
Turner, 2012).
Extending this research further, there is some evidence that parenting interventions can be successfully delivered through the
medium of television. Sanders, Calam, Durand, Liversidge, and Carmont (2008) assessed the impact on viewers of a six-episode
documentary series that followed five families of children with severe conduct problems as the parents underwent an eight-session
‘Group Triple P’ intervention. Parents were randomly assigned either to watching the show alone or to the enhanced condition that
included internet support and a structured self-directed program.
Both groups showed significant improvements in parent-reported child behaviour and parenting styles. However, the
enhanced group had the strongest effects and was most satisfied with the program. These findings suggest that effective
interventions delivered through the blending of highly accessible media have the potential to reach a very large number of
families who might not otherwise receive treatment. In reaching broad sections of the community, such innovative approaches
could help undermine pervasive myths that downplay the severity of psychological problems in childhood and prevent children
gaining the help they need.
There are also increasing calls for a public health approach that focuses on both prevention and treatment (Biglan, Flay, Embry, &
Sandler, 2012). Such an approach aims to affect the prevalence rates of childhood emotional and behavioural problems by working
at the population (rather than the individual) level, by implementing interventions that can be widely disseminated in a cost-effective
manner. A public health approach has the potential to reach a greater proportion of children and to ensure that problems are
addressed before they become more persistent and severe.
KEY TERMS
androgen. . . . . . . . . . . . . . . . . . . . . . . . 462 encopresis. . . . . . . . . . . . . . . . . . . . . . . 477 perinatal. . . . . . . . . . . . . . . . . . . . . . . . . 456
attention-deficit/hyperactivity enuresis. . . . . . . . . . . . . . . . . . . . . . . . . 477 pervasive developmental
disorder (ADHD). . . . . . . . . . . . . . . . . . 450 executive functions . . . . . . . . . . . . . . . 451 disorders. . . . . . . . . . . . . . . . . . . . . . . . 457
autism spectrum disorder. . . . . . . . . . 455 experimental study . . . . . . . . . . . . . . . 465 postnatal . . . . . . . . . . . . . . . . . . . . . . . . 460
bell and pad method. . . . . . . . . . . . . . 478 externalising disorders. . . . . . . . . . . . 460 prenatal. . . . . . . . . . . . . . . . . . . . . . . . . 456
cognitive behaviour therapy heritability . . . . . . . . . . . . . . . . . . . . . . . 454 reading disorder. . . . . . . . . . . . . . . . . . 453
(CBT). . . . . . . . . . . . . . . . . . . . . . . . . . . . 474 intellectual disability. . . . . . . . . . . . . . 457 selective mutism. . . . . . . . . . . . . . . . . . 476
concordance rate. . . . . . . . . . . . . . . . . 456 meta-analysis . . . . . . . . . . . . . . . . . . . . 450 separation anxiety disorder. . . . . . . . 472
conduct disorder . . . . . . . . . . . . . . . . . 461 oppositional defiant disorder. . . . . . . 461 specific learning disorder. . . . . . . . . . 453
correlational study. . . . . . . . . . . . . . . . 465 parasympathetic nervous system. . . . 478
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REVIEW QUESTIONS
LO 14.1
14.1 List some commonly reported problems of child behaviour identified by parents.
14.2 What are some challenges associated with research on psychological disorders in children?
LO 14.2
14.3 What are the two main categories of childhood disorders that are used to dichotomise psychological disorders
in children listed in the DSM-5?
LO 14.3
14.4 Describe the similarities and differences between various neurodevelopmental disorders.
LO 14.4
14.5 What are the key characteristics of an externalising disorder?
14.6 Provide a biopsychosocial understanding of the causes of oppositional defiant disorder.
14.7 Describe three evidence-based approaches that have been developed to treat externalising disorders.
Provide examples where possible.
LO 14.5
14.8 Describe the three pathways that contribute to the development and maintenance of separation anxiety disorder.
14.9 Describe the elements of CBT in the treatment of separation anxiety disorder.
LO 14.6
14.10 What treatments for elimination disorders have been found to be most effective?
REFERENCES
Alexander, J. F. (1973). Defensive and supportive communications Australian Human Rights Commission (2014). The forgotten children:
in normal and deviant families. Journal of Consulting and Clinical National inquiry into children in immigration detention. Sydney:
Psychology, 40, 223–231. Author. Retrieved from https://www.humanrights.gov.au/sites/
Alexander, J. F., Barton, C., Schiavo, R. S., & Parsons, B. V. (1976). default/files/document/publication/forgotten_children_2014.pdf.
Behavioral intervention with families of delinquents: Therapist Bader, G., Neveus, T., Kruse, S., & Sillen, U. (2002). Sleep of
characteristics and outcome. Journal of Consulting and Clinical primary enuretic children and controls. Sleep, 25, 579–583.
Psychology, 44, 656–664. Bailey, A., Le Couteur, A., Gottesman, I., & Bolton, P. (1995).
American Psychiatric Association (1980). Diagnostic and statistical Autism as a strongly genetic disorder: Evidence from a British twin
manual of mental disorders (DSM-III) (3rd ed.). Washington, DC: study. Psychological Medicine, 25, 63–77.
Author. Baron-Cohen, S. (1995). Mindblindness: An essay on autism and
American Psychiatric Association (1986). Diagnostic and statistical theory of mind. Cambridge: MIT Press.
manual of mental disorders (DSM-III-R) (3rd ed., revised). Baron-Cohen, S., Scott, F. J., Allison, C., Williams, J., Bolton, P.,
Washington, DC: Author. Matthews, F. E., & Brayne, C. (2009). Prevalence of autism-
American Psychiatric Association (1994). Diagnostic and statistical spectrum conditions: UK school-based population study. British
manual of mental disorders (DSM-IV) (4th ed.). Washington, DC: Journal of Psychiatry, 194, 500–509.
Author. Barrett, P. M., Farrell, L. J., Ollendick, T. H., & Dadds, M. (2006).
American Psychiatric Association (2000). Diagnostic and statistical Long-term outcomes of an Australian universal prevention trial
manual of mental disorders (DSM-IV-TR) (4th ed., text revision). of anxiety and depression symptoms in children and youth: An
Washington, DC: Author. evaluation of the Friends Program. Journal of Clinical Child and
American Psychiatric Association (2013). Diagnostic and statistical Adolescent Psychology, 35, 403–411.
manual of mental disorders (DSM-5) (5th ed.). Arlington: Author. Basten, M., Tiemeier, H., Althoff, R. R., van de Schoot, R., Jaddoe,
Anstendig, K. (1998). Selective mutism: A review of the treatment V. W. V., Hofman, A., . . . van der Ende, J. (2016). The stability
literature by modality from 1980–1996. Psychotherapy, 35, 381–391. of problem behavior across the preschool years: An empirical
rie66620_ch14_443-490.indd 481 07/31/17 05:27 PM

approach in the general population. Journal of Abnormal Child Brady, S. A. (1991). The role of working memory in reading disability.
Psychology, 44, 393–404. In S. A. Brady & D. P. Shankweiler (Eds.), Phonological processes
Bateman, B., Warner, J. O., Hutchinson, E., Dean, T., Rowlandson, in literacy: A tribute to Isabelle Y. Liberman (pp. 129–151).
P., Gant, C., . . . Stevenson, J. (2004). The effects of a double Hillsdale: Lawrence Erlbaum.
blind, placebo controlled, artificial food colourings and benzoate Breier, J. I., Gray, L., Fletcher, J. M., Diehl, R. L., Klaas, P., Foorman,
preservative challenge on hyperactivity in a general population B. R., . . . Molis, M. R. (2001). Perception of voice and tone onset
sample of preschool children. Archives of Diseases in Childhood, time continua in children with dyslexia with and without attention
89, 506–511. deficit/hyperactivity disorder. Journal of Experimental Child
Baving, L., Laucht, M., & Schmidt, M. H. (2000). Oppositional Psychology, 80, 245–270.
children differ from healthy children in frontal brain activation. British Psychological Society (2012). DSM-5: The future of psychiatric
Journal of Abnormal Child Psychology, 28, 267–275. diagnosis (2012—final consultation). Leicester: Author.
Bawkin, H. (1973). The genetics of enuresis. In I. Kolvin, C. Shapiro, Bronfenbrenner, U. (1979). The ecology of human development:
& F. Boquiren (Eds.), Bladder control and enuresis (pp. 73–77). Experiments by nature and design. Cambridge: Harvard University
London: William Heineman. Press.
Bayer, J. K., Hiscock, H., Ukoumunne, O. C., Price, A., & Wake, M. Brotman, M. A., Schmajuk, M., Rich, B. A., Dickstein, D. P., Guyer,
(2008). Early childhood aetiology of mental health problems: A A. E., Costello, E. J., . . . Leibenluft, E. (2006). Prevalence, clinical
longitudinal population-based study. Journal of Child Psychology correlates, and longitudinal course of severe mood dysregulation in
and Psychiatry, 49, 1166–1174. children. Biological Psychiatry, 60, 991–997.
Beckwith, L. (2000). Prevention science and prevention programs. Brown, T. E. (2006). Executive functions and attention deficit hyperactivity
In C. H. Zeanah (Ed.), Handbook of infant mental health (2nd ed.) disorder: Implications of two conflicting views. International Journal
(pp. 439–456). New York: Guilford Press. of Disability, Development and Education, 53, 35–46.
Belsky, J., & Pluess, M. (2009). Beyond diathesis stress: Differential Burke, J. D., Rowe, R., & Boylan, K. (2014). Functional outcomes
susceptibility to environmental influences. Psychological Bulletin, of child and adolescent oppositional defiant disorder symptoms in
135, 885–898. young adult men. Journal of Child Psychology and Psychiatry, 55,
Biglan, A., Flay, B. R., Embry, D. D., & Sandler, I. N. (2012). The 264–272.
critical role of nurturing environments for promoting human well- Burt, S. A. (2009). Rethinking environmental contributions to child
being. American Psychologist, 67, 257–271. and adolescent psychopathology: A meta-analysis of shared
Bischof, G. H., & Benson, B. M. (2004). Childhood enuresis: A environmental influences. Psychological Bulletin, 135, 608–637.
biopsychosocial systems approach. Journal of Family Psychotherapy, Butler, R., & Heron, J. (2008). An exploration of children’s views of
15, 1–17. bed-wetting at 9 years. Child: Care, Health and Development, 34,
Bishop, D. V. M., Whitehouse, A. J. O., Watt, H. J., & Line, E. A. 65–70.
(2008). Autism and diagnostic substitution: Evidence from a Caldwell, P. H. Y., Nankivell, G., & Sureshkumar, P. (2013). Simple
study of adults with a history of developmental language disorder. behavioural interventions for nocturnal enuresis in children.
Developmental Medicine and Child Neurology, 50, 341–345. Cochrane Database of Systematic Reviews, 7.
Black, B. (1996). Social anxiety and selective mutism. American Canino, G., Polanczyk, G., Bauermeister, J., Rohde, L., & Frick, P.
Psychiatric Press Review of Psychiatry, 15, 469–495. (2010). Does the prevalence of CD and ODD vary across cultures?
Black, B., & Udhe, T. W. (1992). Elective mutism as a variant of Social Psychiatry and Psychiatric Epidemiology, 45, 695–704.
social phobia. Journal of the American Academy of Child and Carlson, J. S., Mitchell, A. D., & Segool, N. (2008). The current state
Adolescent Psychiatry, 31, 1090–1094. of empirical support for the pharmacological treatment of selective
Black, B., & Udhe, T. W. (1994). Treatment of elective mutism with mutism. School Psychology Quarterly, 23, 354–372.
fluoxetine: A double-blind, placebo-controlled study. Journal of Cartwright-Hatton, S., McNicol, K., & Doubleday, E. (2006). Anxiety
the American Academy of Child and Adolescent Psychiatry, 33, in a neglected population: Prevalence of anxiety disorders in pre-
1000–1006. adolescent children. Clinical Psychology Review, 26, 817–833.
Black, B., & Udhe, T. W. (1995). Psychiatric characteristics of children Centers for Disease Control and Prevention (2009). Prevalence of
with selective mutism: A pilot study. Journal of the American autism spectrum disorders: Autism and Developmental Disabilities
Academy of Child and Adolescent Psychiatry, 34, 847–856. Monitoring Network. Surveillance Summaries, 58, 1–24.
Borowitz, S., Cox, D. J., Sutphen, J., & Kovatchev, B. (2002). Chamberlain, P., & Reid, J. B. (1998). Comparison of two community
Treatment of childhood encopresis: A randomized trial comparing alternatives to incarceration for chronic juvenile offenders. Journal
three treatment protocols. Journal of Pediatric Gastroenterology of Consulting and Clinical Psychology, 66, 624–633.
and Nutrition, 34, 378–384. Chorpita, B. F., Daleiden, E. L., Ebesutani, C., Young, J., Becker,
Bowlby, J. (1982). Attachment (2nd ed.). New York: Basic Books. K. D., Nakamura, B. J., . . . Starace, N. (2011). Evidence-based
Boylan, K., Vaillancourt, T., Boyle, M., & Szatmari, P. (2007). treatments for children and adolescents: An updated review of
Comorbidity of internalizing disorders in children with oppositional indicators of efficacy and effectiveness. Clinical Psychology:
defiant disorder. European Journal of Child Adolescent Psychiatry, Science and Practice, 18, 154–172.
16, 484–494. Cicchetti, D. (1993). Developmental psychology: Reactions,
Bradley, M. C., & Mandell, D. (2005). Oppositional defiant disorder: reflections and projections. Developmental Review, 13, 471–502.
A systematic review of evidence of intervention effectiveness. Clark, T. C., Fleming, T., Bullen, P., Denny, S., Crengle, S., Dyson,
Journal of Experimental Criminology, 1, 343–365. B., . . . Utter, J. (2013). Youth’12 overview: The health and
rie66620_ch14_443-490.indd 482 07/31/17 05:27 PM

wellbeing of New Zealand secondary school students in 2012. defiant disorder during middle childhood: A meta-analysis. Journal
Auckland, New Zealand: The University of Auckland. of Abnormal Child Psychology, 45, 313–325.
Collins, W. A., Maccoby, E. E., Steinberg, L., Hetherington, E. M., & Devlin, J. B. (1991). Prevalence and risk factors for childhood
Bornstein, M. H. (2000). Contemporary research on parenting: nocturnal enuresis. Irish Medical Journal, 84, 118–120.
The case for nature and nurture. American Psychologist, 55, Dodge, K. A. (1993). Social-cognitive mechanisms underlying the
218–232. development of conduct disorder and depression. Annual Review of
Comer, J. S., Chow, C., Chan, P. T., Cooper-Vince, C., & Wilson, L. Psychology, 44, 559–584.
A. (2013). Psychosocial treatment efficacy for disruptive behavior Doleys, D. M. (1983). Enuresis and encopresis. In T. H. Ollendick &
problems in very young children: A meta-analytic examination. M. Hersen (Eds.), Handbook of child psychopathology
Journal of the American Academy of Child & Adolescent (pp. 201–226). New York: Plenum Press.
Psychiatry, 52, 26–36. Dorn, L. D., Kolko, D. J., Susman, E. J., Huang, B., Stein, H., Music,
Compton, D. L., & Carlisle, J. F. (1994). Speed of word recognition E., Bukstein, O. G. (2009). Salivary gonadal and adrenal hormone
as a distinguishing characteristic of reading disability. Educational differences in boys and girls with and without disruptive behavior
Psychology Review, 6, 115–140. disorders: Contextual variants. Biological Psychology, 81, 31–39.
Compton, S. N., Nelson, A. H., & March, J. S. (2000). Social phobia Dow, S. P., Sonies, B. C., Scheib, D., Moss, S. E., & Leonard, H.
and separation anxiety symptoms in community and clinical L. (1995). Practical guidelines for the assessment and treatment of
samples of children and adolescents. Journal of the American selective mutism. Journal of the American Academy of Child and
Academy of Child and Adolescent Psychiatry, 39, 1040–1046. Adolescent Psychiatry, 34, 836–846.
Conduct Problems Prevention Research Group (2002). The Drews, C. D., Murphy, C. C., & Yeargin-Allsopp, M. (1996). The
implementation of the Fast Track Program: An example of a large- relationship between idiopathic mental retardation and maternal
scale prevention science efficacy trial. Journal of Abnormal Child smoking during pregnancy. Pediatrics, 97, 547–553.
Psychology, 30, 1–17. Dunlop, A. (2005). Meeting the needs of parents and pediatric
Conger, R. D., & Donnellan, M. B. (2007). An interactionist patients: Results of a survey on primary nocturnal enuresis.
perspective on the socioeconomic context of human development. Clinical Pediatrics, 44, 297–303.
Annual Review of Psychology, 58, 175–199. Dunn, S. E., Lochman, J. E., & Colder, C. R. (1997). Social problem-
Consortium of International Scientists (2002). International solving skills in boys with conduct and oppositional defiant
consensus statement on ADHD. Clinical Child and Family disorders. Aggressive Behavior, 23, 457–469.
Psychology Review, 5, 89–111. Dykens, E. M. (2000). Psychopathology in children with intellectual
Copeland, W. E., Shanahan, L., Costello, J., & Angold, A. (2009). disability. Journal of Child Psychology and Psychiatry, 41,
Childhood and adolescent psychiatric disorders as predictors of 407–417.
young adult disorders. Archives of General Psychiatry, 66, 764–772. Egger, H. L., & Angold, A. (2006). Common emotional and
Cox, D. J., Morris, J. B., Jr., Borowitz, S. M., & Sutphen, J. L. (2002). behavioral disorders in preschool children: Presentation, nosology,
Psychological differences between children with and without and epidemiology. Journal of Child Psychology and Psychiatry,
chronic encopresis. Journal of Pediatric Psychology, 27, 585–591. 47, 313–337.
Cox, D. J., Sutphen, J., Ling, W., & Quillian, W. (1996). Additive Ellis, B. J., Boyce, W. T., Belsky, J., Bakermans-Kranenburg, M.
benefits of laxative, toilet training, and biofeedback therapies in the J., & van Ijzendoorn, M. H. (2011). Differential susceptibility to
treatment of pediatric encopresis. Journal of Pediatric Psychology, the environment: An evolutionary–neurodevelopmental theory.
21, 659–670. Development and Psychopathology, 23, 7–28.
Crowell, S. E., Beauchaine, T. P., Gatzke-Kopp, L., Sylvers, P., Ellis, B., & Nigg, J. (2009). Parenting practices and attention-deficit/
Mead, H., & Chipman-Chacon, J. (2006). Autonomic correlates hyperactivity disorder: New findings suggest partial specificity of
of attention-deficit/hyperactivity disorder and oppositional defiant effects. Journal of the American Academy of Child and Adolescent
disorder in preschool children. Journal of Abnormal Psychology, Psychiatry, 48, 146–154.
115, 174–178. Erdogan, A., Akkurt, H., Boettjer, N. K., Yurtseven, E., Can, G., &
Cunningham, C. E., McHolm, A., Boyle, M. H., & Patel, S. (2004). Kiran, S. (2008). Prevalence and behavioural correlates of enuresis
Behavioral and emotional adjustment, family functioning, in young children. Journal of Paediatrics and Child Health, 44,
academic performance, and social relationships in children with 297–301.
selective mutism. Journal of Child Psychology and Psychiatry, 45, Erskine, H. E., Baxter, A. J., Patton, G., Moffitt, T. E., Patel, V.,
1363–1372. Whiteford, H. A., & Scott, J. G. (2016). The global coverage of
Dadds, M. R., Fraser, J., Frost, A., & Hawes, D. J. (2005). prevalence data for mental disorders in children and adolescents.
Disentangling the underlying dimensions of psychopathy and Epidemiology and Psychiatric Sciences, 20, 1–8.
conduct problems in childhood: A community study. Journal of Evans, S. W., Owens, J. S., & Bunford, N. (2014). Evidence-
Consulting and Clinical Psychology, 73, 400–410. based psychosocial treatments for children and adolescents with
Dallaire, D. H., & Weinraub, M. (2005). Predicting children’s attention-deficit/hyperactivity disorder. Journal of Clinical Child
separation anxiety at age 6: The contributions of infant–mother & Adolescent Psychology, 43, 527–551.
attachment security, maternal sensitivity, and maternal separation Feigon, S. A., Waldman, I. D., Levy, F., & Hay, D. A. (2001). Genetic
anxiety. Attachment and Human Development, 7, 393–408. and environmental influences on separation anxiety disorder
Demmer, D. H., Hooley, M., Sheen, J., McGillivray, J. A., & Lum, symptoms and their moderation by age and sex. Behavior Genetics,
J. A. G. (2017). Sex differences in the prevalence of oppositional 31, 403–411.
rie66620_ch14_443-490.indd 483 07/31/17 05:27 PM

Flint, J., & Wilike, A. O. M. (1996). The genetics of mental Hale, W. W. III, Raaijmakers, Q., Muris, P., van Hoof, A., &
retardation. British Medical Bulletin, 52, 435–464. Meeus, W. (2008). Developmental trajectories of adolescent
Foley, D. L., Pickles, A., Maes, H. M., Silberg, J. L., & Eaves, L. anxiety disorder symptoms: A 5-year prospective community
J. (2004). Course and short-term outcomes of separation anxiety study. Journal of the American Academy of Child and Adolescent
disorder in a community sample of twins. Journal of the American Psychiatry, 47, 556–564.
Academy of Child and Adolescent Psychiatry, 43, 1107–1114. Hasson, R., & Fine, J. G. (2012). Gender differences among children
Fombonne, E. (2003). Epidemiological surveys of autism and other with ADHD on continuous performance tests: A meta-analytic
pervasive developmental disorders: An update. Journal of Autism review. Journal of Attention Disorders, 16, 190–198.
and Developmental Disorders, 33, 365–382. Higa-McMillan, C. K., Francis, S. E., Rith-Najarian, L., & Chorpita,
Ford, M. A., Kratochwill, T. R., Sladeczek, I., & Carlson, J. S. (1998). B. F. (2016). Evidence base update: 50 years of research on
Selective mutism: Development, identification, characteristics, treatment for child and adolescent anxiety. Journal of Clinical
etiology and school experience. School Psychology Quarterly, 13, Child & Adolescent Psychology, 45, 91–113.
192–227. Houts, A. C., & Abramson, H. (1990). Assessment and treatment for
Ford, T., Goodman, R., & Meltzer, H. (2003). The British Child and functional childhood enuresis and encopresis: Toward a partnership
Adolescent Mental Health Survey 1999: The prevalence of DSM- between health psychologists and physicians. In S. B. Morgan &
IV disorders. Journal of the American Academy of Child and T. M. Okwumabua (Eds.), Child and adolescent disorders:
Adolescent Psychiatry, 42, 1203–1211. Developmental and health psychology perspectives (pp. 47–103).
Forsythe, W. I., & Redmond, A. (1974). Enuresis and spontaneous Hillsdale: Erlbaum.
cure rate: Study of 1,129 enuretics. Archives of Disease in Houts, A. C., Berman, J. S., & Abramson, H. (1994). Effectiveness of
Childhood, 49, 259–263. psychological and pharmacological treatments for nocturnal enuresis.
Fossum, S., Handegård, B. H., Adolfsen, F., Vis, S. A., & Wynn, R. Journal of Consulting and Clinical Psychology, 62, 737–745.
(2016). A meta-analysis of long-term outpatient treatment effects Hublin, C., Kapiro, J., Partnen, M., & Koskenvuo, M. (1998). Nocturnal
for children and adolescents with conduct problems. Journal of enuresis in a nationwide twin cohort. Sleep, 21, 579–585.
Child and Family Studies, 25, 15–29. Immunization Safety Review Committee (2004). Immunization
France, A. (2012). DSM-5 is guide not bible—ignore its ten worst Safety Review: Vaccines and Autism. Washington, DC: National
changes. Psychology Today, December 2. Retrieved from www. Academies Press. Retrieved from www.nap.edu.
psychologytoday.com/blog/dsm5-in-distress/201212/dsm-5-is- Jurbergs, N., & Ledley, D. R. (2005). Separation anxiety. Psychiatric
guide-not-bible-ignore-its-ten-worst-changes. Annals, 35, 728–735.
Frigerio, A., Ceppi, E., Rusconi, M., Giorda, R., Raggi, M. E., & Karen, R. (1994). Becoming attached: First relationships and how
Fearon, P. (2009). The role played by the interaction between they shape our capacity to love. New York: Oxford University
genetic factors and attachment in the stress response in infancy. Press.
Journal of Child Psychology and Psychiatry, 50, 1513–1522. Kazdin, A. E. (1996). Combined and multimodal treatments in
Friman, P. C., & Jones, K. M. (1998). Elimination disorders in child and adolescent psychotherapy: Issues, challenges and
children. In T. S. Watson & F. M. Gresham (Eds.), Handbook of research directions. Clinical Psychology: Science and Practice,
child behavior therapy (pp. 239–260). New York: Plenum Press. 3, 69–100.
Fritz, G., & Armbrust, J. (1982). Enuresis and encopresis. Psychiatric Kazdin, A. E., & Blase, S. L. (2011). Rebooting psychotherapy
Clinics of North America, 5, 283–296. research and practice to reduce the burden of mental illness.
Fritz, G., Rockney, R., Bernet, W., Arnold, V., Beitchman, J., Benson, Perspectives on Psychological Science, 6, 21–37.
R. S., . . . Stock, S. (2004). Practice parameter for the assessment Kazdin, A. E., Esveldt-Dawson, K., French, N. H., & Unis, A. S.
and treatment of children and adolescents with enuresis. Journal (1987). Problem-solving skills training and relationship therapy in
of the American Academy of Child and Adolescent Psychiatry, 43, the treatment of antisocial child behavior. Journal of Consulting
1540–1550. and Clinical Psychology, 55, 76–85.
Galuschka, K., Ise, E., Krick, K., & Schulte-Körne, G. (2014). Kearney, C. A., Sims, K. E., Pursell, C. R., & Tillotson, C. A. (2003).
Effectiveness of treatment approaches for children and adolescents Separation anxiety disorder in young children: A longitudinal
with reading disabilities: A meta-analysis of randomized controlled and family analysis. Journal of Clinical Child and Adolescent
trials. PLOS ONE, 9, e89900. Psychology, 32, 593–598.
Gershon, J., & Gershon, J. (2002). A meta-analytic review of gender Keenan, K., Shaw, D. S., Delliquardi, E., Giovannelli, J., & Walsh,
differences in ADHD. Journal of Attention Disorders, 5, 143–154. B. (1998). Evidence for the continuity of early problem behaviors:
Gillon, G., & Dodd, B. (1997). Enhancing the phonological Application of a developmental model. Journal of Abnormal Child
processing skills of children with specific reading disability. Psychology, 26, 441–445.
European Journal of Communication Disorders, 32, 67–90. Keenan, K., & Wakschlag, L. S. (2004). Are oppositional defiant and
Greenberg, M. T., Speltz, M. L., & DeKlyen, M. (1993). The role conduct disorder symptoms normative behaviors in preschoolers?
of attachment in the early development of disruptive behaviour A comparison of referred and nonreferred children. American
problems. Development and Psychopathology, 5, 191–213. Journal of Psychiatry, 161, 356–358.
Gross, R. T., & Dornsbusch, S. M. (1982). Enuresis. In M. D. Levine, King, S. M., Iacono, W. G., & McGue, M. (2004). Childhood
W. B. Carey, A. C. Crocker & R. T. Gross (Eds.), Developmental externalizing and internalizing psychopathology in the prediction
behavioral pediatrics (pp. 574–586). Philadelphia: Saunders. of early substance use. Addiction, 99, 1548–1559.
rie66620_ch14_443-490.indd 484 07/31/17 05:27 PM

