Updating Watson & Marks (1971): How Has Our Understanding of the
Mechanisms of Extinction Learning Evolved And Where Is Our Field Going
Next?

Anu Asnaani, Carmen P. McLean, Edna B. Foa

PII: S0005-7894(16)00019-8
DOI: doi: 10.1016/j.beth.2016.02.003
Reference: BETH 611

To appear in: Behavior Therapy

Received date: 8 June 2015

Revised date: 2 February 2016
Accepted date: 3 February 2016

Please cite this article as: Asnaani, A., McLean, C.P. & Foa, E.B., Updating Wat-
son & Marks (1971): How Has Our Understanding of the Mechanisms of Extinction
Learning Evolved And Where Is Our Field Going Next?, Behavior Therapy (2016), doi:
10.1016/j.beth.2016.02.003

This is a PDF file of an unedited manuscript that has been accepted for publication.
As a service to our customers we are providing this early version of the manuscript.
The manuscript will undergo copyediting, typesetting, and review of the resulting proof
before it is published in its final form. Please note that during the production process
errors may be discovered which could affect the content, and all legal disclaimers that
apply to the journal pertain.
 ACCEPTED MANUSCRIPT

RUNNING HEAD: Understanding Mechanisms of Extinction Learning

PT
RI
Updating Watson & Marks (1971): How Has Our Understanding of the Mechanisms of

SC
Extinction Learning Evolved And Where Is Our Field Going Next?

NU
Anu Asnaani
MA
Carmen P. McLean

Edna B. Foa
D
TE

University of Pennsylvania, Philadelphia, PA

P
CE

Corresponding author for proofs and reprints:

AC

Anu Asnaani, Ph.D.

Department of Psychiatry
Center for the Treatment and Study of Anxiety
3535 Market St, Suite 600 North
Philadelphia, PA 19104
aasnaani@mail.med.upenn.edu
 ACCEPTED MANUSCRIPT

Abstract

J.P. Watson and I.M. Marks published a seminal article in Behavior Therapy entitled

“Relevant and Irrelevant Fear in Flooding – A Crossover Study of Phobic Patients” in 1971 that

PT
paved the way for important theoretical developments and empirical studies that examined the

RI
mechanisms underlying extinction learning. Indeed, in the 44 years since their article was

published, our knowledge about how exposure therapy works has increased considerably. In this

SC
review, we explore the progress our field has made in understanding extinction learning and how

NU
Watson and Marks’ important work has influenced this progress. We provide a brief summary of

the design and major findings of the Watson and Marks (1971) study, followed by a brief
MA
description of several theoretical conceptualizations of fear extinction that were developed

following the article’s publication. We also review empirical studies that illustrate the “state of
D

the science” with regard to the following key issues that were explored in Watson and Marks’
TE

paper: (1) the effect of specificity of exposure stimuli content in exposure therapy on outcome;
P

(2) fear activation as a mechanism of exposure; and (3) the associations between within- and
CE

between-session extinction learning and treatment outcome. The major findings of these three
AC

issues over the past 4 decades are summarized and discussed.

Keywords: exposure therapy; mechanisms; fear reduction; extinction learning; anxiety disorders
 ACCEPTED MANUSCRIPT

Updating Watson & Marks (1971): How Has Our Understanding of the Mechanisms of

Extinction Learning Evolved And Where Is Our Field Going Next?

The paper published by J.P. Watson and I.M. Marks in Behavior Therapy entitled

PT
“Relevant and Irrelevant Fear in Flooding – A Crossover Study of Phobic Patients” (Watson &

RI
Marks, 1971) 44 years ago raised several fundamental questions about the efficacy and

SC
mechanisms of exposure techniques. Their important work set off a cascade of research that has

helped improve exposure therapy approaches to treating anxiety-related disorders, and has

NU
increased our understanding about the mechanisms underlying fear extinction. This article
MA
explores how our field has progressed since this seminal paper published in 1971. After a brief

summary of the design and major findings of this study, we describe several predominant
D

theoretical conceptualizations of fear extinction both at the time the article was written as well as
TE

subsequent theoretical developments. Next, we discuss empirical studies that illustrate the “state

of the science” with regard to the following key issues that were explored in Watson and Marks’
P
CE

paper: (1) the effect of specificity of content in exposure therapy on outcome; (2) fear activation

as a mechanism of exposure; and (3) the associations between within- and between-session
AC

extinction learning and treatment outcome.