Klein, R. G. (1995). Is panic disorder associated with childhood separation Mannuzza, S., Klein, R. G., Abikoff, H., & Moulton, J. L., III. (2004).
anxiety disorder? Clinical Neuropharmacology, 18, S7–S14. Significance of childhood conduct problems to later development
Kochanska, G., Philibert, R. A., & Barry, R. A. (2009). Interplay of conduct disorder among children with ADHD: A prospective
of genes and early mother–child relationship in the development follow-up study. Journal of Abnormal Child Psychology, 32,
of self-regulation from toddler to preschool age. Journal of Child 565–573.
Psychology and Psychiatry, 50, 1331–1338. Mash, E. J., & Dozois, D. J. A. (2003). Child psychopathology: A
Kopp, S., & Gillberg, C. (1997). Selective mutism: A population- developmental-systems perspective. In E. J. Mash & R. A. Barkley
based study: A research note. Journal of Child Psychology and (Eds.), Child Psychopathology (2nd ed.) (pp. 3–71). New York:
Psychiatry, 38, 257–262. Guilford Press.
Kristensen, H. (2000). Selective mutism and comorbidity with Masi, G. (2004). Pharmacotherapy of pervasive developmental
developmental disorder/delay, anxiety disorder and elimination disorders in children and adolescents. CNS Drugs, 18, 1031–1052.
disorder. Journal of the American Academy of Child and Adolescent Maughan, B., Rowe, R., Messer, J., Goodman, R., & Meltzer, H.
Psychiatry, 39, 249–256. (2004). Conduct disorder and oppositional defiant disorder in a
Kumpulainen, K., Rasanen, E., Raaska, H., & Somppi, V. (1998). national sample: Developmental epidemiology. Journal of Child
Selective mutism among second-graders in elementary school. Psychology and Psychiatry, 45, 609–621.
European Child and Adolescent Psychiatry, 7, 24–29. Max, J. E., Castillo, C. S., Bokura, H., Robin, D. A., Lindgren, S.
Lahey, B. B., Loeber, R., Quay, H. C., Applegate, B., Shaffer, D., D., Smith, W. L., Jr., . . . Mattheiss, P. J. (1998). Oppositional
Waldman, I., . . . Bird, H. R. (1998). Validity of DSM-IV subtypes defiant disorder symptomatology after traumatic brain injury: A
of conduct disorder based on age of onset. Journal of the American prospective study. Journal of Nervous and Mental Disease, 186,
Academy of Child and Adolescent Psychiatry, 37, 435–442. 325–332.
Lavigne, J. V., Cicchetti, C., Gibbons, R. D., Binns, H. J., Larsen, Mayes, S. D., Waxmonsky, J. D., Calhoun, S. L., & Bixler, E. O.
L., & DeVito, C. (2001). Oppositional defiant disorder with (2016). Disruptive mood dysregulation disorder symptoms and
onset in preschool years: Longitudinal stability and pathways to association with oppositional defiant and other disorders in a
other disorders. Journal of the American Academy of Child and general population child sample. Journal of Child and Adolescent
Adolescent Psychiatry, 40, 1393–1400. Psychopharmacology, 26, 101–106.
Lavigne, J. V., LeBailly, S. A., Hopkins, J., Gouze, K. R., & Binns, H. Mazzucchelli, T., & Sanders, M. (2010). Facilitating practitioner
J. (2009). The prevalence of ADHD, ODD, depression, and anxiety flexibility within an empirically supported intervention: Lessons
in a community sample of 4-year-olds. Journal of Clinical Child from a system of parenting support. Clinical Psychology: Science
and Adolescent Psychology, 38, 315–328. and Practice, 17, 238–252.
Lawrence, D., Johnson, S., Hafekost, J., Boterhoven De Haan, K., McArthur, D., & Adamson, L. B. (1996). Joint attention in preverbal
Sawyer, M., Ainley, J., & Zubrick, S. R. (2015). The mental health children: Autism and developmental language disorder. Journal of
of children and adolescents: Report on the second Australian Child Autism and Developmental Disorders, 26, 481–496.
and Adolescent Survey of Mental Health and Wellbeing. Canberra: McBurnett, K., Lahey, B. B., Rathouz, P. J., & Loeber, R. (2000).
Department of Health. Low salivary cortisol and persistent aggression in boys referred for
Leibenluft, E. (2011). Severe mood dysregulation, irritability, and disruptive behavior. Archives of General Psychiatry, 57, 38–43.
the diagnostic boundaries of bipolar disorder in youths. American McGee, R., Share, D. L., Moffitt, T., Williams, S., & Silva, P. A.
Journal of Psychiatry, 168, 129–142. (1998). Reading disability, behaviour problems and juvenile
Levy, F., Hay, D. A., & Bennett, K. S. (2006). Genetics of attention delinquency. In D. H. Saklofske & S. B. G. Eysenck (Eds.),
deficit hyperactivity disorder: A current review and future Individual differences in children and adolescents (pp. 158–172).
prospects. International Journal of Disability, Development and New Brunswick: Transaction Publishers.
Education, 53, 5–20. McGee, R., Williams, S., Moffitt, T., & Anderson, J. (1989). A
Loeber, R., Burke, J. D., Lahey, B. B., Winters, A., & Zera, M. comparison of 13-year-old boys with attention deficit and/or
(2000). Oppositional defiant and conduct disorder: A review of the reading disorder on neuropsychological measures. Journal of
past 10 years, Part I. Journal of the American Academy of Child Abnormal Child Psychology, 17, 37–53.
and Adolescent Psychiatry, 39, 1468–1484. Moffatt, M. E. K., Harlos, S., Kirshen, A. J., & Burd, L. (1993).
Loeber, R., Burke, J., & Pardini, D. A. (2009). Perspectives on Desmopressin acetate and nocturnal enuresis: How much do we
oppositional defiant disorder, conduct disorder, and psychopathic know? Pediatrics, 92, 420–425.
features. Journal of Child Psychology and Psychiatry, 50, 133–142. Moffitt, T. E. (1993). Adolescence-limited and life-course-persistent
Luman, M., Oosterlaan, J., & Sergeant, J. A. (2005). The impact of antisocial behavior: A developmental taxonomy. Psychological
reinforcement contingencies on AD/HD: A review and theoretical Review, 100, 674–701.
appraisal. Clinical Psychology Review, 25, 183–213. Molina, B. S. G., Hinshaw, S. P., Swanson, J. M., Arnold, E., Vitiello,
MacGregor, R., Pullar, A., & Cundall, D. (1994). Silent at school: B., Jensen, P. S. . . . The MTA Cooperative Group (2009). The MTA
Elective mutism and abuse. Archives of the Disabled Child, 70, at 8 Years: Prospective follow-up of children treated for combined-
540–541. type ADHD in a multisite study. Journal of the American Academy
Malicky, G. V., & Norman, C. A. (1999). Phonological awareness and of Child & Adolescent Psychiatry, 48, 484–500.
reading: An alternative interpretation from a clinical perspective. Morawska, A., Sanders, M. R., Goadby, E., Headley, C., Hodge, L.,
Alberta Journal of Educational Research, 45, 18–34. McAuliffe, C., . . . Anderson, E. (2011). Is the Triple P-Positive
rie66620_ch14_443-490.indd 485 07/31/17 05:27 PM

Parenting Program acceptable to parents from culturally diverse Polanczyk, G. V., Salum, G. A., Sugaya, L. S., Caye, A., & Rohde,
backgrounds? Journal of Child and Family Studies, 20, 614–622. L. A. (2015). Annual research review: A meta-analysis of the
Munkvold, L., Lundervold, A., Lie, S. A., & Manger, T. (2009). worldwide prevalence of mental disorders in children and
Should there be separate parent and teacher-based categories adolescents. Journal of Child Psychology and Psychiatry, 56,
of ODD? Evidence from a general population. Journal of Child 345–365.
Psychology and Psychiatry, 50, 1264–1272. Polanczyk, G. V., Willcutt, E. G., Salum, G. A., Kieling, C., & Rohde,
Murphy, C. C., Boyle, C., Schendel, D., Decoufle, P., & Yeargin- L. A. (2014). ADHD prevalence estimates across three decades:
Allsopp, M. (1998). Epidemiology of mental retardation in An updated systematic review and meta-regression analysis.
children. Mental Retardation and Developmental Disabilities International Journal of Epidemiology, 43, 434–442.
Research Reviews, 4, 6–13. Porjes, M. D. (1992). Intervention with the selectively mute child.
Murphy, C. C., Yeargin-Allsopp, M., Decoufle, P., & Drews, C. D. Psychology in the Schools, 29, 367–376.
(1995). The administrative prevalence of mental retardation in Poulton, R., Milne, B. J., Craske, M. G., & Menzies, R. G. (2001). A
10-year-old children in metropolitan Atlanta, 1985 through 1987. longitudinal study of the etiology of separation anxiety. Behaviour
American Journal of Public Health, 85, 319–323. Research and Therapy, 39, 1395–1410.
Nigg, J. T. (2005). Neuropsychologic theory and findings in attention- Prinz, R. J., & Sanders, M. R. (2007). Adopting a population-level
deficit/hyperactivity disorder: The state of the field and salient approach to parenting and family support interventions. Clinical
challenges for the coming decade. Biological Psychiatry, 57, Psychology Review, 27, 739–749.
1424–1435. Purvis, K. L., & Tannock, R. (2000). Phonological processing, not
NSW Department of Health (2001). New South Wales Child Health inhibitory control, differentiates ADHD and reading disability.
Survey 2001. Sydney: Epidemiology and Surveillance Branch, Journal of the American Academy of Child and Adolescent
NSW Department of Health. Psychiatry, 39, 485–494.
O’Connor, T., Bredenkamp, D., & Rutter, M. (1999). Attachment Rapee, R. M. (2012). Family factors in the development and
disturbances and disorders in children exposed to early severe management of anxiety disorders. Clinical Child and Family
deprivation. Infant Mental Health Journal, 20, 10–29. Psychology Review, 15, 69–80.
Ohan, J. L., & Johnston, C. (2005). Gender appropriateness of Rapee, R. M., Abbott, M. J., & Lyneham, H. J. (2006). Bibliotherapy
symptom criteria for attention-deficit/hyperactivity disorder, for children with anxiety disorders using written materials for
oppositional defiant disorder, and conduct disorder. Child parents: A randomized controlled trial. Journal of Consulting and
Psychiatry and Human Development, 35, 359–381. Clinical Psychology, 74, 436–444.
Owens, J. S., & Hoza, B. (2003). Diagnostic utility of DSM-IV-TR Remschmidt, H., Poller, M., Herpertz-Dahlmann, B., Hennigause, K.,
symptoms in the prediction of DSM-IV-TR ADHD subtypes and & Gutenbunner, C. (2001). A follow-up study of 45 patients with
ODD. Journal of Attention Disorders, 7, 11–27. elective mutism. European Archives of Psychiatry and Clinical
Patterson, G. R. (1982). Coercive family process. Eugene: Castalia Neuroscience, 251, 284–296.
Publishing Co. Reynolds, W. M. (Ed.) (1992). Internalizing disorders in children and
Patterson, G. R., & Bank, L. (1989). Some amplifying mechanisms adolescents. New York: Wiley.
for pathologic processes in families. In M. R. Gunnar & E. Thelen Ritterband, L. M., Ardalan, K., Thorndike, F. P., Magee, J. C., Saylor,
(Eds.), Systems and development: Minnesota Symposium on Child D. K., Cox, D. J., . . . Borowitz, S. M. (2008). Real world use of an
Development (vol. 22) (pp. 167–209). Hillsdale: Erlbaum. Internet intervention for pediatric encopresis. Journal of Medical
Paul, R. (2003). Promoting social communication in high functioning Internet Research, 10, e16.
individuals with autistic spectrum disorders. Child and Adolescent Rittig, S., Knudsen, U. B., Norgaard, J. P., Pedersen, E. B., &
Psychiatric Clinics of North America, 12, 87–106. Djurhuus, J. C. (1989). Abnormal diurnal rhythm of plasma
Pelsser, L. M., Frankena, K., Toorman, J., Savelkoul, H. F., Dubois, A. vasopressin and urinary output in patients with enuresis. American
E., Pereira, R. R., . . . Buitelaar, J. K. (2011). Effects of a restricted Journal of Physiology, 25, 664–671.
elimination diet on the behaviour of children with attention-deficit Rockney, R. M., McQuade, W. H., Days, A. L., & Linn, H. E.
hyperactivity disorder (INCA study): A randomised controlled (1996). Encopresis treatment outcome: Long-term follow-up of 45
trial. The Lancet, 377, 494–503. cases. Journal of Developmental and Behavioral Pediatrics, 17,
Pelsser, L. M. J., Frankena, K., Toorman, J., Savelkoul, H. F. J., 380–385.
Pereira, R. R., & Buitelaar, J. K. (2009). A randomised controlled Rogers, S. J. (1996). Brief report: Early intervention in autism.
trial into the effects of food on ADHD. European Child and Journal of Autism and Developmental Disorders, 26, 243–246.
Adolescent Psychiatry, 18, 12–19. Rossignol, D. A., & Frye, R. E. (2012). A review of research trends in
Petitclerc, A., Boivin, M., Dionne, G., Zoccolillo, M., & Tremblay, physiological abnormalities in autism spectrum disorders: Immune
R. E. (2009). Disregard for rules: The early development and dysregulation, inflammation, oxidative stress, mitochondrial
predictors of a specific dimension of disruptive behavior disorders. dysfunction and environmental toxicant exposures. Molecular
Journal of Child Psychology and Psychiatry, 50, 1477–1484. Psychiatry, 17, 389–401.
Petty, C. R., Monuteaux, M. C., Mick, E., Hughes, S., Small, J., Rubin, K. H., Stewart, S. L., & Chen, X. (1995). Parents of aggressive
Faraone, S. V., . . . Biederman, J. (2009). Parsing the familiality and withdrawn children. In M. H. Bornstein (Ed.), Handbook of
of oppositional defiant disorder from that of conduct disorder: A parenting: Vol. 1 Children and parenting (pp. 255–284). Mahwah:
familial risk analysis. Journal of Psychiatric Research, 43, 345–352. Erlbaum.
rie66620_ch14_443-490.indd 486 07/31/17 05:27 PM

Rutter, M. (2000). Resilience reconsidered: Conceptual considerations, of adolescent antisocial behaviour: Outcomes and connections.
empirical findings, and policy implications. In J. P. Shonkoff & S. Third report. Melbourne: Australian Institute of Family Studies.
J. Meisels (Eds.), Handbook of early childhood intervention (pp. Smart, D., Sanson, A., & Prior, M. (1996). Connections between
651–682). Cambridge: Cambridge University Press. reading disability and behavior problems: Testing temporal and
Sameroff, A. J., & Fiese, B. H. (2000). Models of development and causal hypotheses. Journal of Abnormal Child Psychology, 24,
developmental risk. In C. H. Zeanah (Ed.), Handbook of infant 363–383.
mental health (2nd ed.) (pp. 3–19). New York: Guilford Press. Smart, D., Vassallo, S., Sanson, A., Richardson, N., Dussuyer, I.,
Sanders, M. R. (1999). Triple P-Positive Parenting Program: McKendry, B., . . . Oberkleid, F. (2003). Patterns and precursors
Towards an empirically validated multilevel parenting and family of adolescent antisocial behaviour: Types, resiliency and
support strategy for the prevention of behavior and emotional environmental influences. Second report. Melbourne: Australian
problems in children. Clinical Child and Family Psychology Institute of Family Studies.
Review, 2, 71–90. Snowling, M. (1998). Dyslexia as a phonological deficit: Evidence and
Sanders, M. R., Baker, S., & Turner, K. M. T. (2012). A randomized implications. Child Psychology and Psychiatry Review, 3, 4–11.
controlled trial evaluating the efficacy of Triple P online with Sonuga-Barke, E. J. S., Brandeis, D., Cortese, S., Daley, D., Ferrin,
parents of children with early-onset conduct problems. Behaviour M., Holtmann, M., . . . Group, E. A. G. (2013). Nonpharmacological
Research & Therapy, 50, 675–684. interventions for ADHD: Systematic review and meta-analyses
Sanders, M., Calam, R., Durand, M., Liversidge, T., & Carmont, S. of randomized controlled trials of dietary and psychological
A. (2008). Does self-directed and web-based support for parents treatments. American Journal of Psychiatry, 170, 275–289.
enhance the effects of viewing a reality television series based Speltz, M. L., McClellan, J., DeKlyen, M., & Jones, K. (1999).
on the Triple P–Positive Parenting Programme? Journal of Child Preschool boys with oppositional defiant disorder: Clinical
Psychology and Psychiatry, 49, 924–932. presentation and diagnostic change. Journal of the American
Sanders, M. R., Haslam, D. M., Calam, R., Southwell, C., & Academy of Child and Adolescent Psychiatry, 38, 838–845.
Stallman, H. M. (2011). Designing effective interventions for Spence, S. H., Holmes, J. M., March, S., & Lipp, O. V. (2006). The
working parents: A survey of UK parents. Journal of Children’s feasibility and outcome of clinic plus internet delivery of cognitive-
Services, 6, 186–200. behavior therapy for childhood anxiety. Journal of Consulting and
Sanders, M. R., Markie-Dadds, C., Rinaldis, M., Firman, D., & Baig, Clinical Psychology, 74, 614–621.
N. (2007). Using household survey data to inform policy decisions Sroufe, L. A. (1990). Considering normal and abnormal together:
regarding the delivery of evidence-based parenting interventions. The essence of developmental psychopathology. Development and
Child: Care, Health and Development, 33, 768–783. Psychopathology, 2, 335–347.
Schill, M. T., Kratochwill, T. R., & Gardner, W. I. (1996). An Streissguth, A. P., Barr, H. M., & Sampson, P. D. (1990). Moderate
assessment protocol for selective mutism: Analogue assessment prenatal alcohol exposure: Effects on child IQ and learning
using parents as facilitators. Journal of School Psychology, 34, problems at age 7.5 years. Alcoholism: Clinical and Experimental
1–21. Research, 14, 662–669.
Schoenwald, S. K., & Henggeler, S. W. (2005). Multisystemic therapy Suveg, C., Aschenbrand, S. G., & Kendall, P. C. (2005). Separation
for adolescents with serious externalizing problems. In J. L. anxiety disorder, panic disorder, and school refusal. Child and
Lebow (Ed.), Handbook of clinical family therapy (pp. 103–127). Adolescent Psychiatric Clinics of North America, 14, 773–795.
Hoboken: Wiley. Swanson, H. L., & Berninger, V. W. (1995). The role of working
Schulman, S. L., Colish, Y., von Zuben, F. C., & Kodman-Jones, memory in skilled and less skilled readers’ comprehension.
C. (2000). Effectiveness of treatments for nocturnal enuresis in a Intelligence, 21, 83–108.
heterogeneous population. Clinical Pediatrics, 39, 359–364. Szatmari, P., Jones, M. B., Zwaigenbaum, L., & MacLean, J. E.
Shaffer, D. (1985). Enuresis. In M. Rutter & L. Herso (Eds.), Child (1998). Genetics of autism: Overview and new directions. Journal
and adolescent psychiatry: Modern approaches (pp. 465–481). of Autism and Developmental Disorders, 28, 351–368.
London: Blackwell. Szymanski, L., & King, B. H. (1999). Practice parameters for the
Shreeram, S., He, J.-P., Kalaydjian, A., Brothers, S., & Merikangas, K. assessment and treatment of children, adolescents, and adults
R. (2009). Prevalence of enuresis and its association with attention- with mental retardation and comorbid mental disorders. Journal
deficit/hyperactivity disorder among U.S. children: Results from a of the American Academy of Child and Adolescent Psychiatry, 38
nationally representative study. Journal of the American Academy (Supp.), 5S–31S.
of Child and Adolescent Psychiatry, 48, 35–41. Tancer, N. K. (1992). Elective mutism: A review of the literature.
Silk, J. S., Nath, S. R., Siegel, L. R., & Kendall, P. C. (2000). In B. B. Lahey & A. E. Kazdin (Eds.), Advances in clinical child
Conceptualizing mental disorders in children: Where have we been psychology (vol. 14) (pp. 265–288). New York: Plenum Press.
and where are we going? Development and Psychopathology, 12, Tanguay, P. E. (2000). Pervasive developmental disorders: A 10-year
713–735. review. Journal of the American Academy of Child and Adolescent
Simon, P. G., Joshi, M., & Williams, K. A. (1999). Not all reading Psychiatry, 39, 1079–1095.
disabilities are alike. Journal of Learning Disabilities, 32, 120–137. Thomas, R., Sanders, S., Doust, J., Beller, E., & Glasziou, P. (2015).
Smart, D., Richardson, N., Sanson, A., Dussuyer, I., Marshall, B., Prevalence of attention-deficit/hyperactivity disorder: A systematic
Toumbourou, J., . . . Oberkleid, F. (2005). Patterns and precursors review and meta-analysis. Pediatrics, 135, e994–e1001.
rie66620_ch14_443-490.indd 487 07/31/17 05:27 PM

Tidmarsh, L., & Volkmar, F. R. (2003). Diagnosis and epidemiology Wakefield, A. J., Murch, S. H., Anthony, A., Linnell, J., Casson, D. M.,
of autism spectrum disorders. Canadian Journal of Psychiatry, 48, Malik, M., . . . Walker-Smth, J. A. (1998). Ileal-lymphoid-nodular
517–525. hyperplasia, non-specific colitis, and pervasive developmental
Torgesen, J. K. (2000). Individual differences in response to early disorder in children. The Lancet, 351, 637–641.
intervention in early reading: The lingering problem of treatment Webster-Stratton, C. (1990). Long-term follow-up of families with
resisters. Learning Disabilities Research and Practice, 15, 55–64. young conduct problem children: From preschool to grade school.
Tremblay, R. E. (2010). Developmental origins of disruptive Journal of Clinical Child Psychology, 19, 144–149.
behaviour problems: The original sin hypothesis, epigenetics and Weems, C. F. (2008). Developmental trajectories of childhood
their consequences for prevention. Journal of Child Psychology anxiety: Identifying continuity and change in anxious emotion.
and Psychiatry, 51, 341–367. Developmental Review, 28, 488–502.
Turk, C. L., Heimberg, R. G., & Hope, D. A. (2001). Social anxiety Weiss, B., Dodge, K. A., Bates, J. E., & Pettit, G. S. (1992).
disorder. In D. H. Barlow (Ed.), Clinical handbook of psychological Some consequences of early harsh discipline: Child aggression
disorders: A step-by-step treatment manual (3rd ed.) (pp. 114–153). and a maladaptive social information processing style. Child
New York: Guilford Press. Development, 63, 1321–1335.
Tuvblad, C., Zheng, M., Raine, A., & Baker, L. A. (2009). A common Weisz, J. R., Doss, A. J., & Hawley, K. M. (2005). Youth
genetic factor explains the covariation among ADHD ODD and CD psychotherapy outcome research: A review and critique of the
symptoms in 9–10 year old boys and girls. Journal of Abnormal evidence base. Annual Review of Psychology, 56, 337–363.
Child Psychology, 37, 153–167. Weisz, J. R., & Gray, J. S. (2008). Evidence-based psychotherapy for
van Goozen, S. H. M., van den Ban, E., Matthys, W., Cohen-Kettenis, children and adolescents: Data from the present and a model for the
P. T., Thijssen, J. H. H., & van Engeland, H. (2000). Increased future. Child and Adolescent Mental Health, 13, 54–65.
adrenal androgen functioning in children with oppositional defiant Weisz, J. R., Weiss, B., Alicke, M. D., & Klotz, M. L. (1987).
disorder: A comparison with psychiatric and normal controls. Effectiveness of psychotherapy with children and adolescents: A
Journal of the American Academy of Child and Adolescent meta-analysis for clinicians. Journal of Consulting and Clinical
Psychiatry, 39, 1446–1451. Psychology, 55, 542–549.
van Lier, P. A. C., Vuijk, P., & Crijnen, A. A. M. (2005). Understanding Willcutt, E. G., Pennington, B. F., Boada, R., Ogline, J. S., Tunick, R.
mechanisms of change in the development of antisocial behavior: A., Chhabildas, N. A., & Olson, R. K. (2001). A comparison of the
The impact of a universal intervention. Journal of Abnormal Child cognitive deficits in reading disability and attention-deficit/hyperactivity
Psychology, 33, 521–535. disorder. Journal of Abnormal Psychology, 110, 157–172.
Van Oort, F. V. A., Greaves-Lord, K., Verhulst, F. C., Ormel, J., Williams, K., Glasson, E. J., Wray, J., Tuck, M., Helmer, M., Bower,
& Huizink, A. C. (2009). The developmental course of anxiety C. I., . . . Olson, R. K. (2005). Incidence of autism spectrum
symptoms during adolescence: The TRIALS study. Journal of disorders in children in two Australian states. Medical Journal of
Child Psychology and Psychiatry, 50, 1209–1217. Australia, 182, 108–111.
Vassallo, S., Smart, D., Sanson, A., Dussuyer, I., McKendry, B., Willoughby, M. T. (2003). Developmental course of ADHD
Toumbourou, J., Prior, M., . . . Oberkleid, F. (2002). Patterns
symptomatology during the transition from childhood to

and precursors of adolescent antisocial behaviour. First report. adolescence: A review with recommendations. Journal of Child
Melbourne: Australian Institute of Family Studies. Psychology and Psychiatry, 44, 88–106.
Viana, A. G., Beidel, D. C., & Rabian, B. (2009). Selective mutism: Wong, C., Odom, S. L., Hume, K. A., Cox, A. W., Fettig, A.,
A review and integration of the last 15 years. Clinical Psychology Kucharczyk, S.,  . . 
. Schultz, T. R. (2015). Evidence-based
Review, 29, 57–67. practices for children, youth, and young adults with autism
Vidair, H. B., & Gunlicks-Stoessel, M. L. (2009). Innovative child spectrum disorder: A comprehensive review. Journal of Autism
and adolescent treatment research for anxiety and depressive and Developmental Disorders, 45, 1951–1966.
disorders. Depression and Anxiety, 26, 307–308. Wright, H. H., Holmes, G. R., Cuccaro, M. L., & Leonhardt, T. V.
Volkmar, F., Cook, E. H., Jr., Pomeroy, J., Realmuto, G., & Tanguay, (1994). A guided bibliography of the selective mutism (elective
P. (1999). Practice parameters for the assessment and treatment of mutism) literature. Psychological Reports, 74, 995–1007.
children, adolescents, and adults with autism and other pervasive Yakinci, C., Mangen, B., Durmaz, Y., Balbay, D., & Karabiber, H.
developmental disorders. Journal of the American Academy of (1997). Autonomic nervous system functions in children with
Child and Adolescent Psychiatry, 38 (Supp.), 32S–54S. nocturnal enuresis. Brain and Development, 19, 485–487.
von Gontard, A., Heron, J., & Joinson, C. (2011). Family history of Yeargin-Allsopp, M., Murphy, C. C., Cordero, J. F., & Decoufle,
nocturnal enuresis and urinary incontinence: Results from a large P. (1997). Reported biomedical causes and associated medical
epidemiological study. Journal of Urology, 185, 2303–2307. conditions for mental retardation among 10-year-old children.
Wadsworth, S. J., Olson, R. K., Pennington, B. F., & DeFries, J. Developmental Medicine and Child Neurology, 39, 142–149.
C. (2000). Differential genetic etiology of reading disability as a Zero to Three (1994). Diagnostic classification of mental health and
function of IQ. Journal of Learning Disabilities, 33, 192–199. development disorders of infancy and early childhood: DC:0–3.
Wåhlstedt, C., Thorell, L. B., & Bohlin, G. (2009). Heterogeneity Washington, DC: Author.
in ADHD: Neuropsychological pathways, comorbidity and Zero to Three (2005). Diagnostic classification of mental health and
symptom domains. Journal of Abnormal Child Psychology, 37, development disorders of infancy and early childhood: DC:0–3R.
551–564. Washington, DC: Author.
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490
GRADUATE SPOTLIGHT
NAME: FRANCO SCALZO
Degree studied: Master of Psychology (Clinical

Psychology)
University: The University of Melbourne
Current position: Psychologist/Case Manager
Employer: Orygen, The National Centre of Excellence in

Youth Mental Health

I have always wanted to help people and to give something back to the community, and I am fascinated
by how the mind works and what motivates people to behave in certain ways. Working as a psychologist
in a community mental health setting enables me to help people and to keep learning about challenging
presentations such as personality disorders, psychosis and addiction.

I work in a public mental health clinical service that specialises in early intervention for young people with
psychosis. I have also maintained an interest in research by working in a neuroscience laboratory at the
University of Melbourne.

I provide individual psychological interventions to assist with the management of early psychosis and
the treatment of comorbid psychological disorders. However, case management involves more than just
individual counselling; it also includes referrals to Orygen’s psychosocial recovery program, vocational
consultant, family and peer support services, accommodation providers, legal services, and sexual and
physical health professionals. The laboratory work involves the use of cognitive-behavioural tests in
conjunction with neuroimaging to manipulate and observe cognitive processes that are implicated in
various clinical groups, in particular, individuals with problematic substance use.

I am inspired by the ability of clients to persevere and contribute to the community despite a highly
challenging mental illness. The most enjoyable aspect of research is each new insight into how the mind
works and how that knowledge is translated into treatment.

If you have the passion and curiosity for a career in psychology, then persevere; it is worth the hard work.
I would also encourage graduates to grasp any opportunity to get started, even if this means a move
interstate or further afield.
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CHAPTER 15
Ageing and psychological

disorders
Nancy A. Pachana
CHAPTER OUTLINE
● Ageing
● Psychological disorders in later life: the dementias
● Psychological disorders in later life: depression and anxiety
● Life events associated with later life: retirement, grandparenting, driving cessation and bereavement
● Positive or successful ageing
● Ageing organisations and resources in Australia, New Zealand and worldwide
● Summary

15.1 Describe the changes in physical, psychological and interpersonal functioning that are part of normal ageing and
how these fit within a lifespan perspective of psychology.
15.2 Describe how dementia (neurocognitive disorder) can affect an older person’s functioning and what the specific
diagnostic and treatment implications are for such disorders in later life.
15.3 Describe how psychological disorders such as depression or anxiety can affect an older person’s functioning
and what the specific diagnostic, assessment and treatment implications are for such disorders in later life.
15.4 Describe significant events that may occur in later life with respect to their impact on psychological wellbeing.
15.5 Describe how successful or positive ageing can be fostered in older adults.
15.6 Identify organisations and resources from Australia, New Zealand and globally that can enhance the
psychological functioning of older adults.
AGEING AND PSYCHOLOGICAL DISORDERS: AN AUSTRALASIAN FOCUS

Throughout history, and in all parts of the world, people have been interested in questions about ageing. What are the
keys to living a long and healthy life? What can older adults contribute to society? These questions are being asked with
even greater importance today, in Australia as well as in the rest of the world. This is because population demographics
tell us that the percentages of older adults aged 65 and over are increasing across both the developed as well as the
developing world.
These questions were also asked in ancient times. The Greek philosophers Plato and Socrates both believed that one
of the benefits of growing older is the ability to use accumulated knowledge and experiences gained earlier in life to help
oneself and one’s family and friends, and to contribute positively to one’s community. Similar sentiments are expressed
by modern researchers who focus on the benefits of ageing, such as positive changes in social networks in later life, the
growth in wisdom with age and the factors that influence successful ageing.
continued
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These more positive views of ageing are to be contrasted with

common negative understandings of what it means to grow older—
with a common view being that ageing inevitably leads to a loss of
functioning and the ability to enjoy life. Shakespeare, who did not
have many good things to say about ageing, expressed this concern:
All the world’s a stage,
And all the men and women merely players;
They have their exits and their entrances,
And one man in his time plays many parts,
His acts being seven ages . . . Last scene of all,
That ends this strange eventful history,
Is second childishness and mere oblivion,
Sans teeth, sans eyes, sans taste, sans everything.
The idea that ageing, even in the face of illnesses such as dementia,
precludes quality of life is not true. This has been highlighted by
several Australian authors who themselves have dementia. For
instance, Christine Bryden was diagnosed with dementia when
she was 46. Since then she has been a strong public speaker and
advocate for people living with dementia. Her book Dancing with
Dementia: My Story of Living Positively with Dementia (2005)
chronicles her experiences and how she has continued to lead an
DAL
active and productive life while coping with dementia. In an interview
on the All in the Mind program for the radio station ABC RN (2005),
Christine discussed her book, including the reason she chose the title, saying that it is ‘a metaphor for trying to live
positively with dementia. It talks about the dance floor of dementia, changing my dance every few months or so because
I have to do new steps because I don’t function as well. Then there’s my care partner Paul helping me around the floor.’
In terms of bringing a positive attitude to her experience of dementia, Christine has even described the condition as a
gift in that ‘it’s given me time to reflect, time to think, makes you think about what’s important in life, to focus on what’s
important in terms of the human being. That with this journey with dementia I’ve become less of a cognitive self . . . but
what I am becoming is more of a spiritual self . . . You know I’ve seen people at various stages and I know from talking
to people who nurse people at all stages that in the latest stages we do retain a knowledge of spiritual things . . . So the
spiritual self remains intact, the appreciation of love and beauty and nature.’
Despite the positive approach Christine has brought to coping with her illness, she does not minimise the challenge
that living with dementia entails. Using another metaphor, she describes herself as a swan: ‘You look at me, people
say oh, you don’t sound like there’s anything wrong with you but what they see is the swan gliding on the surface . . .
Underneath I’m in the muddy water and my legs are frantically paddling trying to stop me from sinking and to keep me
moving.’ Among the challenges Christine faces are losing precious life memories with an ever-growing ‘black hole of life
unremembered’ and of anticipatory grief as she realises the losses that await her such as ‘driving, independence or being
able to get a sentence out without stumbling over all of the thoughts when they come out’.
Yet in the midst of these daily challenges, Christine has advocated strongly for those with dementia. Part of her
activism involves giving talks about her illness, including at dementia conferences. Although it is somewhat more
common now for dementia conferences to have sessions for people with dementia and caregivers, and to have some
speakers with dementia giving talks, this was certainly not the case when Christine started her journey with dementia.
Some physicians refused to believe that a person with dementia could give a talk about their illness. In the book she
refers to ‘coming out’ as someone with dementia.
Unfortunately, there is still a great deal of stigma attached to the diagnosis of dementia, and Christine’s story of a life
well-lived is inspiring as well as directly challenging of this stigma. In Christine’s own words: ‘We go to a doctor and we
get a diagnosis and then [at] some other stage of this disease we die . . . Now there’s a whole journey between those
two points and it’s a journey of being present not a journey of being absent. Certainly a journey of fading for me, fading
in cognition but growing spiritually. So I just really object to the whole stigma.’
Older adults experience a range of changes associated with age, and in some cases changes associated with physical
or psychological illnesses, to which they need to adapt in order to be able to continue to participate in activities as well as in
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Chapter 15 Ageing and psychological disorders 493
their communities. Psychologists can contribute to helping older adults make sense of these physical and mental changes,
and help those with illnesses, including dementia, get the most out of living.
Current psychological research on ageing has moved away from an emphasis on disease states and decline to
include the study of strengths and the positive aspects of ageing. A focus on positive as well as negative aspects
of ageing will ultimately contribute the most to helping individuals live out their later years productively and to age
successfully. The present chapter aims to present an overview of current understandings regarding the psychology
of ageing. It will begin by presenting information regarding the demographics and epidemiology of ageing followed
by historical approaches to the psychology of ageing. The cognitive, emotional and social changes associated with
normal ageing will then be presented. As well as providing a more balanced view of the ageing process to counter
negative stereotypes, understanding normal ageing is essential for identifying the presence of illness in later life (i.e.,
when the changes in functioning are beyond what would be considered normal). Against this normal developmental
backdrop, the chapter will then describe the two major classes of disorders in later life: (a) dementing conditions, and
(b) depression and anxiety disorders. Finally, special topics of interest to psychologists, including retirement,
grandparenting, driving cessation, bereavement and positive ageing, will be covered. Issues with respect to culture
will be interwoven throughout the chapter. It is hoped that such a broad introduction will stimulate new lines of thinking
about what it really means to grow old. As the poet Robert Browning wrote to his beloved:
Grow old along with me! The best is yet to be. . .
Source: Christine Bryden material reproduced by permission of Australian Corporation—Library Sales © ABC
LO 15.1 Ageing
The demographics and epidemiology of ageing
Everyone is the age of their heart.
Guatemalan proverb
The study of the population characteristics of a country or other group is called demography, and the
demographics of older populations in Australia, as well as the rest of the world, have been a focus of
much research in recent years. The populations of many industrialised countries are ‘greying’, meaning
that the proportion of the population comprising people over the age of 65 is increasing. In the many
countries experiencing this population trend, lower fertility rates and declining mortality rates due to
improvements in healthcare and medical technology are primarily responsible for these changes. In the
2011 Australian Census, 3.1 million people, or 14 per cent of the population of Australia, were aged
65 and over (Australian Bureau of Statistics [ABS], 2013). In this census there were 2500 centenarians
(persons over age 100) recorded; this number will continue to rise in the coming years. In addition,
similar to overseas data, those aged 85+ years represent the fastest-growing proportion of the Australian
population (ABS, 2015), again spurred on by medical advances. As shown in Figure 15.1, this has
resulted in a rectangularisation of the population curve over time (i.e., with increasing numbers in the
older age groups), which is projected to continue into the future.
Lifespan is also increasing in Australia, as is generally the case for countries globally. The average
life expectancy at birth in Australia is 80.2 years. To put this statistic into context, in the United
Kingdom the figure is 78.3, in the United States it is 77.3, and in Indonesia the figure is 66.5 (ABS,
2006). In nearly all countries, females outlive males due largely to decreases in mortality from
childbirth but also to increases in the general health of the female relative to the male population.
The most recent figures from the Australian Bureau of Statistics suggest that a male born in Australia
between the years 2007 and 2009 could expect to live to an average age of 79.3 years, while for
females this figure jumps to 83.9 years (ABS, 2011). Contrary to the common, pessimistic view that
most older adults live in institutions, approximately 85 per cent of older persons in Australia live in
their own home (ABS, 2005a; 2008).
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Males Age Females
1999 85+
80–84
2051
75–79
70–74
65–69
60–64
55–59
50–54
45–49
40–44
35–39
30–34
25–29
20–24
15–19
10–14
5–9
0–4
900 750 600 450 300 150 0 0 150 300 450 600 750 900
’000 ’000
FIGURE 15.1 The number of Australians in different age groups as measured in 1999 and projected to
exist in 2051
Source: From Australian Bureau of Statistics. (2001). Australian Social Trends, 2001 (cat. no. 4102.0). Canberra: Author.
The average age of Australia’s population of Aboriginal and Torres Strait Islander peoples is
relatively young, with a median age of 21 years (ABS, 2005b). It is of great concern that Indigenous
Australians experience an earlier age of onset for most chronic illnesses, and this contributes to a
markedly lowered life expectancy for Indigenous males (59.4 years) and females (64.8 years) compared
to the general Australian population.
Epidemiology is the study of the distribution and determinants of diseases and injuries in
human populations. The types and frequencies of illnesses affecting older Australians have changed
dramatically over time. For example, in the 1900s the most common causes of morbidity (illness)
and mortality (death) were acute illnesses such as pneumonia and tuberculosis. In contrast, the most
common causes of morbidity and mortality today are chronic illnesses such as heart disease and
cancer. In Indigenous groups in Australia, the mortality rates for diseases such as diabetes are between
7 and 11 times the rates for non-Indigenous people (ABS, 2005b).
Information from the 2015 Survey of Disability, Ageing and Carers (SDAC) showed that older
Australians living in the community were more active than in prior surveys, with the proportion that
participated in physical activities for exercise or recreation increasing from 44.5 per cent in 2012
to 49.2 per cent in 2015 (ABS, 2016). This survey also found that while the proportion of older
Australians has increased as a percentage of the overall population, the prevalence of disability in
this group has decreased to 50.7 per cent of older people living with disability in 2015, compared to
52.7 per cent in 2012.
Psychologists would do well to inform themselves about such population statistics, as the
increasing proportion of older adults in the population has important impacts on both research and
clinical practice (Laidlaw & Pachana, 2009). Unhelpful negative ageist stereotypes or attitudes can
lead to poorer health outcomes, both via the older person internalising these stereotypes (Levy, 2003),
as well as through misinformed decisions made by health professionals (such as the failure to provide
helpful treatments for depression due to the stereotype that depression is an inevitable part of ageing)
(Currey, 2008; Garner & Evans, 2010). For example, if people believe that some of the deterioration
of ageing is preventable or manageable, they are more likely to be active in their own self-care or more
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likely to look for solutions to health problems. Therefore, education about important biopsychosocial
aspects of ageing needs to be provided to health professionals and the general population.
In order to measure and help address gaps in knowledge and misconceptions about ageing, a Facts
on Aging Quiz (FAQ1) was created (Palmore, 1977). The FAQ1 has already been used in over 100
studies worldwide (Harris & Changas, 1994) and it has been adapted for use in Australia (Luszcz, 1982;
Pachana, Helmes, & Gudgeon, 2013) and New Zealand (Pennington, Pachana, & Coyle, 2001). Sample
questions from the Australian revision of the FAQ1 are shown in Table 15.1. Most of these studies have
found that knowledge about ageing is very limited, with the average person with a high-school education
scoring barely above 50 per cent (Pennington et al., 2001). Not surprisingly, the best predictor of scores
on the FAQ1 is education. Improving training in mental health care for older adults is therefore vital.
This requires attracting students into the gerontological sub-discipline, ensuring that curricula match
the needs of older adults and providing high-quality placement experiences for students in aged care
settings (Pachana, 2013). Although such training is lacking overall, even in Australia (Pachana, Emery,
Konnert, Woodhead, & Edelstein, 2010), progress is slowly being made in knowledge and improvement
of mental health issues, services and policies with regards to older adults (Pachana, 2013).
TABLE 15.1 Sample questions from the Australian revision of the Facts on Aging Quiz
1. In old age, a person’s height:

A. does not change.
B. only appears to change.
C. tends to decline.*
D. depends on how active one is.
2. Compared with younger persons, more older persons (65 years or over) are limited in their activity by which type of illness?
A. acute illnesses (short term)
B. colds and flu
C. infections
D. chronic illnesses*
3. Which type of illnesses do older persons have less frequently than younger persons?
A. chronic illness
B. arthritis
C. stroke
D. acute illness*
4. Compared with younger persons, older persons have:
A. more injuries in the home.*
B. about the same number of injuries in the home.
C. fewer injuries in the home.
D. twice the likelihood to be injured in the home.
5. Older workers’ absenteeism rates:
A. are higher than among younger workers.
B. cannot be trusted.
C. are about the same as among younger workers.
D. are lower than among younger workers.*
6. The life expectancy of Indigenous Australians at age 65 years:
A. is higher than that of Whites.
B. is lower than that of Whites.*
C. is about the same as that of Whites.
D. has not been determined.
*Correct answers
Source: From Pachana, N., Helmes, E., & Gudgeon, S. (2013). An Australian Facts on Ageing Quiz. Australian Journal on Ageing, 32, 117–121.
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Historical overview of the psychology of ageing