Summary of Watson & Marks (1971) article

The principal aim of Watson and Marks’ study was to examine the impact of flooding

(i.e., prolonged exposure, typically imaginal exposure) using cues that are relevant to the

patients’ fears during flooding versus flooding using cues that are irrelevant to patients’ fears.

Participants in the study were patients with specific phobias (N = 6; including “spiders, birds,

thunderstorms, wearing clean shirts and public violin playing”) and agoraphobia (N = 10). Half

of the participants first received 8 sessions of fear-relevant imaginal flooding, which entailed
 ACCEPTED MANUSCRIPT

listening to the therapist repeatedly describe the patients’ feared situation or object for 50

minutes including the feared consequences of facing the feared situation, followed by 8 sessions

of fear-irrelevant imaginal flooding, which entailed situations that the authors defined as

PT
“normally frightening to anybody” including scenarios where the participant was eaten by a tiger

RI
(12 participants), burned to death (three participants), or drowned (1 participant). The other half

of the participants first received 8 sessions of fear-irrelevant imaginal flooding sessions followed

SC
by 8 sessions of fear-relevant imaginal sessions. Sessions were scheduled 2-3 times per week

NU
with a 4-8 day break between the two 8-session conditions, for an average treatment time of six

weeks. Half the participants (four in each order condition) were treated as inpatients due to the
MA
severity of their fears, and the remaining patients were treated as outpatients. Assessments of

participants’ symptoms (both with clinical and physiological measures) occurred just prior to the
D
TE

start of treatment, 2-4 days after sessions 8 and 16, and at 3-month and 6-month follow-up

periods. During these assessments, participants underwent psychophysiological measurement

P

during an imagery task whereby they were asked to imagine three different scenarios for 40
CE

seconds twice each, in counterbalanced order: (1) a neutral scene, (2) a control fear situation, and
AC

(3) a major phobic situation.

The study results indicated that although 8 sessions of either treatment alone led to

significantly improved clinical outcomes, the combination of the two treatments (i.e., 16

sessions) resulted in the most significant improvements in clinical and heart-rate measures

regardless of the order in which the treatment conditions were delivered. Interestingly, the fear-

irrelevant condition, but not the fear-relevant condition, produced significant improvement in

heart-rate and skin conductance during assessment. The authors also found that the fear-

irrelevant condition was significantly more effective than the fear-relevant condition in reducing
 ACCEPTED MANUSCRIPT

subjective anxiety when individuals were imagining their feared phobic-specific situation during

the imagery assessment task. The gains from pre- to post-treatment were maintained at 6 months

follow-up (the 3-month follow-up results were not provided).

PT
Other results reported by Watson and Marks (1971) suggested that differential

RI
mechanisms underlie success in each of the treatment conditions. Specifically, heightened

physiological activity during the imagery task before treatment predicted good outcome to the

SC
fear-relevant flooding, but not to the fear-irrelevant flooding. In addition, high levels of pre-

NU
treatment subjective anxiety during the imagery assessment predicted poor outcome to fear-

irrelevant flooding. Finally, high subjective anxiety reported during treatment sessions predicted
MA
good outcome to fear-irrelevant flooding, but was not associated with outcome in fear-relevant

flooding. The authors concluded that while flooding to both relevant and fear-irrelevant stimuli
D
TE

reduced phobic anxiety in participants, this reduction was achieved via different mechanisms

across conditions. They further hypothesized that these differing mechanisms may not be
P

mutually exclusive, and might also be additive in their effects on fear reduction.
CE