Ageing as a discipline of scientific inquiry has a relatively short history. In fact, one of the first
comprehensive textbooks on the psychology of ageing was produced by James Birren as recently as
1964. However, people have been interested in ageing, or more precisely in how to combat the ageing
process and lengthen life, for thousands of years.
Fascination with ageing often takes the form of searching for ways to lengthen the lifespan. The
search for a so-called ‘fountain of youth’ takes several forms. Throughout history, from the time of
the ancient Greeks and Chinese, people have searched for individuals living in remote parts of the
world who are incredibly long-lived, such as the Hyperboreans of Greek mythology. These ancient
pursuits have a contemporary counterpart in today’s centenarian studies (research on older adults
living past the age of 100), which are providing important information on the positive aspects of
ageing). Throughout history there have been searches for fountains or springs conferring longevity, as
well as the use of alchemy (i.e., the study of the properties of elements in search of an elixir to cure
diseases). Gerocomy, the belief and practice that older men can gain health and freedom from disease
through contact, particularly sexual contact, with younger women, was popular in Asian and Eurasian
cultures centuries ago and is still believed and practised in some cultures today (Busse, 1989).
The modern understanding of ageing continues to make great strides as new technologies and
research techniques increase awareness of the ageing process. For example, researchers have become
increasingly aware of the limitations of cross-sectional research designs. Previously, many studies
comparing the brain weights of younger and older adults had concluded that the size of the brain
decreased with age; often cell death or cerebral atrophy was thought to be the culprit. While some
brain size reduction does occur with ageing, much of the supposed brain changes with age were in
cohort effect fact cohort effects—that is, where differences between younger and older groups are not due to age
An effect that but to the different life circumstances that have been experienced between these two age groups.
occurs when Specifically, the average male brain increased in size by 0.66 grams and the average female brain size
people born in by 0.28 grams between 1860 and 1940, largely due to improvements in public health and nutrition
one historical
period are at a
over this time (Kril, 2003; Miller & Corsellis, 1977).
different risk for a Similarly, cognitive functioning and particularly intelligence were presumed to decrease in the
disorder than are face of increasing age. The cross-sectional studies of the 1940s and 1950s, which compared younger
people born in and older cohorts, appeared to support this view of steep and inevitable declines in intelligence with
another historical ageing. However, the insights gained from longitudinal surveys of cognitive functioning, such as the
period. Seattle Longitudinal Study of ageing and cognition (Schaie, 2005), have largely discredited this view.
In fact, studies demonstrate that many aspects of cognitive functioning hold steady into even advanced
old age. For example, crystallised intelligence (learning from past experiences or prior learning)
does not decline significantly into the eighth decade of life and beyond, whereas fluid intelligence
(the ability to solve novel problems) declines far earlier—in about the third or fourth decade of life
(Christensen, 2001). Verbal abilities, particularly vocabulary and language usage, also have minimal
declines in later life (Anstey, Luszcz, & Hofer, 2003). In contrast, speed of cognitive processing and
memory, particularly episodic memory, are examples of aspects of cognition that not only decline with
increasing age, but also have a relatively accelerated rate of decline at more advanced ages (Anstey et
al., 2003; Christensen, 2001).
Both the brain weight and cognitive studies demonstrate the value of longitudinal studies over
cross-sectional studies when the goal is to try to establish changes due to ageing. In longitudinal
studies, the same individuals are followed over time, whereas cross-sectional studies compare different
age groups at a particular point in time. Longitudinal studies are a more reliable way of ascertaining
changes due to ageing since in cross-sectional studies it is impossible to determine which changes are
due to ageing and which are due to cohort effects. While cohort effects are minimised in longitudinal
studies, a limitation of this design is that the original participants may drop out over time and new
participants cannot be recruited as the study progresses.
In addition to improved research designs and methodologies, even the definition of what constitutes
‘old age’ has changed dramatically through recent history. One only has to compare Australian life
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expectancies of males and females born

between 1900 and 1910 (55 and 59 years,
respectively) to those of children born
today to gauge the magnitude of change
experienced in the past century. Today,
the term ‘older adults’ generally refers to
persons aged 65 years and over. How did
this common idea of ‘older’ come about?
Many cite the German pension system as an
instigator. Germany was the first Western
country to adopt a national public pension
program in 1889, designed by Otto von
Bismarck, Germany’s chancellor at the time.
Germany initially set age 70 as the retirement
COURTESY OF THE UNIVERSITY OF QUEENSLAND

age; 27 years later (in 1916) the age of
retirement was lowered to 65. At this time,
many countries were considering similar
schemes and 65 as the age of entitlement for
such a pension was widely adopted.
In Australia, much of the development
in the field of psychology and ageing can
be attributed to the pioneering work of
Dr Elsie Harwood, a major figure in
Australian psychology. Harwood was born
in London in 1911 and emigrated with her
family to Australia in 1914. She attended Dr Elsie Harwood, a pioneering figure in Australian
the University of Queensland in Brisbane psychology generally and the psychology of ageing
as a student from 1931, at a time when in particular.
psychology was taught in the Philosophy/
Classics Department. In 1955, partly through her efforts, a Department of Psychology was established
at the University of Queensland. In terms of research, Harwood was perhaps best known for her
longitudinal studies of older adults. She initiated the first study of older adults in Australia in 1966;
what was supposed to be a 10-year project, ‘Operation Retirement’, in fact lasted 20 years. This study
contributed to knowledge of longevity and cognitive processes in older adults including perception,
memory and learning (among other activities, participants in the studies were required to learn German
and to play the recorder). Harwood received many awards during her life, including life membership
of the Australian Association of Gerontology, an Order of Australia and a Fellowship of both the
British Psychological Society and the Australian Psychological Society (APS). In 1992, the APS
Psychology and Ageing Interest Group instituted the Elsie Harwood Award to be awarded for the best
postgraduate thesis on ageing. Epitomising the field’s growing focus on the positive aspects of ageing,
Harwood remained quite active in retirement. She would regularly attend Friday afternoon Greek and
Latin reading group discussions in the University of Queensland Classics Department (reading, of
course, in the original Greek and Latin). To the end, although beset by illness, she maintained a lively
and inquisitive mind.
Normal ageing processes: cognitive, emotional

and social functioning
An important distinction to be made in terms of illnesses that are more common in later life is to
distinguish those that are a product of ‘normal’ ageing (i.e., illness or decline in functioning due to
the simple passage of time) from those that are due to the presence of a disease state. The former,
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often referred to as primary ageing, are the result of changes due to the passage of chronological time.
They include such familiar changes as the greying of hair, decreases in white blood cell production
and decreases in memory functioning in later life that, while frustrating, do not impede everyday
functioning or the capacity to live independently. The latter, often referred to as secondary ageing,
include acquired disabilities such as head trauma as well as disease states such as coronary disease,
Alzheimer’s major depression and Alzheimer’s disease. These conditions are not a normal part of ageing; their
disease cause lies in an identifiable disease state or an acquired disability, and if everyone lived to over
A progressive 100 years of age, not everyone would be afflicted with these conditions.
neurological To confuse primary and secondary ageing processes can have a profoundly negative effect on
disorder that is
older adults. For example, if a health professional erroneously believes that ageing is invariably
the most common
form of dementia. associated with depression, s/he may simply assume that the older person’s depression is ‘normal’
and thus should not or cannot be treated. Since depression is one of the most treatable conditions in
later life, this is not only a gross error but unnecessarily deprives the depressed older adult of quality
of life and wellbeing.
Thus, before one can appreciate the meaning and significance of any changes or declines in
functioning in later life, it is vital to have a solid understanding of the normal developmental changes
associated with ageing. In this section, changes in cognitive, emotional and interpersonal functioning
as a result of primary ageing will be described.
COGNITIVE CHANGES WITH INCREASING AGE

Which cognitive functions remain relatively stable in the face of increasing age and which decline?
General answers to this question are difficult to provide given that there are pronounced differences
between older individuals in cognitive functioning, affected by such diverse influences as health status
and emotional dysfunction, as well as demographic factors such as occupation or hobbies. For example,
several studies support the hypothesis that contextual factors such as an ‘enriched environment’ aid
the cognitive functioning of older adults (Couillard-Despres, Iglseder, & Aigner, 2011; Hess, 2005).
In other words, the level of participation with the environment, including cognitive, physical and
social activities, is thought to affect cognitive health in old age. Involvement in activities that are
cognitively stimulating in earlier life has also been shown to protect against the cognitive deficits
(including dementia) associated with ageing. For example, more intensive leisure-time physical
activity in midlife was associated with a reduced risk of dementia (Andel et al., 2008; Carlson
et al., 2008), whereas occupational physical activity, which is often associated with low intellectual
demand, or leisure activities with low cognitive demand (such as watching television), did not show
this protective effect or could even be detrimental (Rovio et al., 2007; Wang et al., 2006).
Attention
In general, complex attention processes, such as attempts to switch between cognitive tasks or
to complete two separate tasks at the same time, are most affected by increasing age. Executive
attention, defined as the ability to control one’s attentional processes (e.g., the ability to block out
distractions), is one of the complex attentional processes that has been found to decrease with age.
Mahoney, Verghese, Goldin, Lipton, and Holtzer (2010) looked at executive attention and blood
pressure and found that reduced blood flow to the frontal lobes could explain executive attention
dementia declines in older adults without a diagnosis of dementia. In contrast to complex attention processes,
Neurological the ability to focus attention on single tasks remains relatively intact with age, even in the context of
disorder in which such illnesses as dementia.
a gradual decline
of intellectual Memory
functioning Lapses in memory with increasing age are also part of the normal, primary ageing process. The
occurs.
hippocampus, the seat of memory functioning, is one of the areas of the brain most affected by ageing
(Couillard-Despres et al., 2011). Changes in memory may include decreases in both the amount of
information recalled as well as the speed of retrieval. Memories for facts (often termed semantic
memories) tend to be more resistant to ageing effects than memories for events (episodic memories).
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Prospective memory, or remembering to remember,

is also affected by ageing.
Yet some individuals appear to age better than
others—and this pertains to both their brains as
well as to their objective memory test results. In one
study of the brains of these so-called ‘superagers’,
their brains appeared more similar to individuals
much younger than themselves, and these preserved
areas of the brain corresponded to cortical areas
related to memory performance (Sun et al., 2016).
Understanding how some older people can have
such preserved memory functioning remains a key
area for future research.
Language
In contrast to complex attention and memory tasks,
DAL
the expression and understanding of language is Lapses in memory (including memories of episodes that have occurred
the cognitive skill that is most robust in the face in the person’s life) are part of the normal, primary ageing process.
of ageing processes (Rabaglia & Salthouse, 2011). In contrast, memories for facts tend to be less affected by the process
This is why any changes in language abilities, such of normal ageing.
as losing the ability to understand speech or find
words for common items, warrants investigation as it may be a sign of illness. However, common
lapses in language use, such as an inability to think of a person’s name in a social situation, are not in
themselves unusual (nor is this a phenomenon solely confined to the later years). neuroimaging
Range of
Executive functioning techniques used
Executive functioning comprises a diverse group of cognitive tasks, including planning, reasoning to image the
and problem solving. In one study, increasing age, coupled with higher self-reported depression, was structure and/
associated with poorer executive abilities (Currell, Byrne, & Pachana, 2014). Other studies show a or function of
positive effect of physical activity on executive functioning in later life (Gajewski & Falkenstein, the brain such
2015). These studies highlight the importance of addressing psychological issues in later life so as to as computerised
tomography (CT),
prevent declines in cognitive abilities, such as executive functioning, which are important in enabling
positron emission
the person to maintain independence. They also highlight how physical activity can have a beneficial tomography (PET)
influence on cognition. and magnetic
Theoretical accounts of age-related cognitive changes resonance
imaging (MRI)
Several theories have evolved and continue to be tested to account for the changes in cognition in later
scans.
life. Craik (1986) and Salthouse (1996) have contributed to theories of cognitive ageing based on
information-processing capacity. Studies have demonstrated that age-related declines occur in tasks computerised
requiring effortful processing of information, or in those involving a need for speed of processing. tomography (CT)
However, tasks that are more automatic and do not require large amounts of conscious effort, or Method of
analysing brain
those tasks for which speed is not essential, do not decline. This is postulated to be due to age-related
structure by
declines in information-processing capacity (Spencer & Raz, 1995). passing narrow
A different theory to explain age-related cognitive declines has been put forward by Shimamura X-ray beams
(1995). The frontal lobe theory rests upon the fact that functions located in the frontal lobes deteriorate through an
with normal ageing. Tasks related to the frontal lobes, which decline in later life, include planning the individual’s head
steps to achieve a goal, using strategies to complete a task or monitoring one’s own performance to from several
offer self-corrections while performing a task. As performance of the frontal lobes declines, attentional angles to produce
measurements
resources and particularly working memory are negatively affected.
from which a
Support for both the information processing and the frontal lobe theories of cognitive changes with computer can
ageing comes from laboratory studies, longitudinal studies and neuroimaging studies (Shimamura, construct an
2002). The last involve using advanced imaging techniques to look at either the structure of the brain image of the
(e.g., computerised tomography [CT] or computerised axial tomography [CAT] scanning using brain.
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positron emission X-rays) or the functioning of the brain (e.g., using positron emission tomography [PET] to measure
tomography (PET) emissions from radioactively labelled metabolically active chemicals such as glucose that have been
Method of injected into the bloodstream).
localising and
measuring Wisdom
brain activity Thus far, mention has been made of the cognitive abilities that either decline or remain stable with
by detecting age. However, certain skills actually improve with age. One cognitive skill that has received attention
photons that
for its improvement with age is wisdom. Baltes and colleagues conducted a series of studies at the
result from the
metabolisation Max Planck Institute in Berlin to try to understand wisdom in later life (Baltes & Staudinger, 1993;
of an injected 2000; Staudinger & Pasupathi, 2003). They define wisdom as expert knowledge and judgment about
isotope. important, difficult or uncertain questions encountered during life. For example, a sample question
might be: ‘Somebody gets a phone call from a good friend who says that s/he cannot go on anymore
and that s/he has decided to commit suicide. What should one do and consider?’ Baltes and his
colleagues tested individuals of varying ages using hypothetical scenarios such as this to try to assess
their varying levels of wisdom. The results suggest that greater wisdom is generally associated with
greater age, although it is also related to other factors such as personality characteristics and attitudes.
As an example of the latter, evidence has emerged that those who view negative life situations as
opportunities for growth and who successfully overcome life crises are more likely to develop wisdom
(Ardelt & Jacobs, 2009).
The Life and Living in Advanced Age: A Cohort Study in New Zealand, Te Puawaitanga o Ngā
Tapuwae Kia Ora Tonu (LiLACS NZ)
The LiLACS NZ study (Kerse, Muru-Lanning, Rolleston, & Teh, 2016) aims to assess the health,
social, cultural and environmental status of Māori and non-Māori people in later life, using measures
of these variables to predict the quality of life of its participants, among other indicators, over time.
In the next 40 years, the New Zealand population over age 65 will increase from 13 per cent to
25 per cent, and those over age 85 will at that stage be 6 per cent of the total population (Statistics New
Zealand, 2012). Currently, the Māori population, who make up approximately 14.6 per cent of the
total New Zealand population (Statistics New Zealand, 2013), is ageing more rapidly. In other words,
the proportion of Māori older people is increasing even more quickly than the growing proportion of
non-Māori older people (Ministry of Health, 2011).
The LiLACS NZ study is informed by Kaupapa Māori methods and ideology, and is based on
a Māori worldview which acknowledges that knowledge and ways of knowing are firmly rooted
in cultural contexts. This study began in 2010 with 927 initial participants. The participants were
invited to take part in an interview, a health assessment and a blood test, and asked to consent to the
researchers accessing their medical records. The results to date have revealed interesting comparative
findings between the two participant groups. For example, despite differences in education and
socioeconomic status, neither self-rated health nor rates of falls differed between Māori and non-Māori
elders. However, older Māori people were more likely to have certain illnesses (such as congestive
heart failure, diabetes and dementia), while Māori women were observed to experience the highest
prevalence of depression. Such data will assist both health professionals and psychologists to better
target the care of all New Zealanders.
EMOTION AND PERSONALITY IN LATER LIFE

As with cognition, early research into emotional and personality changes suggested decreases in
functioning with increasing age. However, more recent studies using longitudinal data, as well as
meta-analysis meta-analyses of data across a large number of studies, have revealed a far more positive picture of
Statistical emotional and personality functioning in later life.
technique for
summarising Mood
results across It is now generally accepted that depression and most other psychiatric conditions decrease in
several studies. incidence in later life. Jorm (2000) suggests that this may be at least partly due to the fact that
older adults have mastered better coping strategies for managing distressing emotions. Research into
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coping across the adult lifespan supports this. For example, Scheibe and Carstensen (2010) suggest
that the experience older adults obtain in dealing with emotional situations over the course of their
lives results in their gaining important knowledge about emotional processes, which then increases
their effectiveness in handling emotional situations. In fact, research suggests that, as people age,
they represent their emotional states in more complex and abstract ways (Strongman & Overton,
1999). For example, older adults have typically experienced the complexities of relationships with
family members and friends—in which both positive and negative emotions feature—and know
that this complexity can be tolerated and the relationship can still be satisfying despite its negative
aspects. In addition, older adults have had extensive life experience in analysing emotional cues
in interpersonal communication (Phillips, MacLean, & Allen, 2002). Magai (2001) suggests that,
because of these accumulated interpersonal experiences across the lifespan, older people develop
better abilities to understand, anticipate and react to the emotional responses of other people. Older
adults are also more confident than younger adults that they can control their emotional responses
(Kessler & Staudinger, 2009).
Older adults’ greater skill at regulating their emotions (Charles & Pasupathi, 2003; Roecke, Li, &
Smith, 2009) may not only have the effect of lowering the risk of psychiatric illness, but may also
help to increase levels of wellbeing. Population studies involving wellbeing and life satisfaction
show improvements with increasing age. For example, a study by Stone, Schwartz, Broderick, and
Deaton (2010) analysed wellbeing using a telephone assessment of 340 840 US adults aged 18 to
85 years, with the aim of investigating changes in wellbeing with age. Wellbeing was defined as
a person’s general appraisal of his/her life (or ‘global wellbeing’), as well as his/her positive and
negative affective state (or ‘hedonic wellbeing’). The results demonstrated that global and positive
hedonic wellbeing had U-shaped age profiles, such that these forms of wellbeing decreased at mid-
life and then increased after the age of 50. Aspects of negative hedonic wellbeing displayed distinctly
different patterns: stress and anger declined sharply from the early 20s, worry was noticeable through
middle age and then declined, and sadness had an essentially flat profile throughout. Overall, the
findings indicated that wellbeing improves, or at least stays stable, with age. These results are in
agreement with several other studies showing that emotional states generally improve with increasing
age (Carstensen, Pasupathi, Mayr, & Nesselroade, 2000; Charles, Reynolds, & Gatz, 2001; Riediger,
Schmiedek, Wagner, & Lindenberger, 2009).
Personality
In terms of personality and ageing, an influential theory is Erikson’s (1950) stages of psychosocial
development. According to this approach, development is characterised by movement through
various stages in different life periods. As shown in Figure 15.2, each stage entails a qualitative shift
in personality functioning entailing the need to resolve opposing tendencies (e.g., generativity versus
self-absorption in the middle years of life and integrity versus despair in later life). The resolution
of these conflicts throughout life is thought to influence the development of the personality of the
individual. Specifically, unsuccessful resolution of the challenges of a particular stage may result in
emotional or coping difficulties.
In contrast to Erikson’s qualitatively different personality themes at different stages of life, Costa
and McCrae’s (1980) theory of personality development is based on personality traits used to describe
individuals irrespective of age. In their five factor (‘big five’) model of personality, neuroticism (the
tendency to experience negative feelings), extroversion (seeking stimulation), conscientiousness
(reliability), agreeableness (compliance with the wishes of others) and openness (ability to cope with
the unfamiliar) are the broad traits that make up the human personality. These traits have been found
to be remarkably stable over adult life. Thus the answer to the question as to whether personality
changes or remains stable over the course of ageing is dependent on the aspects of personality and
the theoretical model adopted: Erikson emphasised change whereas Costa and McCrae’s model
emphasises stability.
In addition, researchers propose that within older age there may be other psychological and
developmental changes of note. For example, Cohen (2001a; 2001b) claims that there are four
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1 Basic trust vs basic mistrust

In this stage, very early in childhood, trust, security, and optimism are learned if the child is well-nurtured. In the
absence of such nurturing, mistrust and insecurity can develop.
2 Autonomy vs shame
After the second year of life the child’s task is to discover a sense of autonomy, or confidence in him/herself.
If such autonomy is not developed, a lack of confidence and feelings of shame can result.
3 Initiative vs guilt
In the preschool years, activities such as imaginative play and cooperation with others afford the child the chance to
learn to take the initiative. If the child is instead filled by feelings of self-reproach fear and undue dependence on
adults may result.
4 Industry vs inferiority
For the school-aged child, learning to master the basic skills of life (e.g., relating to peers and working well in school)
results in a sense of meaningful industry. Deficits in trust, autonomy or initiative from earlier stages will result instead
in feelings of inferiority predominating.
5 Identity vs identity diffusion

In adolescence, acquiring a sense of one’s own identity, through experimentation and exploration within the
environment and with peers, is the core task. A strong self-identity is the result of successful negotiation of this stage,
whereas self-consciousness and self-doubt characterise failure to master this stage.
6 Intimacy vs isolation
Young adulthood sees the experience and mastery of true intimacy as the core objective. Isolation and frustration in
relationships are the consequence if difficulties from earlier stages surface.
7 Generativity vs self-absorption
In adulthood, generativity or productivity, both in the sense of relationships (including raising children) as well as
working productively and creatively are the signs of mastery of this stage. Self-absorption and lack of productivity
signal failure to fully master this stage.
8 Integrity vs despair
If the previous seven stages have been successfully negotiated, the mature adult displays the peak of adjustment:
integrity. The individual is able to explore new horizons comfortably, and trust, independent thought, and action come
easily. Thus, a self-satisfying identity has evolved. If one or more of the earlier psychosocial stages have not been
successfully negotiated, at this later stage of life the adult may view life with regret and despair.
FIGURE15.2 Erikson’s eight stages of psychosocial development and their associated tasks
Adapted from Erikson, E. H. (1950). Childhood and society. New York: Norton.
stages in mature and later life. These stages are not invariant and there can be overlap between
the stages. Cohen calls the first phase Midlife Re-evaluation, which occurs from the 40s to the 60s
and is described as a time of exploration and transition. In this phase, most adults are driven by a
quest-like energy to reconsider their lives and strive to make them more rewarding. After this first
phase comes the liberation stage, which begins from age 60 through to the early 70s and mainly
comprises a yearning to experiment. In this phase, people are inclined to feel comfortable within,
knowing that if they make a mistake it will not destroy the image that they (or others) have of them.
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The Summing-up phase, often occurring during the 70s, is a time of recapitulation, resolution and
review. People in this stage feel the need to find greater meaning in the story of their lives, through a
process of looking back, summing up and giving back. Finally, the Encore phase, usually occurring
from age 80 onwards, is characterised by the desire to make a final statement or yet additional
contributions on an individual or community level, or to take care of unfinished business.
SOCIAL CHANGES WITH AGE

Carstensen’s (1992) socioemotional selectivity theory describes the motivational forces that shape
social network size and composition, as well as how these relationships change from a lifespan
perspective. Previous theories (e.g., activity theory; see Maddox, 1970) focused on older adults coping
with negative changes in their social networks, such as the decreasing number of close friends and the
death of spouses. Moreover, older adults were viewed as passive with regard to their social networks
and relationships rather than as driving events themselves. Despite this picture of the older adult
passively responding to negative interpersonal events, research repeatedly revealed the intriguing
finding that older adults were as satisfied, if not more satisfied, with their social relationships as
younger adults (Lansford, Sherman, & Antonucci, 1998). For example, Cavallero, Morino-Abbele,
and Bertocci (2007) surveyed nearly 1000 older Italians and found that participants were generally
satisfied with their social life. Australian data also support the existence of equivalent, if not higher,
social satisfaction among older adults. Specifically, von Hippel, Henry, and Matovic (2008) compared
the social satisfaction of 38 younger adults (aged 18–30 years) and 40 older adults (aged 66–91 years).
These researchers found that their community sample of older adults showed neither greater nor lesser
social satisfaction than the community-based sample of younger adults. Indeed, once age-related
decreases in social activity levels were controlled for in the analyses, it was found that older adults
actually reported greater social satisfaction than did younger adults.
Carstensen’s (1992) theory can help to explain these findings. This theory suggests that social
interactions are to some extent shaped by the perception in later years that there is a finite amount of
time remaining for pursuing many goals and activities, including social engagement. With this sense
of finitude in mind, more meaningful and fulfilling relationships are given a higher priority over those
that are less able to meet the emotional needs of the older person. This active prioritisation thus shapes
the size and the quality of the older adult’s social network. While the overall number of social contacts
tends to decline in later life, Carstensen (1992) maintains that this decline is not uniform in that older
adults actively discard peripheral or unsatisfying relationships while investing more in their important
connections. Age-related decreases in networks are driven primarily by excluding less meaningful,
casual acquaintances from the network (Fung, Carstensen, & Lang, 2001; Yeung, Fung, & Lang,
2008). However, the number of emotionally close social partners remains highly stable (Fung et al.,
2001) or slightly increases with increasing age (Yeung et al., 2008). In short, there is a reduction in
quantity but an increase in the quality of the social network in later life.
Carstensen (1992) also maintains that this outcome with respect to social relationships in later life is
the product of a continuing process of change and evolution in the nature of social relationships across the
lifespan. In adolescence and early adulthood, friendships assist with gathering information so as to make
greater sense of an often hectic and chaotic period of life. People ask friends for advice on topics as diverse
as clothes, university courses and relationships. Thus, having a wide network of acquaintances is an
effective strategy if information-gathering is the goal. Later, in middle adulthood, relationships may form
out of important life tasks and events. At this stage, friendships develop around shared activities such as
childrearing, work and recreational activities. In later life, people more strongly select relationships based
on their contribution to emotional wellbeing. Through this ‘selective pruning of the social network’, older
adults tend to eliminate unimportant or harmful relationships while retaining important relationships such
as those with close family and friends (Carstensen, Gross, & Fung, 1998, p. 326).
Research suggests that such changes in network composition are indeed generally voluntary. Older
adults report highest levels of positive emotional experiences when interacting with family members, which
are higher in this regard than that reported by younger adults (Charles & Piazza, 2007). In fact, longitudinal
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data from a study by Shaw, Krause, Liang, and Bennett (2007) demonstrate that, with increasing age, older
adults reported markedly less contact with friends but relatively stable levels of contact with family.
Social networks, then, are much more important than their size. It is the perceived amount of social
support that best predicts outcomes such as satisfaction with one’s relationships. People use networks
to obtain different kinds of support. Two kinds of social support often discussed in the literature are
instrumental (or practical) and emotional (or affective) social support. Social networks are important
to older adults as they assist them in coping with adversity, through both instrumental activities (such
as having someone to drive one to a medical appointment) and emotional activities (such as being
able to share points of view and derive comfort). In their study, Shaw and colleagues (2007) show that
older adults receive increasingly more instrumental support, while levels of emotional support remain
fairly stable throughout time.
Social support has been shown to influence a range of health and psychosocial outcomes in later life.
For example, lower levels of social support predict poorer mental health outcomes such as depression
in older adults (Bellini & Matteucci, 2001). Conversely, increasing social support has been mooted as
a potential intervention strategy for a wide range of problems and has even been purported to decrease
the risk of developing Alzheimer’s disease (Bennett, Schneider, Tang, Arnold, & Wilson, 2006).
Gender is often an important variable in discussing social relationships. Although much research
supports the view that women have social support networks that may be more
extensive and robust than those of men, these can come at a price, such as the
need to continue to provide support in such an extended network (Antonucci,
Akiyama, & Lansford, 1998). Shaw and colleagues (2007) found that older
men generally receive and give less support than older women; the fact that
they give less support may have accounted for the finding that men were more
satisfied than women with their support interactions. For both genders, poor
mental health and sensory impairments are associated with smaller social
networks and lower satisfaction with social support (McLaughlin, Vagenas,
Pachana, Begum, & Dobson, 2010).
Finally, being meaningfully engaged in social relationships requires
allowing for such relationships to be reciprocal. At all points in the lifespan,
people prefer generally to under-benefit from unsolicited or non-reciprocal
help (Antonucci & Jackson, 1990). What this means is that, as a rule, people
prefer being in a position to give help more frequently than being in a
position to need to ask for or receive aid. This results in people building up
a measure of ‘support credits’ that can then be exchanged if they are in need
of assistance. However, later in life people may try to prevent older persons
from reciprocating if a favour is done for them. The older person is being
told, in effect, that they can no longer participate in the social exchange on an
equal footing, which the older person may experience as demeaning.
One source of unconditional and non-judgmental support for older
adults comes from their pets or companion animals (Hafen, Rush, Reisbig,
DAL
Owning a pet may have a beneficial effect on McDaniel, & White, 2007; Pachana, Massavelli, & Robleda-Gomez, 2011).
the wellbeing of older adults. In their review, Pachana and colleagues (2011) outline how, throughout
the lifespan, animals play an important role in maintaining physical and
emotional wellbeing, influence recovery from illness and have an impact on reactions to loss or grief.
Longitudinal research in Australia has found that people who continuously own pets are the healthiest
group, compared with those who no longer have pets or have never had one (Headey & Grabka, 2007).
With older adults specifically, it has been shown that the ability to perform activities of daily living is
higher in pet owners than non-pet owners (Raina, Waltner-Toews, Bonnett, Woodward, & Abernathy,
1999). Moreover, Raina and colleagues (1999) suggest that pet ownership may buffer the harmful
effects of lack of social support on psychological wellbeing. Therefore, it is important to consider
companion animals as potential sources of emotional support for older adults.
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LO 15.2 Psychological disorders in later life:

the dementias
The definition of dementia and neurocognitive disorder
Many people mistakenly believe that disorders such as dementia are to be expected as one grows
old. In reality, there is a substantial difference between the memory lapses associated with normal
ageing and the significant memory impairments seen in dementias such as Alzheimer’s disease.
Moreover, dementia does not affect all adults or even a majority of older adults. There are many forms
of dementia, with distinct aetiologies and symptom profiles. However, in all cases dementia is not a
part of normal or primary ageing but represents a neurological disease process (secondary ageing)
characterised by distinct changes in the brain.
Dementia has been regarded as a term for a broad class of neurological disorders associated with
cognitive, personality and behavioural changes in later life. However, in the current edition of the
Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (American Psychiatric Association
[APA], 2013), the term dementia has been eliminated and replaced with major or mild neurocognitive
disorder. Major neurocognitive disorders include diagnoses such as dementia from the previous
edition of the DSM (DSM-IV-TR) (APA, 2000) which constitute a substantial level of cognitive
decline (two or more standard deviations) from previous functioning and interfere with the person’s
ability to function independently (Siberski, 2012). In contrast, mild neurocognitive disorder describes
a level of cognitive deterioration that goes beyond declines associated with normal ageing changes
but is not yet at the level of a major neurocognitive disorder. The mild neurocognitive disorder
diagnosis requires that the person is experiencing cognitive changes that negatively affect functioning;
that are observable by the individual, others or on objective cognitive testing; and that require the
affected individual to engage in compensatory strategies to help maintain independence and perform
the activities of daily living. However, critics have pointed out that while early identification of a
person with such a decline may improve access to assistance and potential early interventions, it
may not be straightforward to ascertain such changes accurately (Morris, 2012). After a clinician
determines whether the neurocognitive disorder is major or minor, then a subtype is listed (e.g., ‘major
neurocognitive disorder due to Alzheimer’s disease’).
As the DSM-5 change replacing the term dementia with the term neurocognitive disorder
is relatively recent, most of the existing literature still refers to dementia. The use of the term
neurocognitive disorder rather than dementia may assist with alleviating negative stereotypes around
the use of the term dementia. However, in this transitional period there will be much overlap in
the usage of both terms, which may result in confusion in the short term. In this chapter, the term
dementia is used for the most part, due to the fact that it includes research that was conducted prior
to the formal introduction of the mild and major neurocognitive disorder categories. For example, the
US National Institute on Aging–Alzheimer’s Association (NIA–AA) research criteria and guidelines
for diagnosing dementia due to Alzheimer’s disease (McKhann et al., 2011) still refer to dementia,
and some clinicians and researchers continue to do so. But an important concept underpinning these
changes, welcomed by both clinicians and researchers alike, is the idea that impaired memory might
not be the first sign or symptom of neurocognitive decline indicating possible dementia, and that it is
important to try to identify cognitive changes that adversely affect the individual as early as possible
(i.e., even while still of a mild nature).
The prevalence of dementia in Australia is similar to that of other industrialised countries. Meta-
analyses of survey data suggest that the prevalence of dementia in 2003 among Australians aged
65 years or older was between 136 000 and 193 000 (5.3–7.6%) (Australian Institute of Health and
Welfare [AIHW], 2006). In Australia, the prevalence of dementia is expected to triple by 2050
(AIHW, 2012), similar to estimates in other developed countries. The financial costs of caring for
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persons with dementia is staggering—direct health costs total $3.2 billion, of which $2.9 billion is
spent on residential care costs. By 2050, dementia costs to the federal government may exceed 3 per
cent of gross domestic product (GDP), up from the nearly 1 per cent of GDP spent today (Alzheimer’s
Australia, 2003).
Although most research on dementia has been carried out in more developed, primarily Western
countries, the 10/66 Dementia Research Group aims to change this state of affairs (Prince, 2000).
These researchers carry out population-based research into dementia, non-communicable diseases
and ageing in middle- and low-income countries. The moniker ‘10/66’ refers to the fact that
66 per cent of people from around the world who have dementia are from the developing world,
whereas only 10 per cent or less of population-based research has been carried out in these regions.
The 10/66 Dementia Research Group is part of Alzheimer’s Disease International, an international
federation of Alzheimer’s associations throughout the world, which is also associated with the
World Health Organization.
Alzheimer’s disease
There are many distinct types of dementia. Alzheimer’s disease is the most common form of dementia
and represents approximately 50–70 per cent of all cases of dementia diagnosed. The average age
of onset for the disease is 65, with a course lasting between 8 and 10 years before death. Women
are somewhat more at risk of developing Alzheimer’s disease than men, even after women’s longer
lifespans are taken into account.
Alzheimer’s disease was initially described by Alois Alzheimer, who was born in Germany in
1864. In 1903 he became a research assistant to Emil Kraepelin at the Munich medical school where
he created a new laboratory for brain research. Having published many papers on diseases of the
brain, in 1906 Alzheimer gave the lecture that made him famous, identifying an ‘unusual disease of
the cerebral cortex’ affecting a female patient, Auguste D., that caused memory loss, disorientation,
neurofibrillary hallucinations and ultimately her death aged only 55. The autopsy revealed various abnormalities
tangles of the brain previously encountered only in much older individuals. Kraepelin named the disease
Twists or tangles
of filaments
after Alzheimer. Today, the pathological signs used in the diagnosis of Alzheimer’s disease are still
generally the same as in Alzheimer’s day, although many other advances in neuroscience have allowed
within nerve
cells, especially a greater understanding of the underlying biological processes.
prominent in Alzheimer’s disease is characterised by the presence of neurofibrillary tangles (twisted masses
the cerebral of tiny filaments inside nerve cells) and neuritic plaques (abnormal clumps of degenerating brain
cortex and cells surrounding a protein core) in the brain as first described by Alzheimer over a century ago. A
hippocampus, toxic molecule known as amyloid beta produces these plaques and tangles, which microglial cells (the
common in the
‘defenders’ of the nervous system) are unable to eliminate (Michaud et al., 2013). These changes in
brains of patients
with Alzheimer’s the brain begin most commonly in critical brain areas such as the hippocampus and gradually spread
disease. to more lateral and frontal areas in the cortex of the brain.
The course of Alzheimer’s disease is characterised by increasing cognitive dysfunction,
neuritic plaques
including difficulties with remembering new information and changes in language, particularly the
Deposits
of amyloid ability to name objects, people and places. Alzheimer’s disease also includes changes in personality
protein that and emotional functioning, such as apathy and agitation, and behavioural problems such as
accumulate in wandering and toileting difficulties. Psychiatric symptoms in dementia are often quite disturbing
the extracellular for caregivers. Functional and cognitive impairment, as well as lack of support and assistance in
spaces of the daily living, are among the primary causes of institutionalisation in Alzheimer’s patients (Luppa
cerebral cortex, et al., 2010).
hippocampus and
A major feature of neurocognitive impairment due to Alzheimer’s disease is memory impairment
other forebrain
structures in
(although as previously mentioned, this may not be the first cognitive change to appear). Memory
patients with impairment (i.e., impaired ability to learn new information or to recall previously learnt information)
Alzheimer’s may be evidenced, for example, by losing valuables such as wallets and keys, forgetting food cooking
disease. on the stove, and becoming lost in familiar environments. As the disorder progresses, the memory
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CENTRE FOR ADVANCED IMAGING

Magnetic resonance imaging (MRI) brain scans of a non-affected adult (left) and an adult with Alzheimer’s
disease (right). The arrow points to a major fissure on the brain surface, called the lateral fissure. Note the
increased width of the lateral fissure and other fissures in comparison with the normal brain scan. This
increased width is due to a loss of grey matter (nerve cells).
impairment may be so severe that the person forgets basic details such as his/her occupation, birthday
and even his/her name.
This memory impairment must be accompanied by declines in one or more of the following areas:
∙ aphasia (language disturbance), which may be evidenced by vague or empty speech, excessive use
of terms of indefinite reference such as ‘thing’, and difficulty comprehending written and spoken
language
∙ apraxia (impaired ability to carry out motor activities despite intact motor function) resulting in
difficulty performing daily tasks such as cooking and dressing
∙ agnosia (failure to recognise or identify objects despite intact sensory function), which, at later
stages of the disorder, might include being unable to recognise family members or the individual’s
own reflection in the mirror
∙ disturbance in executive functioning (including planning, organising, sequencing and abstract
thinking abilities).
The memory and accompanying cognitive disturbances must result in significant impairment in
social or occupational functioning and represent a significant decline from prior functioning for the
diagnosis to be given. Also, other possible causes of cognitive decline such as other mental disorders
(e.g., major depression) or physical disorders (e.g., brain tumours) must be ruled out before the
diagnosis is given.
In terms of the aetiology of Alzheimer’s disease, for many years researchers have recognised
the importance of genetic risk factors. For example, a literature review identified more than 1000
publications related to the study of genetic risk factors for Alzheimer’s disease, with 308 genes
implicated (Bertram, McQueen, Mullin, Blacker, & Tanzi, 2006). However, to date, only one gene,
ApoE, has been consistently confirmed as a genetic susceptibility factor for Alzheimer’s disease
(Hsiung & Sadovnick, 2007). The ApoE gene, on chromosome 19, is polymorphic (i.e., it has different
forms): ApoE e2, ApoE e3 and ApoE e4. While ApoE e3 is the most common form in the general
population, approximately 40–60 per cent of people with Alzheimer’s disease carry at least one copy
of ApoE e4 (Farrer et al., 1997).
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vascular In attempting to understand the causes of Alzheimer’s disease, it is important to note that studies
dementia have shown that the mere presence of the neurobiological markers of plaques and tangles is not enough
Type of dementia to cause the disease to manifest itself. In the famous Nun Study, a longitudinal study of ageing and
associated with Alzheimer’s disease funded by the United States National Institute of Ageing, 678 members of the
symptoms of
cerebrovascular
School Sisters of Notre Dame religious order aged 75 years and over were followed for 15+ years
disease (i.e., (Snowden, 2001). Several interesting findings have emerged from this study. First, the nun with the
tissue damage greatest amount of neuropathology at autopsy (in other words, the largest concentration of plaques
in the brain due and tangles) demonstrated little to no cognitive decline in life. Moreover, among those nuns with the
to a blockage of neuropathological features of Alzheimer’s disease at autopsy, those with additional cerebrovascular
blood flow). disease were much more likely to have had dementia during life. Finally and most intriguingly, a
stroke retrospective analysis of the available autobiographies of the nuns in the study was undertaken. These
Sudden damage autobiographies were written by the sisters in their late teens, before they took their vows. After careful
to the brain due analysis of writing style and content, it was found that low linguistic ability and low ideational complexity
to a blockage as displayed in the autobiographical essays was associated with increased risk of the development of
of blood flow or Alzheimer’s disease pathology later in life. Overall, the findings from the Nun Study indicate that the
haemorrhaging. characteristic neurobiological features of plaques and tangles are not sufficient for Alzheimer’s disease
aphasia to develop and that non-biological factors (such as cognitive ability) may also be relevant.
Impaired ability
to produce or
comprehend Vascular dementia
language. Depending on the country, vascular dementia is either the second or the third most common form of
apraxia dementia, and represents approximately 10–30 per cent of all cases of dementia diagnosed (Mendez &
Impaired ability to Cummings, 2003). Vascular dementia is more common in parts of Asia than elsewhere in the world.
perform common For example, in Japan it accounts for 50 per cent of all dementias that occur in individuals older than
voluntary 65 years (Ikeda et al., 2001). In contrast, in Australia the corresponding estimate for the prevalence of
behaviours. vascular dementia is 40 and 25 per cent of total cases of all types of dementias for men and women,
agnosia respectively (Australian Institute of Health and Welfare, 2006). Part of these differing prevalence
Impaired ability to rates may be due to differences in diagnostic practices, with as many as half of all vascular dementia
recognise objects patients having mixed vascular-Alzheimer’s pathology (Rockwood, 2003). The prevalence of vascular
or people. dementia is higher in men than in women, and the risk of developing the disease increases with age,
with onset rising steeply after age 60.

The three most common causes of vascular
dementia are multiple cortical infarcts, a single
infarct in a critical brain region, and small vessel
disease in the brain. An infarct (stroke) occurs when
an artery in the brain becomes blocked, causing cell
death in the area. These infarcts may occur in both
cortical and subcortical tissue in the brain. Thus risk
factors for vascular (blood vessel) disease such as
high blood pressure, diabetes and high cholesterol
levels are all risk factors for vascular dementia.
Similar to Alzheimer’s disease, memory
impairment is a central feature, accompanied by
declines in one or more of the following areas:
aphasia, apraxia, agnosia or a disturbance in
executive functioning (APA, 2013). These cognitive
disturbances must result in significant impairment
in social or occupational functioning and represent
DAL
a significant decline from prior functioning for the

The cognitive disturbances characteristic of Alzheimer’s disease and
diagnosis to be given. Compared to Alzheimer’s
vascular dementia result in significant impairment in daily functioning,
disease, vascular dementia has a more sudden
including the individual’s ability to socialise.
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onset, is associated with vascular disease risk factors and focal neurological symptoms (e.g., weakness
or tingling in extremities), and often has evidence of extensive small strokes on neuroimaging. In
contrast to Alzheimer’s disease, however, there are focal neurological symptoms such as problems focal neurological
with gait (how one walks) or weakness of muscles in the arms or legs, or evidence from neuroimaging symptoms
scans of past strokes, all of which are judged to be related to the cognitive symptoms displayed. As Symptoms (such
with Alzheimer’s disease, other possible causes of the cognitive deficits, such as other mental or as weakness or
tingling in the
physical disorders, must be ruled out before the diagnosis is given.
extremities) whose
causation can
be localised to a
Other forms of dementia and related disorders specific anatomical
Affecting up to 4 per cent of dementia patients are frontotemporal dementias, with an average age of site in the central
nervous system.
onset in the fifth decade of life (Brunnstrom, Gustafson, Passant, & Englund, 2009). Core features of
these dementias include prominent changes in personality and behaviour, whereas memory changes
may not appear until the later stages of the disease. A hallmark feature of frontotemporal dementia is a
decline in interpersonal conduct such as rude behaviours, inappropriate sexual comments or behaviours,
and general disinhibition. The usual duration of frontotemporal dementia is less than 10 years, with
males and females equally affected by the disease. While the underlying causes of frontotemporal
dementia remain unknown, genetic factors are strongly implicated (Mendez & Cummings, 2003). As
judgment and insight are often profoundly impaired in the early stages of the disease, it is important
that safety issues, including possible cessation of driving, be considered.
Lewy body dementia affects over 10 per cent of those diagnosed with dementia. Changes introduced
in the DSM-5 (APA, 2013) include the incorporation of ‘probable Lewy body dementia’ (requiring
two core features or one suggestive feature with one or more core features) or ‘possible Lewy body
visual
dementia’ (requiring one core feature or one or more suggestive features). The core and suggestive
hallucination
features of Lewy body dementia are shown in Table 15.2. Core features of this type of dementia Visual perception
include waxing and waning cognition (e.g., pronounced variations in attention and alertness), recurrent of something that
complex visual hallucinations, and spontaneous features of parkinsonism (uncontrolled movements is not actually
similar to those seen in Parkinson’s disease). Lewy body dementia is characterised by Lewy bodies— present.
that is, abnormal cells present in the lower or subcortical regions of the brain in Parkinson’s disease neuroleptics
but seen in cortical areas of the brain in Lewy body dementia. It is important that Lewy body dementia
Drugs used to
be distinguished from psychotic disorders, as one feature of the disease is a severe sensitivity to treat psychotic
neuroleptics (antipsychotic medications) in up to 50 per cent of patients (Mendez & Cummings, 2003). symptoms.
TABLE 15.2 Core and suggestive features of Lewy body dementia
Core diagnostic features of Lewy body dementia

• Fluctuating (waxing and waning) cognition with pronounced variations in attention and alertness
• Recurrent visual hallucinations that are typically well formed and detailed
• Spontaneous features of parkinsonism with onset at least one year later than the cognitive impairment
Suggestive diagnostic features of Lewy body dementia

• Rapid eye movement sleep behaviour disorder
• Severe sensitivity to neuroleptic medications
• Low dopamine transporter uptake in the basal ganglia region as demonstrated by SPECT or PET imaging
The assessment, treatment and prevention of dementia

The accurate diagnosis of dementia is important, as misdiagnosis can lead to inappropriate or
ineffective interventions, safety issues and family distress. To ensure an accurate diagnosis, a
comprehensive assessment process is required, which typically includes taking a careful clinical
history (including assessing for a family history of neurological disorders), neuropsychological
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assessment (including testing of relevant areas of cognitive functioning such as memory) to ascertain
current cognitive functioning and to estimate premorbid cognitive functioning (before the individual
began to decline) and neuroimaging investigations to rule out other disease processes such as tumours
and to check for vascular changes. There is no simple biological marker or test for dementias in life;
thus the diagnosis can be confirmed only at autopsy after death or by brain biopsy (although the latter
is performed only rarely, most often in a research context). Until such confirmation, one can only
refer to ‘possible’ or ‘probable’ dementia.
EARLY DIAGNOSIS
Early and accurate diagnosis of dementia leads to optimal treatment outcomes. Diagnosis at an
early stage of the illness enables people to seek out information and support and become informed
telemedicine about treatment options, just as in most illnesses. However, as dementia is a disease of later life, it is
Use of sometimes assumed by both health professionals and family that it is perhaps best not to tell the person
telecommunication affected that s/he has dementia. Unfortunately, this can deprive the person with dementia of the right
technologies for
to make decisions such as settling their estate or repairing fractured family relationships before their
the assessment,
treatment, illness progresses and they lose this opportunity forever. Early diagnosis facilitates taking actions such
prevention and as a planned reduction of work hours if appropriate, gradually curtailing driving and putting in place
research of health a plan for alternative transportation options, and engaging support services such as those offered by
issues. Alzheimer’s Australia for both persons with dementia and their families.
Part of trying to facilitate early diagnosis
of Alzheimer’s disease includes the use of
telemedicine to bring health experts ‘virtually’
to older people in regional and rural areas that
lack geriatric specialist services. Telemedicine
(or telehealth) involves the use of various
telecommunication technologies (such as
videoconferencing) for the assessment, treatment,
prevention and research of health issues, and to
provide training for healthcare professionals. An
important element of the delivery of telehealth
services is to ensure that the care administered

is comparable to face-to-face consultations.
Wong, Martin-Khan, Rowland, Varghese, and
DAL
Gray (2012) in Australia, for example, have

Telemedicine may facilitate the diagnosis of Alzheimer’s disease in regional trialled the use of a cognitive screening tool, the
and rural areas. Rowland Universal Dementia Assessment Scale
(RUDAS; Rowland, Basic, Storey, & Conforti,
2006), in a telemedicine setting, and found that videoconferencing administration of the scale did not
significantly differ from face-to-face administration.
Although progress may seem slow in finding a cure for diseases such as Alzheimer’s, a remarkable
amount of progress has occurred given the relatively recent research focus on this condition during the
acetylcholine past 30 years, as displayed in Table 15.3.
Type of
neurotransmitter MEDICATION
that forms the Treatments for dementias include pharmacological, psychological and behavioural interventions.
cholinergic Medications for dementia, particularly Alzheimer’s disease, include cholinesterase inhibitors, which
system in the act to inhibit the reuptake of acetylcholine in the synapses, thus increasing the availability of this
central nervous
neurotransmitter, which is almost always depleted in dementia. However, although the action of
system and
contributes
the drug on the neurotransmitter system often results in improved cognitive function, the effect is
to movement, temporary as the drug has no impact on the underlying disease process. Thus it delays rather than
attention and prevents cognitive decline. Researchers are also working on potential vaccinations with molecules
arousal. that may stimulate activity in the brain’s immune cells, to help destroy the neuritic plaques formed
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TABLE 15.3 Progress in the research into Alzheimer’s disease in the past 100 years
100 years ago

• Dementia first described by Alois Alzheimer
30 years ago
• Research efforts into examining causes and potential cures for Alzheimer’s disease begin
15 years ago
• Examination into the genetics of Alzheimer’s disease begins
10 years ago
• Animal models of Alzheimer’s begin to be developed
5 years ago
• Still working to identify more accurately those at increased risk of Alzheimer’s disease
• Research focusing on increasing knowledge about factors that can promote and maintain brain health
1 year ago
• Dementia reclassified as ‘major neurocognitive disorder’ in the DSM-5
in Alzheimer’s disease. Studies with a molecule known as MPL (monophosphoryl lipid A) found
that weekly injections of it eliminated up to 80 per cent of neuritic plaques in mice. These mice
also showed improvements in cognitive function (Michaud et al., 2013). This is a major step towards
potentially administering injections to people with Alzheimer’s disease to slow the progression of the
illness, or as a preventative measure for people with risk factors for Alzheimer’s disease.
PSYCHOLOGICAL AND BEHAVIOURAL INTERVENTIONS

Psychological and behavioural interventions are quite effective in managing some of the most
challenging symptoms of dementia, that is, the behavioural and psychological symptoms of dementia
(BPSD). BPSD represent a heterogeneous range of psychological reactions and behaviours resulting
from dementia. Approximately 90 per cent of dementia patients will experience at least one such
symptom over the course of their illness (Craig, Mirakhur, Hart, McIlroy, & Passmore, 2005).
Uncontrolled BPSD result in excessive disability, increased rates of hospitalisation and premature
institutionalisation, as well as substantial challenges for the family and suffering for the person with
dementia. BPSD are often unpredictable and can vary over the course of dementia. Thus, interventions
may work for only a limited period of time and carers must be ready to modify strategies to cope with
new symptoms as they emerge. Across studies, carers consider physical aggression to be the most
serious problem they face and the one most likely to lead to institutionalisation. Importantly, physical
aggression against caregivers is a known risk factor for abuse of the person with dementia. In a British
study, for example, caregivers who abused their charges rated their dependants as having significantly
higher levels of behavioural disturbance (i.e., agitation and irritability) than did non-abusing carers
(Cooney, Howard, & Lawlor, 2006).
Detection and monitoring of BPSD, particularly in institutional settings, is key to successful
management. It is critical to understand the causes of BPSD. For example, a person with dementia
who is in pain may cry out or even strike out as s/he lacks the words to describe the suffering. If the
cause of the behaviour can be determined, an effective management plan (in this case, appropriate pain
medication or treatment of the cause of pain) can be put into place. Psychological and behavioural
strategies to cope with BPSD include facilitating effective communication between the patient and
caregivers, modifying the environment to be less confusing or frightening, and providing pleasant and
engaging activities for persons with dementia to avoid frustration and boredom.
One behaviour associated with dementia that can be particularly challenging is wandering. There
is an increasing international literature on the subject of wandering, particularly with respect to
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objectively characterising various patterns of wandering. As shown in Figure 15.3, there are several
subtypes of wandering, including random, lapping and pacing behaviours (Martino-Saltzman, Blasch,
Morris, & McNeal, 1991). Adverse effects of wandering behaviour for persons with dementia include
decreased food intake or skipping meals altogether, weight loss, increased falls, getting lost, premature
institutionalisation and early mortality. Goals of effective wandering management include assuring
the safety of the person with dementia, aiding their navigation, minimising restrictions on their
movements as much as possible, using their preserved skills and supporting abilities, and providing
physical and emotional comfort as part of a person-centred plan of care (Moore, Algase, Powell-Cope,
Applegarth, & Beattie, 2009).
Pacing
Lapping
Random
Direct—not
wandering
FIGURE 15.3 Wandering patterns
In clinical practice, trying to determine the causes of BPSD is more important that simply observing
or reporting such behaviours, if meaningful interventions are to be implemented. It is similar to the
fact that simply observing that a patient has an elevated temperature does not suggest what the best
course of treatment is; the underlying cause of the temperature rise needs to be investigated first,
otherwise a given treatment may not be effective. One method is to systematically work through the
potential causes of BPSD in a manner that has been called the ‘PIECES’ approach (Vitali, Cutaia, &
Vaccaro, 2011). PIECES is an acronym that stands for:
∙ P—physical (e.g., pain from arthritis)
∙ I—intellectual change (e.g., memory loss)
∙ E—emotional (e.g., depression or anxiety)
∙ C—capabilities (e.g., difficulty walking, poor hearing)
∙ E—environment (e.g., cold temperatures in the winter months)
∙ S—social (e.g., interactional styles, cultural norms)
Healthcare professionals can use the PIECES approach to help guide their exploration of the
reasons for a person with dementia displaying a certain behaviour, such as wandering. For example, is
the person cold and looking for a blanket but does not know where to look? Has the person forgotten
where his/her room is in the nursing home? The answers to these questions can help care staff help
the person with dementia by determining what is driving the behaviour. This aspect of dementia care
is a bit like detective work, as the person with dementia cannot explain what s/he may need or want. It
is what makes curiosity and ingenuity key skills in delivering effective care to people with dementia.
THE ROLE OF CAREGIVERS