The study has several limitations. Of most concern is the nature of the “fear irrelevant”
AC

imaginal scenarios. Specifically, it is not clear whether these scenarios were actually irrelevant to

all participants’ fears. For instance, the drowning scenario may not tap into the core pathological

fear of someone with a fear of spiders, but for someone with agoraphobia who fears the physical

symptoms of anxiety (which would include an inability to breathe, which is a central feature of

drowning), such a scenario may be quite relevant to a core agoraphobic concern. These

confounding elements of the study manipulation make it difficult to draw conclusions about the

role of content specificity in exposure. Second, the authors used primarily two-tailed t tests to

test their hypotheses; while this is appropriate given the sample size and is consistent with the
 ACCEPTED MANUSCRIPT

statistical approaches employed at the time the study was published, it limits the inferences and

types of questions (e.g., hypotheses about underlying mechanisms) that can be answered with

such a study design. Related to this choice of analytic approach, the sample of the different

PT
experimental groups (8 individuals in each, which were themselves subdivided by primary

RI
diagnosis of agoraphobia or specific phobia) was very small, and thus the findings need to be

interpreted with caution. Last, while the major focus of this study is on the immediate results

SC
after 8 and 16 sessions, the authors reported that the gains were maintained through 6-month

NU
follow-up, and yet they also noted that the majority of participants (14 of 16) received further

treatment during the follow-up period, including additional imaginal exposure, in vivo exposure
MA
(that is, situational exposure to avoided things, places or activities associated with the feared

stimulus), and antidepressant medications. The robustness or clinical relevance of this reported
D
TE

long-term maintenance of their treatment effects are therefore unclear given the high proportion

who received subsequent treatment.

P
CE

Theoretical underpinnings

Prior to and at the time of this study, the predominant conceptualization of how fear
AC

extinction occurred revolved around the assumption that repeated confrontation with a feared

stimulus in the absence of a feared consequence would lead to a reduction of fear, or habituation.

This assumption was adopted from the impactful work of previous learning theorists (e.g., Ivan

Pavlov and B.F. Skinner, among others) who had developed conditioning models to explain the

acquisition and extinction of fear (Pavlov, 1927; Skinner, 1938). Of note, Watson and Marks

used the terms “extinction” and “habituation” interchangeably, although they reported a

preference for the term habituation because it does not presuppose that the pathological fear

developed through conditioning. In addition, there was very little focus on the mechanisms
 ACCEPTED MANUSCRIPT

underlying conditioning and extinction in these early conditioning theories. Watson and Marks’

study tried to elucidate mechanisms, and much of the theoretical and empirical work that

followed their study has sought to do the same. Thus, several theoretical models were proposed

PT
and subsequently adopted as the framework for empirical work in fear and anxiety in the decades

RI
following the 1971 study; we briefly described a few of these major theoretical models below.

Rescorla-Wagner model of classical conditioning. A theory set forth by Rescorla and

SC
Wagner shortly after the Watson and Marks paper was published delineates a primarily

NU
behavioral model by which fear is maintained and extinguished (Rescorla & Wagner, 1972).

Rescorla and Wagner’s theory relies heavily on the early concepts of the unconditioned stimulus
MA
(US; a biologically potent stimulus that naturally brings on an affective response), conditioned

stimulus (CS; a neutral stimulus), unconditioned response (UR; an unlearned, automatic

D
TE

reflexive response) and conditioned response (CR; a taught response due to repeated US-CS

pairing), all of which are concepts adopted from previous classical and operant conditioning
P

paradigms.
CE

However, Rescorla and Wagner’s (1972) theory uniquely proposes two features not
AC

present in previous conditioning models: (1) organisms learn from the discrepancy between what

they expected to happen and what actually happens and the degree of expectancy violation when

encountering a US is dependent on the associative value of all cues present during this

confrontation with the US; and (2) excitation is the opposite of inhibition and a stimulus can be

one or the other, but not both. Rescorla and Wagner also incorporated principles already

prominent in the prevailing fear extinction theories during the time it was introduced, namely:

the perceived strength of a feared stimulus is directly measurable in the behavior it overtly elicits

or inhibits in an organism; the salience of the CS remains constant throughout old and new
 ACCEPTED MANUSCRIPT

learning; and only the current associative value of a cue to a feared stimulus is relevant to the

amount of learning that occurs (regardless of the prior historical associative value of that cue).