While professional services have much to offer, the vast bulk of caring for individuals with dementia
is performed by family and friends. Caring for persons with dementia is described by most caregivers
as having both positive and negative elements. Depression and anxiety appear to be significant
problems for caregivers. Cuijpers (2005) conducted a systematic literature search and included studies
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examining caregivers of dementia patients that reported the prevalence of major depressive disorder.
Ten studies with a total of 790 caregivers were identified. A total of 176 caregivers (22.3%) reported
a depressive disorder.
The nature of the pre-existing relationship between carers and patients has been found to be
important in predicting stress, with carers who had positive relationships reporting more positive
caregiving experiences (Lopez, Lopez-Arrieta, & Crespo, 2005). Women overall tend to report feeling
more burdened by the caring experience relative to men (Michon et al., 2004).
Most studies suggest that a range of coping strategies (such as taking time for relaxation and self-
care, maintaining a sense of humour and being able to reach out for help if needed) can be effective
for carers. Effective programs for the caregiver typically provide long-term support, allowing the
caregiver to reduce specific risks (such as their level of burden) associated with poor outcomes (for
instance, depression) (Stevens, Lancer, Smith, Allen, & McGhee, 2009).
Interventions that involve both the caregiver and the patient have been found to be more effective
than interventions aimed at the caregiver alone (Schulz et al., 2008; Shelton, Schraeder, Dworak,
Fraser, & Sager, 2001). Thus, research has been moving towards interventions that address the quality
of the relationship between the caregiver and care recipient (Whitlatch, 2001). One study piloted
the use of a home-based music intervention aimed at stimulating meaningful interactions between
caregivers and their dementia care-recipient spouses. The study found that music-sharing experiences
improved the mood of both partners, enhanced the spousal relationship and increased both the
satisfaction with the caregiving and the caregiver’s wellbeing (Baker, Grocke, & Pachana, 2012).
Strategies to help compensate and facilitate memory and communication skills between carers
(professional or family) and the person with dementia have been shown to be useful (Smith et al.,
2011). In this study by Smith and colleagues, using consistent routines (such as always placing needed
objects in one location in the home) and encouraging conversation about interesting and familiar
topics (for instance, familiar holiday traditions or reminiscing over past family vacations using a
scrapbook) can help support memory and communication difficulties in the person with dementia.
These positive and proactive approaches offer carers concrete and simple strategies to facilitate
positive and meaningful interactions on a daily basis.
PREVENTATIVE APPROACHES
Given the immense suffering that dementias can entail for the person with dementia as well as for their
family, friends and carers, interest has arisen in preventative approaches. In recent years, lifestyle factors
have emerged not only as possible risk factors for developing dementia, but also as a route to decreasing
the chances of developing the disorder. Recent studies have shown that lifestyle factors such as increased
physical and mental activity, as well as increased social engagement, have been shown to decrease the risk
of developing dementia (Bennett et al., 2006). Alzheimer’s Australia has developed an excellent campaign
to help people to incorporate these positive lifestyle changes into their daily life. Dubbed the ‘Mind Your
Mind’ campaign, it lists seven ‘signposts’ to living a healthy life and quite possibly reducing the risk of
dementia. These lifestyle suggestions include increasing levels of physical activity (e.g., through moderate
exercise), keeping to a healthy diet low in saturated fats and high in foods rich in antioxidants (such
as blueberries, broccoli and green tea), and keeping the brain active with stimulating activities such as
pursuing hobbies or attending cultural events. Maintaining good social contacts, through regular activities
with friends and family or through volunteer work, keeping up with regular health checks with a GP, and
avoiding unhealthy habits such as smoking and excessive alcohol use (more than two standard drinks per
day, every day), are also believed to yield long-term benefits to overall brain health.
CHALLENGES OF DEMENTIA DETECTION AND TREATMENT FOR ABORIGINAL

AND TORRES STRAIT ISLANDER PEOPLE
Indigenous peoples make up about 6 per cent of the world’s population, composed of approximately
5000 groups spread across at least 70 countries (Horton, 2006). As described earlier, morbidity and
mortality rates for Indigenous persons in Australia are significantly worse than for non-Indigenous
persons; this situation is true across much of the globe. Aboriginal populations around the world
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represent a fast-growing, under-studied and

under-served population, including with
respect to dementia.
Many of the factors that contribute to high
morbidity and mortality in this group are also
risks for cognitive impairment and dementia. In
the first prevalence study of dementia among
Aboriginal and Torres Strait Islander peoples
in Australia, a prevalence rate of 20 per cent
for dementia or suspected dementia was found
(Zann, 1994). A more recent study by Smith and
colleagues (2008) of 363 Indigenous Australians
GARY RADLER PTY LTD
(55% women) aged over 45 years from the

Kimberley region and far north of Western
Australia found that the prevalence of dementia
in those over 45 years was 12.4 per cent, and
the prevalence in those aged over 65 years was
Morbidity and mortality rates for Indigenous persons in Australia are 26.8 per cent. Dementia was more frequent in
significantly worse than for non-Indigenous persons. In recognition of this men than women (17% versus 9% respectively),
fact, ‘old age’ for Indigenous Australians has been officially defined as and the overall prevalence of dementia in this
beginning at age 50. Indigenous community was 5.2 times greater
than in the overall Australian population.
Within Indigenous cultures, the symptoms of dementia may be viewed in a variety of ways. For some,
the person with dementia’s childlike behaviour is a cause for gentle guidance; viewed in a different way,
the abrupt alteration of personality and interpersonal skills may signal that the person is no longer part
of the group, particularly if the person with dementia violates cultural norms (Pollitt, 1997).
The assessment of persons at risk for dementia in Indigenous communities is a complex undertaking.
Fortunately, researchers are tackling the difficult task of adapting Western methods of assessment
so as to have culturally sensitive and appropriate means of assessing dementia. Many factors must
be considered in developing a culturally appropriate assessment tool. First, English may not be the
individual’s first language, or may not even be spoken. As in many cultures, ideas of time, space and
number may differ from Western notions of these concepts. Also, certain information regarding family
or personal issues may be considered inappropriate for discussion in such an assessment context. With
these and other issues in mind, the Kimberley Indigenous Cognitive Assessment tool (KICA) was
developed to systematically gather clinically relevant information, including cognitive and functional
status (LoGiudice et al., 2006). The development of the KICA took into consideration the appropriate
configuration of questions and response formats for older individuals who might have sensory deficits
or limited energy or memory constraints. Linguists, elders in Aboriginal communities in the Kimberley,
clinicians and other health workers were consulted extensively. Items in the scale are designed to be
culturally appropriate, including questions about orientation such as ‘What season is it?’ (rather than
‘What year is it?’), naming pictures of familiar objects such as a crocodile, and a memory item later
asking the individual to recall the pictures s/he was shown. The scale was well accepted by the people
in the Aboriginal communities participating in the validation of the instrument. It was also found to
have excellent psychometric properties and will be a valuable addition to the toolkit of psychologists
working in Indigenous communities.
Dementia is the most common age-related cognitive condition among Aboriginal peoples (Bennett,
2008). Beyond assessment, ensuring optimal care of individuals with dementia in Indigenous
communities is another challenge. For most people in Indigenous communities, care for a person
with dementia is seen primarily as the family’s responsibility. However, this carer’s role may be
unnecessarily burdensome given a lack of knowledge about, and reluctance to use, healthcare services
to assist with care for those with dementia as well as other mental health disorders.
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LO 15.3 Psychological disorders in later life:

depression and anxiety
Age determines to a certain extent the risk of experiencing certain mental illnesses. Younger adults,
for example, are generally at greater risk for eating disorders, while older adults are at greater risk
for dementia. Furthermore, throughout the lifespan, women are more likely than men to report
psychological distress, particularly depression and dysthymia (Kessler, 2003) as well as anxiety
(McLean, Asnaani, Litz, & Hofmann, 2011). However, new evidence from Australia suggests that
age helps to equalise the balance of psychological disorders between genders (Pachana, McLaughlin,
Leung, Byrne, & Dobson, 2012). Most important is the fact that although the later years of life are
often viewed as a time of increased frequency of disorders such as depression, in reality research has
shown a decreased vulnerability to most psychiatric conditions later in life, as mentioned earlier. As
the prevalence of conditions such as depression, anxiety disorders, schizophrenia and bipolar disorder
decreases with age, the increased occurrence of dementing conditions, nearly on its own, keeps the
overall prevalence of mental illness stable throughout adulthood into advanced old age.
Depression
Depression is probably the condition that has the most evidence with respect to prevalence, symptom
presentation, risk factors and treatment efficacy across the lifespan. Throughout life, depression is
more common in females than males, and at all points a family history of depression is a prominent
risk factor. In Australia, a national mental health survey revealed that 1.1 per cent of those aged
65 years and over met diagnostic criteria for major depression or dysthymia (dysthymic disorder) dysthymia
(Henderson, Andrews, & Hall, 2000). This finding is broadly comparable to other international studies (dysthymic
on the prevalence of mood disorders in older populations. However, sampling issues in how and where disorder)
participants are recruited may affect such epidemiological study results. For instance, Anstey, von Depressive
Sanden, Sargent-Cox, and Luszcz (2007) reported that the prevalence of depressive symptoms in disorder that is
less severe than
residential care was 32 per cent compared with 14.4 per cent in community-dwelling older adults.
major depression
but more chronic.

SYMPTOMS
Symptom presentation can vary widely in depression, including changes in the nature of symptoms
with age. In general, children’s experience of depression frequently results in acting-out behaviours
or social withdrawal. In adulthood, vegetative signs and symptoms (e.g., not enough or too much
sleep and noticeable increases or decreases in appetite, often with associated weight gain or loss)
generally become prominent. Feelings of sad mood and anhedonia (a loss of interest in pleasurable anhedonia
activities) and fatigue are common in all ages in those who are depressed. In later years, the most Inability to
prominent symptom reported is a significant loss of memory, particularly short-term memory. While experience
pleasure from
difficulty concentrating and memory loss may be reported in all age groups, it appears particularly
previously
common in the presentation of older adults with depression. It is also important to note that changes pleasurable
in sleep or appetite patterns in older adults, and even the presence of fatigue, may actually reflect activities.
symptoms of other physical illnesses or may reflect medication side effects rather than depression.
Medications with side effects that can mimic depression, or even worsen symptoms of mild mood
disorders, include those for chronic illnesses such as cancer (which can disrupt sleep and appetite and
cause fatigue). Medications such as benzodiazepines for anxiety, as well as sleep medication, can also benzodiazepines
decrease attention and memory functioning in older adults, mimicking both depressive disorders and Drugs (such
mild dementia. Thus it is important to rule out such sources of these changes before a diagnosis of as Valium and
Xanax) that
depression is made.
reduce anxiety
Depression itself is also a common symptom of a number of serious ailments such as cancer, and insomnia.
and so it is always important that an older adult with suspected depression receive a thorough
medical evaluation. Unfortunately, many health professionals less versed in the care of older adults
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often automatically assume that any change in memory is a sign of a dementing condition such as
Alzheimer’s disease, or else there is a belief that depression is a natural part of ageing and therefore
does not warrant investigation or treatment. Both of these false assumptions can have serious negative
impacts and result in inadequate treatment and decreases in quality of life and lifespan. There are many
barriers for older people receiving effective, evidence-based care for their depression, including poor
detection of the symptoms of depression, failure to recognise symptoms of depression as a treatable
illness, and healthcare providers lacking the knowledge and means for adequate referrals to mental
health specialists (Ell, 2006).
CHARACTERISTICS OF LATE-LIFE DEPRESSION

Although depression can occur throughout the lifespan, of particular interest to psychologists
working with older people is the occurrence of ‘late-life depression’, also known as ‘late-onset major
depressive disorder’. Late-life depression has its onset as a first occurrence of major depression
after the age of 60. It is characterised by a presentation, course, prognosis and treatment different
from those in persons who develop depression earlier in life and continue to experience episodes
of depression after age 60. Compared to those with early-onset depression, those with late-onset
depression experience significant cognitive dysfunction, increased comorbidity of medical illnesses,
and higher rates of either lethargy (or fatigue) or agitation. Unlike those with early-onset depression,
those with late-onset depression are less likely to have a family history of depressive or other mood
disorders such as bipolar disorder. These late-onset episodes of depression tend to be quite chronic and
more resistant to treatment. They also have a high rate of mortality and possibly dementia (Baldwin,
Gallagley, Gourlay, Jackson, & Burns, 2006), including Alzheimer’s disease and vascular dementia
(Alexopoulos, 2003).
SUICIDE
People over the age of 60, particularly men over the age of 75, have the highest frequency of suicide
in almost two-thirds of countries worldwide (World Health Organization [WHO], 2007). The specific
types of stressful life events related to suicide in later life differ from those of younger suicide
victims. For example, interpersonal discord, financial or job problems and legal difficulties are more
characteristic of suicides in young and middle-age groups, whereas the experience of physical illness,
pain, loneliness and social isolation are more typical of those in later life (Chiu, Chan, & Tsoh, 2010).
Nevertheless, suicide is of serious concern as a potential outcome of depression, both in younger
and older age groups. Several studies have found that up to 75 per cent of older adults who commit
suicide visited a primary care physician within a month before their suicide (Conwell, 2001). The
most common psychiatric syndrome of older adults at greatest risk for suicide is a single episode of
unipolar depression without either psychotic symptoms or comorbid psychological disorders. These
patients who take their own life are thus the same patients who might have expected a high rate
of recovery from conventional treatments. The fact that their treatable depression resulted in death
underscores the seriousness of the under-diagnosis and under-treatment of depressive disorders in
later life (Conwell, 2001).
Social disconnectedness is emerging as an important potential factor driving suicide, including
suicidal thoughts, among older adults (Van Orden & Conwell, 2011). In fact, a meta-analysis by
Holt-Lunstad, Smith, and Layton (2010) showed that the influence of social disconnectedness on
premature mortality across age groups is comparable to or greater than other well-established risk
factors such as smoking, obesity and physical inactivity. This follows from Van Orden and colleagues’
(2010) interpersonal theory of suicide, the main points of which are illustrated in Figure 15.4. The
theory proposes two causes of suicidality: thwarted belongingness (not feeling connected to others in
a positive way) and perceived burdensomeness (feeling that one’s death is more valued by others than
continuing to live). These two constructs make up social disconnectedness, and failure to address
this, coupled with a person’s motivation and ability to actually carry out a suicide attempt, greatly
increases their likelihood of success. Van Orden and Conwell (2011) suggest that one important
rie66620_ch15_491-536.indd 516 08/03/17 02:01 PM

Psychiatric
illness Neurobiological and
Personality
cognitive processes
Social Functional cognitive

isolation Social impairment behaviour
disconnectedness
therapy (CBT)
Thwarted Perceived Type of
belongingness burdensomeness psychological
+ treatment that
combines both
Acquired cognitive and
capability
Physical illness Access to behavioural
and pain lethal means concepts and
techniques.
Culture
= Life events
reminiscence
Lethal suicidal therapy
behaviour An empirically
based form of
FIGURE 15.4 The interpersonal theory of suicide applied to late life psychotherapy
Source: From van Orden and Conwell (2011). Suicides in late life. Current Psychiatry that involves
Reports, 13, 234–241. discussing past
activities, events
and experiences,
and uses life
histories—
mechanism shared by effective interventions for the prevention of suicide in later life is the promotion written, oral or
of social connectedness. both—to improve
psychological
TREATMENT wellbeing; has
A variety of treatment approaches are effective for depression in later life. Martin Pinquart, a been used in
psychologist who is very interested in which treatments are effective for older adults, uses a the treatment
of older adults,
technique called meta-analysis to examine which types of psychotherapy for depression for older
particularly those
people currently have the most support. Echoing the findings for younger adults, the effectiveness with depression.
of cognitive behaviour therapy (CBT) was demonstrated for older adults in a meta-analytic
interpersonal
review by Pinquart, Duberstein, and Lyness (2007). In examining the effects from 57 intervention
psychotherapy
studies, these researchers found support for both CBT and reminiscence therapy (which involves
(IPT)
the discussion of past experiences) in the treatment of older depressed populations. In addition,
Short-term
interpersonal psychotherapy (IPT) has good support for the treatment of depression in older psychological
adults (Hinrichsen & Clougherty, 2006). Across studies, meta-analyses suggest that treatment treatment
for depression in older adults produces very good outcomes, with 70–80 per cent recovery rates originally
achieved (Pinquart, Duberstein, & Lyness, 2007). However, because of the low rates at which older developed by
adults seek mental health services, the vast majority (as much as 80%) of older adults with mental Gerald Klerman,
illness go undiagnosed and untreated. Myrna Weissman
and their
colleagues for
the treatment
Anxiety disorders of depression;
Anxiety disorders in older adults have received far less attention in the research literature than addresses
the client’s
depression, yet if anything the epidemiological research demonstrates that anxiety is more common
interpersonal
than depression in later life. Anxiety disorders have been found to be 4–8 times more frequent than problems as a way
major depressive disorders in older samples (Beck & Stanley, 1997). Anxiety disorders are associated of improving his/
with high levels of service use and economic burden (Andlin-Sobocki & Wittchen, 2005; Porensky et her psychological
al. 2009; Smit et al., 2006; Teeson et al., 2011). symptoms.
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EPIDEMIOLOGY
Henderson, Andrews, and Hall (2000) report a prevalence rate of 4.5 per cent for anxiety disorders in
Australians over the age of 65. Several studies have reported phobias to be the most common anxiety
disorder among older people, with generalised anxiety disorder (GAD) being slightly less prevalent
(Ritchie et al., 2004). Other anxiety disorders, such as obsessive-compulsive disorder (OCD) and
posttraumatic stress disorder (PTSD), are uncommon in later life.
Research on anxiety disorders lags behind that of mood disorders despite the fact that anxiety
disorders are associated with numerous negative outcomes in older adults. Anxiety symptoms are
associated with diminished wellbeing, reduced quality of life, increased mortality, impaired ability
to carry out basic activities of daily living (such as preparing meals), poorer health and reduced life
satisfaction (Bryant, Jackson, & Ames, 2009; Porensky et al., 2009).
Like most anxiety disorders presenting earlier in life, anxiety disorders presenting later in life
tend to more commonly affect females and those with a comorbid medical illness. Similar to the
presentation of depressive symptoms in later life, the symptoms of anxiety in older adults may
differ from those in younger adults. Older adults with anxiety more often complain of cognitive
(e.g., memory and attention) and vegetative (e.g., poorer sleep and appetite) symptoms than
younger cohorts.
Although anxiety disorders are more prevalent than mood disorders in later life, their overall
prevalence, like that of mood disorders, declines in later life. Diagnostic difficulties encountered in
anxiety disorders may contribute to their possible lower rates of detection in later life (Jeste, Blazer, &
First, 2005). First, the symptoms of anxiety disorders (e.g., shortness of breath and heart palpitations)
mimic the symptoms of medical conditions common in later life, such as illnesses affecting the
heart or lungs. These symptoms can also mimic the side effects of medications commonly used with
older populations, including antidepressant medications (which can sometimes make people feel ‘on
edge’ for the first few weeks) and, paradoxically, benzodiazepines, a class of medications frequently
prescribed for anxiety symptoms. Finally, older adults with anxiety may present with symptoms
including agitation and memory loss. While these symptoms are also common in younger adults with
anxiety disorders, the greater the patient’s age, the more likely they are to be misdiagnosed with a
dementing condition such as Alzheimer’s disease.
DIAGNOSIS OF SYMPTOMS
In order to accurately establish whether symptoms of anxiety are present, reliable and valid instruments
normative data with good normative data must be used. However, most anxiety instruments have been developed for
Average score younger populations and may underestimate rates of psychological disorders in older populations or
obtained by may be less suitable for older adults with mild cognitive deficits (e.g., the wording of items may be
the normative
too long or complex).
sample on any
given measure
A brief inventory of anxiety symptoms in older adults has recently been developed in Australia
against which an with the aim of increasing the accuracy of surveying anxiety symptoms in older populations (Pachana
individual’s score et al., 2007). The Geriatric Anxiety Inventory was designed specifically for use with older adults in
can be compared a wide range of settings, including inpatient and nursing-home settings. The instrument was kept
so as to provide relatively brief (20 items) and was designed with a simple agree/disagree response format for ease
an objective, of use with mildly cognitively impaired older adults. The inventory was designed not to ascertain
external standard a diagnosis of a particular anxiety disorder but rather to measure symptom severity across a range
of performance.
of anxiety disorders and symptoms. Such self-rating symptom-based scales are advantageous in
screening situations as they do not require extensive observation of patients and can be useful in
guiding treatment recommendations. The Geriatric Anxiety Inventory has been shown to have
good psychometric characteristics such as excellent reliability and concurrent validity (Pachana et
al., 2007). A shortened version of the Geriatric Anxiety Inventory with only five items has been
developed for use in epidemiological research and as a brief screening tool (Byrne & Pachana, 2011).
The Geriatric Anxiety Inventory has also been translated into more than two dozen languages spread
across five continents, with psychometric properties remaining largely consistent across translations
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(Pachana & Byrne, 2012). This is important, as it allows for crucial cross-cultural comparisons of
anxiety symptoms in healthy and clinical populations.
TREATMENTS
A variety of treatment approaches are effective for anxiety disorders in later life. Unlike depression,
the use of anti-anxiety medications (commonly called anxiolytics) is not recommended in nearly all
instances of anxiety in later life. This is because such medications tend to be addictive and sedating,
tend to disrupt normal sleep–wake cycles, and tend to result in unsteady balance, resulting in an
increased risk of falls and fractures. For example, Vitry, Hoile, Gilbert, Esterman, and Luszcz (2010)
examined the effects of psychotropic medications, including anxiolytics and sedatives, on the risk of
falls and fractures using data from the Australian Longitudinal Study of Ageing. They found that the
use of psychotropic medications was associated with an increased risk of falls and fractures in females
but not males. In a meta-analysis conducted by Glass, Lanctot, Herrmann, Sproule, and Busto (2005),
adverse events were more common in older adults taking sedatives than in those who did not take such
medication. For example, adverse cognitive events (such as drowsiness, nausea and headaches) were
4.78 times more common, and adverse psychomotor events (such as falls and vehicle crashes) were
2.61 times more common.
There are very few robust treatment studies evaluating the effectiveness of psychological
interventions for anxiety later in life. One of the most controlled and comprehensive of the studies
in the area of late-life anxiety was conducted by Stanley et al. (2003) investigating the efficacy of
cognitive behaviour therapy (CBT) for generalised anxiety disorder. Results indicated a significant
improvement in self-reported and clinician-rated measures of worry, anxiety, depression and quality
of life following CBT compared to the control group, with 45 per cent of those in the CBT condition
classified as having had a good response to treatment.
As with depression, older adults with anxiety disorders do not seek treatment as often as their
younger counterparts. This is sometimes attributed to older adults not wishing to seek psychiatric
treatment due to embarrassment or being stigmatised from talking about mental health issues (Gething
et al., 2003). However, a more recent study found that attitudes towards seeking psychological help in
this population were relatively positive (Woodward & Pachana, 2009). Attitudes towards help-seeking
for mental disorders among older cohorts are in fact similar to those of younger cohorts, at least for
more severe mental disorders, and thus are unlikely to be a major contributor to the under-treatment
of older adults. A study by Robb, Haley, Becker, Polivka, and Chwa (2003) compared older and
younger adults’ attitudes towards mental health care via a postal survey. The questionnaire covered
such areas as their personal experiences with mental health professionals, knowledge of mental health
services, perceived barriers to mental health services, and the likelihood that they would consult a
mental health professional for various disorders. Older adults were found to have been less likely than
younger adults to have used mental health services, were less confident regarding their knowledge
of mental healthcare, and less likely to seek help for ‘less severe’ and more common problems (such
as depression, anxiety, divorce, bereavement and stress). In contrast, however, neither age group
indicated stigmatisation (negative attitudes towards people with a mental illness) as an important
barrier to treatment, and both age groups indicated that access to mental health services was ‘very
important’ and that they would seek help for ‘more severe’ mental disorders such as schizophrenia and
suicidal feelings.
While the rate of older adults consulting mental health professionals in general and psychologists
in particular has been shown to be relatively low (e.g., Smyer & Qualls, 1999), unwillingness to do
so is not the main reason for this. The increasing number of older people has resulted in a shortage
of mental health providers with skills in treating older adults specifically—and this is of particular
concern to psychologists (Laidlaw & Pachana, 2009). In Australia, mental health service provision for
older adults, particularly psychological services, is relatively low compared to that for younger groups
and may in part be the result of a failure to attract mental health professionals to work with older
populations (Koder & Helmes, 2006).
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Furthermore, biases in the treatment of older adults with mental illness have been documented in
the literature. For example, Helmes and Gee (2003) investigated the attitudes of Australian therapists
towards older clients through a postal survey of 707 psychologists and counsellors. Participants
received a case vignette indicative of depression, noting that the white female described was either 42 or
72 years of age. The participants were asked to indicate their opinion on the client’s presenting
problem, prognosis and appropriateness for therapy. They were also asked to rate their ability to
develop an adequate therapeutic relationship with the client and their perceived level of competence in
treating and willingness to accept her as a client. Results indicated that while the client was correctly
diagnosed regardless of her age in an average of 90 per cent of cases, the older client was rated
as less able to develop an adequate therapeutic relationship, to have a poorer prognosis and to be
less appropriate for therapy compared to the younger client. Therapists also indicated that they felt
less competent in treating her and less willing to accept her as a client. Negative attitudes by mental
health professionals may therefore be another barrier for older adults obtaining effective treatment for
psychological disorders.
CASE STUDY: ANXIETY

Cheryl is a 71-year-old retired high school biology teacher in good health. Her husband, Richard, also a teacher, died five
years ago; they were married for over 30 years. Their marriage was one filled with laughter and much travel. They had no
children of their own, but were very invested in the lives of their nieces and nephews.
Cheryl had a bad fall recently, which required a partial hip replacement. Previously a very active gardener and
birdwatcher, Cheryl was confined to bed for an extended period of time due to complications from her surgical procedure.
Her rehabilitation process was slow and she was very discouraged at her slow progress and the amount of pain she
was in.
Cheryl’s younger sister Beth noticed several
changes in her behaviour after this adverse life
event. Cheryl became very afraid of going out,
insisting she might have another fall, even on
relatively short excursions that were objectively
not risky. She became more easily tearful, and
sent long emails almost daily about things

that were concerning her—about washing
machines making ominous noises, neighbours
being inconsiderate and many new vague
physical symptoms. Cheryl was not sleeping or
eating well, and was withdrawing from friends
and family.
Beth was able to convince Cheryl to go with
her to the GP to discuss these concerns. Beth
was convinced that Cheryl was depressed,
DAL
but the GP, after a careful clinical interview Family and friends can be helpful in identifying if an older adult is
and using the Geriatric Anxiety Inventory (GAI) experiencing difficulties and in assisting the older person to seek
screening tool, believed that Cheryl’s main professional support if needed.
problem was anxiety.
This case raises a number of issues, the first
relating to the issue of diagnosis. Why might Beth have thought of depression first in this instance? After someone has a
fall, it might be natural to worry about having another fall. What symptoms did Cheryl display that made her worry seem
beyond what is considered ‘normal’? Assessing for further symptoms of anxiety (such as worry interfering with activities,
or causing physical symptoms such as stomach pain) would help to clarify this. Why might the GP have used a screening
tool such as the GAI? A referral to a psychologist to discuss her concerns would be beneficial for Cheryl, in terms of
helping her to better manage her anxiety as well as the pain relating to her surgery and rehabilitation efforts.
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LO 15.4 Life events associated with later life:

retirement, grandparenting, driving
cessation and bereavement
Retirement
Later in life, individuals typically need to make adjustments to their cognitive, emotional and social
functioning occasioned by significant events such as retirement. For many people, work not only
occupies a substantial portion of their time and energies over their lifespan, but also often facilitates
relationships, structures daily activities and defines, to some extent, a sense of self. Thus, the prospect
of retirement, the process of retirement and actually living in retirement may all have an impact on
wellbeing in the later stages of life.
Retirement is a critical life transition, as supported by both cross-sectional research comparing the
experiences of workers to retirees and longitudinal studies examining personal and social development
after retirement. More recent research suggests that retirement is generally a positive transition. For
example, using data from two large epidemiological surveys, Drentea (2002) examined the relationship
between retirement and mental health and wellbeing. Retirees were found to report less anxiety and
distress and higher positive affect, compared to older adults who had not yet retired.
A range of variables has been identified that can help to predict those who will experience
retirement as a positive experience versus those who will not. Donaldson, Earl, and Muratore (2010)
examined individual characteristics (e.g., age and gender), psychosocial variables (e.g., mastery, sense
of control and planning for retirement) and organisational factors (such as the preparation for and the
timing of retirement) as possible predictors of retirement adjustment in a group of older Australians
(mean age 65). They found that higher income and having better psychological and physical health
predicted better adjustment to retirement. They also found that a higher personal sense of mastery and
more favourable conditions surrounding retirement (such as having a choice in the timing and nature of
the transition) were more important predictors of subsequent retirement adjustment than other factors
such as health and wealth. Very similar results were found by Wong and Earl (2009), such that better
psychological health, higher income and being married predicted better retirement adjustment in a
sample of Australian retirees aged 45–93 years. In terms of the work–retirement transition, individuals
who retire voluntarily are happier than those who are forced out of their job (Calvo, Haverstick, &
Sass, 2009; De Vaus, Wells, Kendig, & Quine, 2007). Thus health, financial constraints and social
networks can all contribute to how one fares in retirement.
One major theory regarding successful life after retirement and ageing generally is Baltes’s
theory of selection, optimisation and compensation (SOC) (Freund, Li, & Baltes, 1999). This theory
proposes that individuals who age successfully use three strategies—selection, optimisation and
compensation—to achieve their desired goals. Selection includes identifying and prioritising goals.
Optimisation refers to maximising performance to ensure successful achievement of the goal. This
may involve learning new skills, looking to others as a model for successful pursuit of the goal,
and developing new or existing resources to meet the goal. Finally, compensation involves adapting
to limitations that hinder the pursuit of goals, and may involve the use of assistive technology or
obtaining help from others.
An important feature of Baltes’s SOC theory is that it underscores the fact that older adults are
making active choices with respect to how they will compensate for any physical, cognitive or other
limitations in the pursuit of their goals. This idea of active accommodation and strategy use has been
replicated in many other areas. For example, in studies of older adults’ driving behaviour, it has
been found that older adults slow down slightly (but still safely) in their driving speeds in order to
compensate for their slower speed of processing and reaction times, and that they may self-limit their
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driving at dawn and dusk when visual difficulties adjusting to the glare from oncoming headlights
and changing lighting conditions are at their worst (Pachana & Long, 2000). In fact, the lack of such
successful accommodation may signal a problem, as when older adults experiencing dementia (who
often lack insight into their own behaviours) fail to adopt these compensatory strategies.
Baltes’s SOC theory has been successfully applied in a number of areas, including leisure pursuits.
For example, in a study of reading among older adults with visual impairments, participants’ coping
strategies were analysed using SOC theory (Ryan, Anas, Beamer, & Bajorek, 2003). Participants
demonstrated selection by discontinuing some types of reading (e.g., where they were unable to
obtain large-print copies of texts), optimisation by learning how to use talking book players, and
compensation by using assistive devices including powerful lights and magnifiers. Thus participants
using an SOC approach were able to achieve success in ageing with respect to their pursuit of leisure
goals, in this case the activity of reading.
Grandparenting
Older Australians are the largest providers of non-parental childcare in this country (Goodfellow,
2003). In 2008, some 660 000 children (or just under one-fifth of Australian children aged 12 years
and under) received grandparent care, far outstripping other forms of childcare such as long day care
and before/after school care (ABS, 2008). In fact, in about 1 per cent of all families with children aged
0–17 years, grandparents are the principal guardians. In nearly two-thirds of these cases, the natural
parents of the children are living elsewhere.
hypertension In several studies, grandparenting as a full- or nearly full-time occupation is related to a
Condition in variety of both positive and negative outcomes. In terms of physical and mental health, custodial
which the blood grandparents are more likely to experience depression, diabetes, hypertension and insomnia
supply through than non-custodial grandparents (Minkler, Fuller-Thomson, Miller, & Driver, 2000). Custodial
the blood vessels grandparents caring for grandchildren with emotional distress and hyperactive symptoms reported
is excessive higher levels of anxiety, stress and depression, and were more likely to report less life satisfaction
and is a major
(Doley, Bell, Watt, & Simpson, 2015). Several sources of stress for grandparents have been
risk factor for
heart disease identified, including deterioration of physical health, social isolation, financial burden and dealing
with grandchildren’s behavioural problems and emotional disturbance (Janicki, McCallion,
and stroke (also

known as high Grant-Griffin, & Kolomer, 2000). Social isolation and inadequate social support are significant
blood pressure). problems for custodial grandparents (Hayslip & Kaminski, 2005). Gerard, Landry-Meyer, and
Roe (2006) found that social support reduced
the amount of stress grandparents reported in the
face of health problems in their grandchildren.
However, since in many cases the children’s
natural parents are alive, grandparents are often
hesitant to seek formal custody or adoption of
their grandchildren. A variety of legal, financial
and interpersonal challenges arise from such
circumstances (Goodfellow, 2003). For example,
without being the legally recognised guardian of
the grandchildren, grandparents are often limited
in terms of which government remuneration
schemes they can access.
Despite the many stresses faced by custodial
grandparents, many also report positive benefits
from their role (Jenkins, 2010). Custodial
DAL
grandparents report feeling closer to their

Grandparent care is by far the most common form of non-parental grandchildren than non-custodial grandparents
childcare in Australia. (Goodman & Silverstein, 2001). Other benefits
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reported by custodial grandparents include obtaining renewed meaning in their own lives (Haglund,
2000). In turn, children raised by their grandparents report unique aspects of their experience. For
example, grandparents in such situations can serve as strong, positive role models and can provide
security and encouragement in a safe and often familiar environment for children who might
otherwise have been in foster care (Hayslip & Kaminski, 2005). In one study, 90 per cent of custodial
grandparents reported that they would still take responsibility for their grandchildren if offered the
choice again (Hayslip & Shore, 2000). Despite these intriguing findings, grandparenting remains an
understudied area, with many opportunities to better understand and assist those who take on this
demanding role in a full-time capacity.
Driving cessation
Older adults in Australia are continuing to drive for more years and to drive for longer distances than
ever before. The ability to drive may influence one’s ability to engage socially and may be tied up with
one’s sense of identity as an independent and mobile adult. Driving cessation can therefore result in
a range of negative consequences for the older individual, including depression, social isolation and
decreased use of health services.
As a person ages there is an increasing chance that health concerns will force him/her to have
to cease driving. Some common reasons why older adults might cease driving include medications
or sleep conditions that interfere with attention and concentration; health-related symptoms (such as
arthritis) limiting strength or movement, or causing pain; visual impairments that hinder driving; or
neurological conditions such as dementia that interfere with driving skills and judgment on the road
(Anstey, Wood, Lord, & Walker, 2005; Tuokko, Rhodes, & Dean, 2007). In Australia, it has been found
that approximately 46 per cent of people aged 65 years and older do not drive, and the proportion of
non-drivers increases dramatically as a function of age and gender. For example, by the age of 85 years,
95 per cent of women and 63 per cent of men reported that they no longer drive (Ross et al., 2009).
According to the World Health Organization’s Global Burden of Disease Project, motor vehicle
accidents will rank third behind heart disease and major depression as a worldwide cause of disability by
2020 (Murray & Lopez, 1996). Accidents (especially multi-car accidents) and fatalities are high in those
over the age of 65 years, even though as a group older adults do not drive as many kilometres per year
as younger cohorts (Langford & Koppel, 2006). Fortunately, the risk of an older adult being involved in
an accident is not as high as other age groups. For example, recent data suggests that adolescent drivers
(15–19 years old) have the highest reported crash rates compared with any age group (Bingham &
Ehsani, 2012; National Highway Traffic Safety Administration, 2009). Furthermore, Hakamies-
Blomqvist, Raitanen, and O’Neill (2002) found that, compared to middle-aged drivers, older drivers
had no increased crash risk per distance driven once different driving distances were controlled for.
Although there is a strong stereotype that some people hold about older adults being less capable drivers
than younger adults, this is untrue. Healthy older adults drive as well as younger age groups (Fitten et al.,
1995) and, in fact, driving is a skill that increases with practice. This means that, in general, older, more
experienced drivers are better at negotiating hazards and anticipating difficulties ahead than younger,
more inexperienced drivers (Deery, 1999; Wallis & Horswill, 2007; Horswill et al., 2009). In the absence
of health conditions that may compromise safe driving, the skill of driving increases with experience—
thus, driving is one aspect of functioning that is positively associated with age.
In contrast to other older adults, of concern are older drivers with cognitive and behavioural
impairments as a result of dementia. Persons with dementia are 19 times more likely to have an accident
than age-matched persons who do not have dementia (Dubinsky, Williamson, & Gray, 1992; Fox,
Bowden, Bashford, & Smith, 1997). Being male and of a younger age with a diagnosis of dementia are
factors more often associated with the refusal to stop driving despite significant cognitive impairment
(Freund & Szinovacz, 2002). In Australia, the statistics for male drivers are troubling, with 42 per
cent of those with probable dementia and 63 per cent with possible cognitive impairment respectively
reporting that they are current drivers (Ross et al., 2009). As insight into how one is performing a task,
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including tasks such as driving a car that can seem so familiar, is often impaired early in the course
of dementia, it is difficult for people with this condition to understand the need to give up driving
for safety reasons. It also poses a burden on family and healthcare professionals, who must try to
manage the older adult who can no longer drive, and who often lacks the insight or ability to grasp this
situation (Liddle et al., 2013). If family dynamics such as those in Figure 15.5 (and described in the
case study on driving) are addressed by healthcare professionals when negotiating driving cessation,
then improved outcomes and satisfaction for all parties, including the person with dementia, can occur
(Liddle et al., 2016). Family members need to feel a sense of unity (‘we are all in it together’) and
participate in active negotiation with respect to driving with the person with dementia to avoid conflict
(‘being at odds with one another’). Providing sensitive and responsive support for families managing
driving cessation is of the utmost importance (Liddle et al., 2016).
Context for driving cessation
Driving cessation:
a continuum of family dynamics
In it Behind the Active

At odds
together scenes negotiations
Collaboration Conflict
FIGURE 15.5 The context for driving cessation

Allen, Shelley et al. (2016). ‘The biggest problem we’ve ever had to face’: How families manage driving cessation with people with dementia.
International Psychogeriatrics, 28, 109–122.
CASE STUDY: DRIVING

Roger is a 72-year-old farmer who lives on a rural property. His wife, Betty, also 72, does not drive. Roger and Betty have
three children: the oldest, Tim, is a builder; the middle daughter, Tracy, is a lawyer and lives in another state; and Nick,
the youngest, is overseas, working in London for a large multinational company in their finance department. Tim lives the
closest to his parents, but he is still 200 kilometres away.
Approximately one year ago, Roger was involved in a minor accident (running into a parked car while doing the
grocery shopping). He insisted that it was not his fault because of the way that the other car was parked. However, when
Tracy heard of the accident, she rang her father’s GP and voiced concerns about her father’s driving: ‘He is erratic and
I’m not comfortable with him driving my kids.’ On a subsequent visit to his GP, Roger was livid that his driving ability was
being questioned: ‘I am a great driver and always have been.’ Nick and Tracy subsequently quarrelled over what he saw
as her ‘meddling’ and what she saw as his ‘ignoring the signs that something is wrong’.
Unfortunately, Roger had a subsequent single car accident when his car went off the road and into a ditch near his
home; Betty was hospitalised with severe internal injuries. This event led to both Tracy and Tim travelling to meet with
the GP. Their father was refusing a referral for cognitive testing, insisting that it was not necessary. Mirroring the types of
family dynamics involved in cases where driving cessation is considered (see Figure 15.5), Tim and Tracy, while initially
at odds with how they saw their father’s ability to drive (fighting with each other about what was the best way forward,
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and not really listening to each other), realised that they were in it together—they had to put their differences aside and
act cooperatively given escalating events about their father’s driving and their mother’s health. In interacting with their
father at home while their mother was in the hospital, both siblings came to realise that their father was lacking insight
about his driving, but that he was also very upset about both the accident and the thought of losing his mobility.
Some behind the scenes discussions between Tim and Tracy, including a Skype call to their brother Nick in London,
led to Tim’s suggestion that an offer be made to help sell the family farm (which was being leased and which none of the
siblings had an interest in retaining). Such behind the scenes discussions between partners, adult children, friends and
health professionals can get these interested parties to agree on a sensitive and sensible approach forward to address
the concerns about the continued driving of the person with dementia. In Roger’s case, the profits realised by selling the
family farm could enable Tim to build a home for his parents on his large coastal property so that he could be close by
to help them.
Active negotiations to enact this plan then began between the siblings and their parents. Such negotiations involve
respectful conversations with the person with dementia about the next best steps to take to mitigate the risks involved
with continuing to drive, and ultimately culminate in a plan to cease driving. While initially resistant, Betty’s slow recovery
and need for extensive rehabilitation gradually helped sway Roger to consider this move: accessing good specialist care
was not possible from their rural location and Tim’s wife was a nurse, so it made sense for Roger and Betty to live close
to Tim. With both Tim and his wife on hand to drive, Roger became less distressed at the thought of stopping driving
since he would still have easy access to transportation.
This case brings up difficult issues of driving cessation, particularly in locations without access to public transport,
and in circumstances where the spouse does not drive. Access to a structured driving cessation program might be
possible in a larger town; increasingly, such programs may be offered in a telehealth format, which could be of great
benefit to people living in rural areas such as Roger and Betty.
As previously mentioned, driving cessation is linked to a range of negative consequences,

including increased depression (Windsor, Anstey, Butterworth, Luszcz, & Andrews, 2007), reduced
social involvement and feelings of social isolation (Liddle, Gustafsson, Bartlett, & McKenna, 2012)
and concerns and feelings about being a burden on family members or caregivers (Finlayson &
Kaufert, 2002). Nevertheless, people affected by dementia are likely to need to stop driving at some
point after becoming ill (Breen, Breen, Moore, Breen, & O’Neill, 2007). Interventions to improve
outcomes for older adults who need to stop driving include participation in structured driving
cessation programs (Liddle et al., 2013; 2014). Such programs involve the participant taking part in
a series of either group or individual sessions with specific aims, for instance, grieving the loss of
driving, coping with public transportation issues and maintaining social connections and activities.
Research has also found that social connectedness can help to offset the negative consequences of
stopping driving, with one study reporting that women who remained actively involved in social
activities maintained a good level of mental health despite driving cessation (Pachana, Leung,
Gardiner, & McLaughlin, 2016).
Bereavement
A number of studies have indicated that while bereavement is common among older adults, it does
not necessarily result in clinically significant psychological distress (Fisher, Zeiss, & Carstensen, clinically
2001). In fact, some research has indicated that younger widows and widowers may experience more significant
symptoms of depression and physical health problems than older persons who are bereaved (Nolen- Meaning the
Hoeksema & Larson, 1999). This may be partly due to the fact that older adults tend to have a support disorder causes
substantial
network more able to help them with such an event than younger adults whose friends may find this
impairment
unexpected situation difficult to deal with. Moreover, the experience of the death of a spouse at an in social,
older age is more expected than the death of a spouse at a younger age; however, unexpected losses occupational or
(as opposed to anticipated losses) may result in poorer mood among older adults (Pachana, 1999). other areas of
Expected losses generally result in lesser degrees of dysfunction than unexpected losses, particularly functioning.
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if the unexpected loss involves suicide. Increased coping with bereavement among older populations
may also reflect the fact that this group may have more experience in coping with death due to a
lifetime of personal losses. This explanation is also congruent with research that demonstrates that
those who have had greater exposure to grief tend to have less severe reactions following a death
(Fisher et al., 2001).
The finding that older adults often fare better than their younger counterparts in responding to
grief is not to minimise the distress that loss occasions in older individuals. Older adults experience
the loss of a spouse from a variety of life circumstances. For instance, they will vary in their level
of closeness with their spouse, their financial and social situation, and their perspective on the
circumstances of the loss. Generally, though, studies have found that older adults report the loss of
a long-term spouse as devastating, with this loss often exacerbating health concerns (Naef, Ward,
Mahrer-Imhof, & Grande, 2013).
Normal grief reactions may include some of the symptoms that occur in depression, such as sadness
and changes in appetite or sleep. Other symptoms, however, suggest that the person’s bereavement has
precipitated a full-blown depressive episode. Distinguishing normal grief reactions from depression is
difficult, but the latter usually includes feelings of worthlessness and pervasive guilt or hopelessness.
This is especially true if such reactions persist for more than six months after the loss. In a controversial
decision, the DSM-5 removed its previous ‘bereavement exclusion’ clause, which meant that a grieving
person could not be diagnosed with depression or an adjustment disorder. This change has been made
in order to provide treatment for the 10–15 per cent of mourners with severe and crippling reactions to
the loss of a loved one. However, opponents to this change argue that it may result in pharmaceutical
companies pathologising and medicalising even normal reactions to loss (Doka, 2013).
It is often assumed that the opportunity to grieve prior to a loss, sometimes referred to as
anticipatory grief, may ease adverse reactions to the loss when it actually occurs. However, this may not
necessarily be the case. For example, Hill, Thompson, and Gallagher (1988) found that older women
who had rehearsed their loss by discussing financial issues or funeral arrangements with others were
more poorly adjusted following their loss, reported significantly greater numbers of health concerns
and tended to show greater levels of depression than widows who had not engaged in such tasks. In
addition to behaviours engaged in before the loss, events after the loss may affect the individual’s
response. A review by Naef and colleagues (2013) suggests that constructing a new identity after the
loss of a partner or spouse and striving for independence in the face of disrupted everyday activities and
routines, loneliness, health concerns and changed interpersonal relationships are important features of
older persons’ bereavement experience.
Unfortunately, currently, psychotherapeutic
interventions cannot be considered evidence-
based treatment (Byrne, 2010). Indeed, the grief
counselling that is often suggested to those who
have experienced bereavement has been shown to
be neither necessary nor effective (Wittouck, Van
Autreve, De Jaegere, Portzky, & van Heeringen,
2011). In fact, a meta-analysis of 61 studies found
that, despite a small positive effect of therapy for
pathological grief at post-treatment, there was
no statistically significant benefit at follow-up
(Currier, Neimeyer, & Berman, 2008). Another
concern is the over-prescription of benzodiazepines
for bereavement in some healthcare settings (Tol
DAL
et al., 2014). However, research in this area is

Bereavement is common among older adults; their ability to cope with slowly increasing, providing useful insights
the death of a loved one such as their spouse may be greater than that into effective therapeutic strategies for assisting
of younger adults. bereaved older adults.
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LO 15.5 Positive or successful ageing