Related to Watson and Marks’ study, Rescorla and Wagner’s model (along with previous

PT
conditioning models) would predict the reduction in fear over time following repeated

RI
confrontation with fear imagery, as the discrepancy between what is expected (feared outcome)

and what actually happens (no harm) continues with each repeated exposure. However, since

SC
Rescorla and Wagner’s theory was introduced after 1971, it is likely that the theoretical basis for

NU
the Watson and Marks study revolved around older, classical conditioning theories that would

predict habituation (i.e., fear reduction) with repeated exposure to the CS in absence to the UCS
MA
without presupposing a mechanism underlying fear reduction.

Bioinformational theory. Shortly after the Rescorla-Wagner model (Rescorla &

D
TE

Wagner, 1972) was introduced and hypotheses emanating from the theory gained empirical

support, Lang (1979) proposed what he termed the bioinformational theory of emotional
P

imagery. Lang’s theory conceptualizes images in the brain as part of a conceptual fear network
CE

that includes both physiological and behavioral activity, patterns, and expression. The experience
AC

of fear would therefore be defined as a structure that is represented by these various parts of the

network. Importantly, the bioinformational theory suggests that physiological and behavioral

response following confrontation with imagery of a fearful stimulus depends on the type and

content of the imaginal exposure. Specifically, the responses depend upon whether there is a

match between the content of the exposure and the underlying fear structure. This point is

relevant to the main hypothesis in the Watson and Marks (1971) study, which was interested in

whether matching exposure content to patients’ fears would impact outcomes. However, Watson

and Marks’ findings were inconsistent with Lang’s hypothesis, because their results suggested
 ACCEPTED MANUSCRIPT

that there was no need for matching the flooding imagery to the underlying phobic fear content

in order to facilitate reduction of the pathological fear.

Lang also hypothesized that the imagery of the fear response to a particular fear stimulus,

PT
rather than the fear stimulus itself, is what activates the fear network. He further suggested that

RI
the structure of an emotional image and its consequent effects on fear arousal and behavior could

be directly manipulated by instructions to shape this imagery or the resultant behavioral

SC
responses to such fears. Because fear is activated by fear response representations and not by

NU
stimuli representations, Lang conceptualized the therapeutic process as emotional processing

because of its reliance on modifying the affective responses to fear imagery (Lang, 1977).
MA
Emotional processing theory. Another major theoretical development since the Watson

and Marks (1971) study was emotional processing theory (EPT; Foa & Kozak, 1986). Expanding
D

on Lang’s bio-informational model (Lang, 1977; 1979), EPT describes the representation of fear
TE

as a cognitive structure embedded in memory that includes information about fear stimuli, fear
P

responses, and their meaning. However, in contrast to the bioinformational theory’s emphasis on
CE

representations of fear response, EPT focuses on the meaning of the feared stimuli and responses
AC

represented within the structure. In addition, EPT suggests that the feared stimuli, responses, and

their meaning are interconnected, such that an input matching one part of the structure will

activate the entire fear structure.

According to EPT, two conditions are necessary for emotional processing, the presumed

mechanism of recovery, to occur. First, the structure must be activated, so it is available for

change. Second, new information that is incompatible with the pathological fear structure must

be available and incorporated into the pathological memory structure. Inconsistent with the

findings of Watson and Marks, EPT suggests that there are specific pathological fear structures
 ACCEPTED MANUSCRIPT

underlying different disorders. It would follow, therefore, that in order to be effective, exposure

must provide information that is inconsistent with the pathological elements of that specific

structure. The fact that Watson and Marks found that exposure to irrelevant-fear stimuli was as

PT
effective in reducing fear as relevant-fear would not be predicted by EPT.

RI
Since its inception, EPT has undergone two revisions to incorporate emerging empirical

evidence (Foa & McNally, 1996; Foa, Huppert, & Cahill, 2006). Influenced by modern learning

SC
theories that conceptualize extinction as the creation of new associations as opposed to the

NU
modification of old associations (e.g., Bouton & Swartzentruber, 1991), Foa and McNally (1996)

proposed that exposure therapy results in the formation of a new, non-pathological structure that
MA
competes with the original pathological fear structure. The old pathological structure and the

new, non-pathological structure contain overlapping elements, such that the same stimuli and
D
TE

responses are capable of activating both structures. Thus, exposures therapy is successful when

the new non-pathological structure is more readily activated, whereas relapse may occur when
P

the old pathological structure is activated. Foa, Huppert, & Cahill (2006) outlined a more
CE

detailed discussion on how EPT applies to the development and maintenance of PTSD and to
AC

social anxiety disorder, highlighting how EPT can guide exposure therapy and cognitive therapy

approaches for these particular disorders.