The afternoon knows what the morning never suspected.
Swedish proverb
There are many criteria for positive, successful ageing. Rowe and Kahn (1998), in their book Successful
Aging, define positive ageing as the ability to sustain three important characteristics and behaviours,
namely:
∙ a low risk of disease and disease-related disability
∙ a high level of mental and physical functioning
∙ an active engagement with life.
Other authors have added such diverse criteria as social competence and productivity, personal
control and life satisfaction to this equation. Essentially, as lifespan continues to grow incrementally,
the goal of later life is not simply to add years of life but to ensure that the time gained is able to be
used as productively and positively as possible.
Today, average life expectancy in developed countries is approximately 75 years (WHO, 2011).
In terms of biological possibilities, the term ‘maximum lifespan’ is often used to denote a theoretical
limit to achievable human lifespan. This number is usually quoted as between 125 and 130 years.
Lifespan continues to increase by an average of 3–4 months per year in developed countries.
In learning how to achieve a lengthy, healthy and productive life, scientists have turned to
centenarian studies. One interesting finding (Evert, Lawler, Bogan, & Perls, 2003) has been that long-
lived individuals fall into three groups:
∙ escapers (20%)—people who have avoided serious illness until after age 100 (or completely)
∙ delayers (40%)—people who have delayed serious illness until after age 80
∙ survivors (40%)—people who develop serious illness before 80 but survive it.
The substantial proportion of long-lived individuals in the ‘survivor’ category indicates that serious
illness during middle age by no means precludes living to a very old age. Moreover, longitudinal
studies of ageing have found that healthy cognitive functioning is a better predictor of independence in
later life than is physical health (Friedrich, 2002).
In research examining the impact of lifestyle on ageing, certain factors have been found to decrease
average life expectancy (e.g., cigarette smoking, obesity and high amounts of daily stress), while other
factors promote longevity (e.g., regular exercise, a healthy diet and regular medical checkups). Studies
such as these can help to inform interventions aimed at achieving longevity and a high quality of life in
later years.
However, beyond physical and mental health, more subtle qualities of life such as a positive view
of oneself and one’s place in the world are increasingly being examined as part of the research into
successful ageing strategies. Martin Seligman is a psychologist noted for his involvement in the
positive psychology movement, which focuses on the attainment and effects of positive subjective
experiences such as contentment, hope and optimism (Seligman & Csikszentmihalyi, 2000).
Regarding the positive aspects of ageing, research within the positive psychology movement has
sought to characterise the types of social interaction that may enhance the experience of growing
older. One intriguing line of research involves the positive benefits of altruism and volunteering
later in life. Dulin, Hill, Anderson, and Rasmussen (2001) found that a group of low-income
participants who engaged in voluntary work, despite being in poorer health and in a suboptimal
financial condition, reported a greater degree of life satisfaction than a healthier, financially more
secure, age-matched reference group not taking part in volunteer activities. Greenfield and Marks
(2004) found that in their sample of volunteers, those who reported being able to replace previous
life roles with their new volunteerism reported greater satisfaction. Similar findings from other
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studies have lent support to the idea that helping

others in turn confers psychological and health
benefits for the volunteer.
Volunteerism is just one factor among many
contributing to positive ageing. Illuminating such
factors is a high priority for future research. What
both cross-sectional and longitudinal studies have
already highlighted is that the later years of life—
provided that there are no major losses in physical,
cognitive or emotional health and wellbeing—are
typically characterised by increasing satisfaction
with life achievements, contentment with
relationships, and a willingness to give back to the
community.
DAL
Volunteerism can contribute to positive ageing.
LO 15.6 Ageing organisations and resources

in Australia, New Zealand and worldwide
A number of key organisations both nationally and internationally work to provide greater understanding
of the psychological issues associated with ageing.
Alzheimer’s Australia (www.alzheimers.org.au) is the peak consumer body in Australia that represents
and supports people living with dementia and their families and carers in terms of providing free
information and support. The Alzheimer’s Australia ‘Mind Your Mind’ campaign, which aims to prevent
dementia through a range of self-help strategies, can be accessed on the Alzheimer’s Australia website.
Alzheimer’s Disease International (https://www.alz.co.uk/) works globally to focus attention on
dementia, while assisting Alzheimer’s associations locally to promote and offer care and support for
people with dementia and their carers. The group is based in London and closely aligned with the
World Health Organization.
The Gerontological Society of America (GSA) (https://www.geron.org/), founded in 1945, is the
largest interdisciplinary organisation devoted to research, education and practice in the field of ageing.
With members from more than 50 countries, the GSA sponsors scientific meetings and conferences,
offers significant networking and mentorship opportunities and publishes several pre-eminent peer-
reviewed journals on the science of ageing.
National Seniors (www.nationalseniors.com.au) is an Australia-wide community organisation that
aims to provide economic and social benefits to adults over the age of 50 living in the community. It
also represents its members’ views to the government and funds research on ageing.
The Psychology and Ageing Interest Group (PAIG) of the Australian Psychological Society
(APS) (www.groups.psychology.org.au/paig) is dedicated to furthering clinical knowledge, research
agendas, teaching and learning initiatives and public policy relating to older adults in Australia. It acts
as a mechanism for psychologists across Australia to stay linked with colleagues who share a clinical,
teaching and research interest in the psychology of ageing. Psychologists with an interest in clinical
work with older adults are found in a variety of university and community settings, in both urban and
regional areas; contacting one of the state representatives of PAIG is one way to make contact with a
local geropsychologist in Australia.
Age Concern (www.ageconcern.org.nz) is the peak body in New Zealand concerned with older
persons’ welfare, such as efforts to prevent elder abuse.
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SUMMARY
The later years of life are often vital and productive, with older adults taking active roles in their families, their communities and
society more generally. The populations of many industrialised countries are ‘greying’, meaning that the number of people over the
age of 65 is increasing as a proportion of the population.
While some small declines in selected cognitive areas such as memory may be expected with normal ageing, other skills (such
as wisdom) may actually improve with age. Illnesses such as dementia, depression and anxiety are not part of normal ageing,
but are due to disease processes. The symptoms of all of these illnesses may be relieved through medication and psychological
approaches, and complete remission of depressive and anxiety symptoms can be achieved. Clinical psychologists who specialise
in the area of ageing remain a minority in Australia as well as many other countries, but have much to offer in the assessment and
treatment of older adults.
Maintaining a healthy lifestyle is key to maintaining good brain functioning. Important lifestyle considerations include increasing
levels of physical activity, observing good nutrition and keeping the brain active. Such positive changes in lifestyle, along with
avoiding excessive stress and seeking meaningful engagement with others, can contribute to positive ageing.
KEY TERMS
acetylcholine. . . . . . . . . . . . . . . . . . . . . 510 computerised tomography (CT). . . . . 499 neuroleptics . . . . . . . . . . . . . . . . . . . . . 509
agnosia . . . . . . . . . . . . . . . . . . . . . . . . . 508 dementia. . . . . . . . . . . . . . . . . . . . . . . . 498 normative data. . . . . . . . . . . . . . . . . . . 518
Alzheimer’s disease. . . . . . . . . . . . . . . 498 dysthymia (dysthymic disorder). . . . . 515 positron emission tomography
anhedonia. . . . . . . . . . . . . . . . . . . . . . . 515 focal neurological symptoms. . . . . . . 509 (PET). . . . . . . . . . . . . . . . . . . . . . . . . . . . 500
aphasia. . . . . . . . . . . . . . . . . . . . . . . . . . 508 hypertension. . . . . . . . . . . . . . . . . . . . . 522 reminiscence therapy . . . . . . . . . . . . . 517
apraxia. . . . . . . . . . . . . . . . . . . . . . . . . . 508 interpersonal psychotherapy (IPT). . . 517 stroke. . . . . . . . . . . . . . . . . . . . . . . . . . . 508
benzodiazepines . . . . . . . . . . . . . . . . . 515 meta-analysis . . . . . . . . . . . . . . . . . . . . 500 telemedicine. . . . . . . . . . . . . . . . . . . . . 510
clinically significant . . . . . . . . . . . . . . . 525 neuritic plaques . . . . . . . . . . . . . . . . . . 506 vascular dementia. . . . . . . . . . . . . . . . 508
cognitive behaviour therapy (CBT). . . 517 neurofibrillary tangles. . . . . . . . . . . . . 506 visual hallucination. . . . . . . . . . . . . . . . 509
cohort effect. . . . . . . . . . . . . . . . . . . . . 496 neuroimaging. . . . . . . . . . . . . . . . . . . . 499
REVIEW QUESTIONS
LO 15.1
15.1 What is the difference between primary and secondary ageing?
15.2 How is age affecting Indigenous people worldwide?
LO 15.2
15.3 Why is it advantageous to diagnose dementia (neurocognitive disorder) early in the course of the disease?
15.4 Are there lifestyle changes that could help lower the risk of dementia?
LO 15.3
15.5 How are symptoms of depression and anxiety different among younger and older adults?
15.6 Are attitudes towards seeking help for mental health disorders different in later life than at younger ages?
LO 15.4
15.7 In general, is retirement good for mental health?
15.8 How did the impact of bereavement change with respect to a diagnosis of depression in the DSM-5 compared
to the previous edition of the DSM?
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LO 15.5
15.9 What lifestyle factors might increase or decrease longevity?
15.10 What are three important characteristics and behaviours for positive ageing listed in Rowe and Kahn’s book
Successful Aging?
LO 15.6
15.11 What are some of the peak bodies concerned with older adults’ health and wellbeing?
REFERENCES
ABC RN (2005). Dementia, (part I)—Dancing with dementia: Australian Bureau of Statistics (2006). ABS Year Book Australia,
Christine Bryden’s story. Retrieved from http://www.abc.net.au/ 2006 (cat. no. 1301.0). Canberra: Author.
radionational/programs/allinthemind/dementia-part-1---dancing- Australian Bureau of Statistics (2008). Australian social trends, 2008
with-dementia-christine/3442734#transcript. (cat. no. 4102.0). Canberra: Author.
Alexopoulos, G. S. (2003). Vascular disease, depression, and dementia. Australian Bureau of Statistics (2011). Australian social trends (cat
Journal of the American Geriatrics Society, 51, 1178–1180. no. 4102.0). Canberra: Author.
Alzheimer’s Australia (2003). The dementia epidemic: Economic impact Australian Bureau of Statistics (2013). Reflecting a nation: Stories from
and positive solutions for Australia. Canberra: Access Economics. the 2011 Census, 2012–2013. (cat. no. 2071.0). Canberra: Author.
American Psychiatric Association (2000). Diagnostic and statistical Australian Bureau of Statistics (2015). Australian demographic
manual of mental disorders (4th ed., text rev.). Washington, DC: statistics, June 2015 (cat. no. 3101.0). Canberra: Author.
Author. Australian Bureau of Statistics (2016). Disability, ageing, and carers,
American Psychiatric Association (2013). Diagnostic and statistical Australia: Summary of findings, 2015 (cat. no. 4430.0). Canberra:
manual of mental disorders (5th ed.). Arlington: Author. Author.
Andel, R., Crowe, M., Pedersen, N. L., Fratiglioni, L., Johansson, Australian Institute of Health and Welfare (AIHW) (2006). Dementia
B., & Gatz, M. (2008). Physical exercise at midlife and risk of in Australia: National data analysis and development (cat. no.
dementia three decades later: A population-based study of Swedish AGE 53). Canberra: Author.
twins. Journals of Gerontology Series A: Biological Sciences and Australian Institute of Health and Welfare (AIHW) (2012). Dementia
Medical Sciences, 63, 62–66. in Australia: National data analysis and development. (cat. no.
Andlin-Sobocki, P., & Wittchen, H. U. (2005). Cost of anxiety disorders AGE 70). Canberra: Author.
in Europe. European Journal of Neurology, 12 (Supp. 1), 39–44. Baldwin, R. C., Gallagley, A., Gourlay, M., Jackson, A., & Burns,
Anstey, K. J., von Sanden, C., Sargent-Cox, K., & Luszcz, M. (2007). A. (2006). Prognosis of late life depression: A three-year cohort
Prevalence and risk factors for depression in a longitudinal, population- study of outcome and potential predictors. International Journal of
based study including individuals in the community and residential Geriatric Psychiatry, 21, 57–63.
care. American Journal of Geriatric Psychiatry, 15, 479–505. Baltes, P. B., & Staudinger, U. M. (1993). The search for a psychology
Anstey, K. J., Wood, J., Lord, S., & Walker, J. G. (2005). Cognitive, of wisdom. Current Directions in Psychological Science, 2,
sensory and physical factors enabling driving safety in older adults. 75–80.
Clinical Psychology Review, 25, 45–65. Baltes, P. B., & Staudinger, U. M. (2000). Wisdom: A metaheuristic
Antonucci, T. C., Akiyama, H., & Lansford, J. (1998). The negative (pragmatic) to orchestrate mind and virtue towards excellence.
effects of close social relations among older adults. Family American Psychologist, 55, 122–136.
Relations, 47, 379–384. Beck, J. G., & Stanley, M. A. (1997). Anxiety disorders in the
Antonucci, T. C., & Jackson, J. S. (1990). The role of reciprocity in social elderly: The emerging role of behavior therapy. Behavior Therapy,
support. In B. R. Sarason, I. G. Sarason, & G. R. Pierce (Eds.), Social 28, 83–100.
support: An interactional view (pp. 173–198). New York: John Wiley. Bellini, M., & Matteucci, V. (2001). Late onset depression and suicide
Ardelt, M., & Jacobs, S. (2009). Wisdom, integrity, and life outcome. Archives of Gerontology and Geriatrics, 7 (Sup p.), 37–42.
satisfaction in very old age. In M. C. S. N. DeFrates-Densch (Ed.), Bennett, D. A. (2008). Cognitive health in indigenous peoples.
Handbook of research on adult learning and development (pp. Neurology, 71, 1466–1467.
732–760). New York: Routledge/Taylor & Francis Group. Bennett, D. A., Schneider, J. A., Tang, Y., Arnold, S. E., & Wilson,
Australian Bureau of Statistics (2001). Australian social trends, 2001 R. S. (2006). The effect of social networks on the relation between
(cat. no. 4102.0). Canberra: Author. Alzheimer’s disease pathology and level of cognitive function
Australian Bureau of Statistics (2005a). Australian social trends, in old people: A longitudinal cohort study. Lancet Neurology, 5,
2005 (cat. no. 4102.0). Canberra: Author. 406–412.
Australian Bureau of Statistics (2005b). The health and welfare of Bertram, L., McQueen, M., Mullin, K., Blacker, D., & Tanzi, R.
Australia’s Aboriginal and Torres Strait Islander Peoples, 2005 (2006). The AlzGene Database: Alzheimer Research Forum.
(cat. no. 4704.0). Canberra: Author. Retrieved from www.alzgene.org.
rie66620_ch15_491-536.indd 530 08/03/17 02:01 PM

Bingham, C. R., & Ehsani, J. P. (2012). The relative odds of clinical geropsychology: International perspectives on practice
involvement in seven crash configurations by driver age and sex. (pp. 278–298). New York: Oxford University Press.
Journal of Adolescent Health, 51, 484–490. Christensen, H. (2001). What cognitive changes can be expected
Birren, J. E. (1964). The psychology of aging. Englewood Cliffs: with normal ageing? Australian and New Zealand Journal of
Prentice Hall. Psychiatry, 35, 768–775.
Breen, D. A., Breen, D. P., Moore, J. W., Breen, P. A., & O’Neill, Cohen, G. D. (2001a). The creative age: Awakening human potential
D. (2007). Driving and dementia. British Medical Journal, 334, in the second half of life. New York: Avalon Books.
1365–1369. Cohen, G. D. (2001b). Creativity with aging: Four phases of potential
Brunnstrom, H., Gustafson, L., Passant, U., & Englund, E. (2009). in the second half of life. Geriatrics, 56, 51–57.
Prevalence of dementia subtypes: A 30 year retrospective survey of Conwell, Y. (2001). Suicide in later life: A review and recommendations
neuropathological reports. Archives of Gerontology and Geriatrics, for prevention. Suicide and Life Threatening Behavior, 31, 32–47.
49, 146–149. Cooney, C., Howard, R., & Lawlor, B. (2006). Abuse of vulnerable
Bryant, C., Jackson, H., & Ames, D. (2009). Depression and anxiety people with dementia by their carers: Can we identify those most at
in medically unwell older adults: Prevalence and short-term course. risk? International Journal of Geriatric Psychiatry, 21, 564–571.
International Psychogeriatrics, 21, 754–763. Costa, P. T., & McCrae, R. R. (1980). Still stable after all these
Bryden, C. (2005). Dancing with dementia: My story of living years: Personality as a key to some issues in adulthood and old
positively with dementia. London, UK: Jessica Kingsley Publishers. age. In P. B. Baltes & O. G. Brim (Eds.), Life span development
Busse, E. W. (1989). The myth, history and science of aging. In E. and behaviour (3rd. ed.) (pp. 65–102). New York: Academic Press.
W. Busse (Ed.), Geriatric psychiatry (pp. 3–34). Washington, DC: Couillard-Despres, S., Iglseder, B., & Aigner, L. (2011). Neurogenesis,
American Psychiatric Press. cellular plasticity and cognition: The impact of stem cells in the
Byrne, G. J. (2010). Bereavement issues in later life. In N. A. adult and aging brain—a mini-review. Gerontology, 57, 559–564.
Pachana, K. Laidlaw, & B. G. Knight (Eds.), Casebook of Craig, D., Mirakhur, A., Hart, D. J., McIlroy, S. P., & Passmore, A.
clinical geropsychology: International perspectives on practice P. (2005). A cross-sectional study of neuropsychiatric symptoms
(pp. 211–225). New York: Oxford University Press. in 435 patients with Alzheimer’s disease. American Journal of
Byrne, G. J. A., & Pachana, N. A. (2011). Development and validation Geriatric Psychiatry, 13, 460–468.
of a short form of the Geriatric Anxiety Inventory: The GAI-SF. Craik, F. I. M. (1986). A functional account of age differences
International Psychogeriatrics, 23, 125–131. in memory. In F. Mix & H. Hagendorf (Eds.), Human memory
Calvo, E., Haverstick, K., & Sass, S. A. (2009). Gradual retirement, and cognitive capabilities: Mechanisms and performances
sense of control, and retirees’ happiness. Research on Aging, 31, (pp. 409–422). Amsterdam: Elsevier Science Publishing Co.
112–135. Cuijpers, P. (2005). Depressive disorders in caregivers of dementia
Carlson, M. C., Helms, M. J., Steffens, D. C., Burke, J. R., Potter, G. G., patients: A systematic review. Aging and Mental Health, 9, 325–330.
& Plassman, B. L. (2008). Midlife activity predicts risk of dementia Currell, M., Byrne, G. J., & Pachana, N. A. (2014). The effect of
in older male twin pairs. Alzheimer’s & Dementia, 63, 62–66. clinical, demographic and lifestyle factors on executive functions
Carstensen, L. L. (1992). Social and emotional patterns in adulthood: in middle aged and older women. International Journal of Clinical
Support for socioemotional selectivity theory. Psychology and Neurosciences and Mental Health, 1, doi.org/10.1155/2013/284780
Ageing, 7, 331–338. Currey, R. (2008). Ageism in healthcare: Time for a change. Aging
Carstensen, L. L., Gross, J. J., & Fung, H. H. (1998). The social context Well, 1, 16.
of emotional experience. In K. W. Schaie & M. P. Lawton (Eds.), Deery, H. A. (1999). Hazard and risk perception among young novice
Annual review of gerontology and geriatrics: Vol. 17. Focus on drivers. Journal of Safety Research, 30, 225–236.
emotion and adult development (pp. 325–352). New York: Springer. De Vaus, D., Wells, Y., Kendig, H., & Quine, S. (2007). Does gradual
Carstensen, L. L., Pasupathi, M., Mayr, U., & Nesselroade, J. (2000). retirement have better outcomes than abrupt retirement? Results
Emotional experience in everyday life across the adult life span. from an Australian panel study. Ageing and Society, 27, 667–682.
Journal of Personality and Social Psychology, 79, 644–655. Doka, K. J. (2013). Grief and the DSM: A brief Q&A. The Huffington
Cavallero, P., Morino-Abbele, F., & Bertocci, B. (2007). The social Post. Retrieved from www.huffingtonpost.com/kenneth-j-doka/
relations of the elderly. Archives of Gerontology and Geriatrics, grief-and-the-dsm_b_3340216.html.
44, 97–100. Doley, R., Bell, R., Watt, B., & Simpson, H. (2015). Grandparents
Charles, S. T., & Pasupathi, M. (2003). Age-related patterns of raising grandchildren: Investigating factors associated with distress
variability in self-descriptions: Implications for everyday affective among custodial grandparent. Journal of Family Studies, 21
experience. Psychology and Aging, 18, 524–536. Donaldson, T., Earl, J. K., & Muratore, A. M. (2010). Extending the
Charles, S. T., & Piazza, J. R. (2007). Memories of social interactions: integrated model of retirement adjustment: Incorporating mastery
Age differences in emotional intensity. Psychology and Aging, 22, and retirement planning. Journal of Vocational Behaviour, 77,
300–309. 279–289.
Charles, S. T., Reynolds, C. A., & Gatz, M. (2001). Age-related Drentea, P. (2002). Retirement and mental health. Journal of Aging
differences and change in positive and negative affect over 23 and Health, 14, 167–194.
years. Journal of Personality and Social Psychology, 80, 136–151. Dubinsky, R., Williamson, A., & Gray, C. (1992). Driving in
Chiu, H., Chan, S., & Tsoh, J. (2010). Suicide in later life. In Alzheimer’s disease. Journal of the American Geriatrics Society,
N. A. Pachana, K. Laidlaw, & B. G. Knight (Eds.), Casebook of 40, 1112–1116.
rie66620_ch15_491-536.indd 531 08/03/17 02:01 PM

Dulin, P., Hill, R. D., Anderson, J., & Rasmussen, D. (2001). Altruism Gething, L., Gridley, H., Browning, C., Helmes, E., Luszcz, M., Tumer,
as a predictor of life satisfaction in a sample of low-income older J., . . . Wells, Y. (2003). The role of psychologists in fostering the
adult service providers. Journal of Mental Health and Aging, 7, wellbeing of older Australians. Australian Psychologist, 38, 1–10.
349–360. Glass, J., Lanctot, K. L., Herrmann, N., Sproule, B. A., & Busto, U. F.
Ell, K. (2006). Depression care for the elderly: Reducing barriers to (2005). Sedative hypnotics in older people with insomnia: Meta-analysis
evidence based practice. Home Health Care Services Quarterly, of risks and benefits. British Medical Journal, 331, 1169–1173.
25, 115–148. Goodfellow, J. (2003). Grandparents as regular childcare providers:
Erikson, E. H. (1950). Childhood and society. New York: Norton. Unrecognised, under-valued and under-resourced. Australian
Evert, J., Lawler, E., Bogan, H., & Perls, T. (2003). Morbidity profiles Journal of Early Childhood, 28, 7–17.
of centenarians: Survivors, delayers and escapers. Journals of Goodman, C. C., & Silverstein, M. (2001). Gran

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CHAPTER 1

LEARNING OBJECTIVES (LO)

ABNORMAL PSYCHOLOGY: AN AUSTRALASIAN FOCUS

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Unfortunately, this number of sessions is inadequate to treat many

COURTESY THE UNIVERSITY OF SYDNEY ARCHIVES

LO 1.1 The definitions of abnormal behaviour

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have been proposed. The most common ones

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LO 1.2 Perspectives on the classification, causation

The biological perspective

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CLASSIFICATION AND CAUSATION FROM THE BIOLOGICAL PERSPECTIVE

Heinrich Neumann, 1859, cited in Hecker, 1871/2004, p. 351

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causes were not yet known, Kraepelin adopted a descriptive approach.

WIKIPEDIA CREATIVE COMMONS

TREATMENT FROM THE BIOLOGICAL PERSPECTIVE

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CONTRIBUTIONS AND LIMITATIONS OF THE BIOLOGICAL PERSPECTIVE

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The psychoanalytic perspective

psychoanalysts acting as the chairs of psychiatry

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Neuroses and psychoses

TREATMENT FROM THE PSYCHOANALYTIC PERSPECTIVE

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CONTEMPORARY PSYCHODYNAMIC PERSPECTIVES

CONTRIBUTIONS AND LIMITATIONS OF THE PSYCHODYNAMIC MODEL

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behavioural KEY CONCEPTS OF BEHAVIOURISM

unconditioned TABLE 1.2 The procedure for Pavlovian (classical) conditioning

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than increase behaviours, through the application of conditioned

WIKIMEDIA COMMONS SILLY RABBIT CC-BY 3.0

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CONTRIBUTIONS AND LIMITATIONS OF THE BEHAVIOURAL PERSPECTIVE

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The cognitive perspective

Beck, 1976, p. 333

observations while treating depressed patients using

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B: Beliefs or interpretations of B: Beliefs or interpretations of

C: Emotional and behavioural C: Emotional and behavioural

detecting possible cues for danger in the environment.

Black and white thinking (all or nothing)

Setting unrealistic expectations

Selective thinking (looking on the dark side)

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Converting positives into negatives (being a cynic)

Magnifying or exaggerating unpleasantness (making mountains out of molehills)

Catastrophising (whatever can go wrong will go wrong in a big way)

Personalising (it’s all my fault)

Mistaking feelings for facts (I feel therefore I am)

Jumping to negative conclusions

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LO 1.1 The definitions of abnormal behaviour

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LO 1.2 Perspectives on the classification, causation

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