A. Specificity of content and its relevance to extinction learning

One of the major conclusions of the Watson and Marks (1971) article was that the

specificity of content for exposure therapy may not be as important as simply inciting non-

specific fear arousal in participants. As noted earlier, theoretical perspectives such as the

bioinformational theory and EPT are inconsistent with such findings, since both theories

emphasize the importance of activating the fear structure relevant to the major phobic concern
 ACCEPTED MANUSCRIPT

and some level of matching in confronted fearful material with the fear structure (Lang, 1977;

Foa & Kozak, 1986). The empirical data that has emerged since this article was published is

discussed next, to assess the degree to which Watson and Marks’ finding that content specificity

PT
is not critical for good exposure therapy outcomes has been subsequently supported or refuted.

RI
Empirical data. Around the time the bioinformational and emotional processing theories

were being developed, several studies examining the necessity of confronting fear-relevant

SC
material during extinction learning were conducted. Specifically, in a follow-up to the Watson

NU
and Marks (1971) study, a two-part animal study examining fear acquisition and extinction

learning in rats was conducted by Baum and LeClerc (1974) that used a similar design to the
MA
human study by Watson and Marks. In the first experiment, extinction of avoidance behaviors

was observed during a fear-relevant stress condition with response prevention and during a fear-
D
TE

irrelevant stress condition, corroborating the notion that a match between the content of the

exposure stimuli and previously conditioned feared stimulus may not be necessary for good
P

outcomes. In this first experiment, extinction testing occurred immediately following the
CE

treatment conditions. However, in their second experiment, the authors inserted a 2-hour delay
AC

between the extinction conditions (relevant stress versus irrelevant stress exposure) and

extinction testing. This second experiment found evidence of extinction learning only in rats

exposed to relevant stress flooding, and not in the irrelevant stress condition. Such findings

suggest that the effects of extinction learning via exposure to fear-irrelevant stimuli might be

only temporary (Baum & LeClerc, 1974).

In another study, Mineka (1976) examined fear extinction in rats to better understand the

role of fear-irrelevant flooding in extinction learning. In the first experiment, both relevant and

irrelevant flooding resulted in extinction of a conditioned avoidance response, and to a similar

 ACCEPTED MANUSCRIPT

degree, which is consistent with Marks and Watson (1971) and Baum and LeClerc (1974). The

second experiment showed that extinction to one conditioned fear response can facilitate

extinction learning to another conditioned stimulus, suggesting generalization of extinction

PT
learning and perhaps explaining the mechanism by which fear-irrelevant flooding was found to

RI
be effective in previous studies. However, inconsistent with the findings by Watson and Marks

(1971), the third experiment failed to find an effect of fear-irrelevant flooding using two stimuli

SC
significantly different from each other and not used in the previous experiments. These findings

NU
therefore support the hypothesis, subsequently supported in theoretical models of fear extinction,

that the match between the exposure stimulus and the individual’s feared stimulus is necessary in
MA
order to facilitate extinction learning to the target fear (Mineka, 1976).

Following these animal studies, an experimental study with humans also examined the
D
TE

role of exposure content specificity (Lang, Levin, Miller, & Kozak, 1983). In this study, non-

clinical participants reporting either high snake fear or social anxiety were exposed to both their
P

primary phobic fear, and the primary phobic fear of the other group (i.e., they completed either a
CE

snake exposure or a public speaking exposure). In addition, participants from both groups were
AC

asked to imagine both types of feared situations as well as control, non-fearful scenes. The

results were inconsistent and only partially in line with Watson and Marks (1971). Specifically,

snake-fearful participants reported greater subjective distress and physiological reactivity in

response to snake exposure than the social anxious participants; however, both groups showed

similar and significant increases in physiological arousal during the speech exposure, even

though the socially anxious participants subjectively reported greater fear in this situation. In

addition, imagery assessments to both feared situations did not result in significant physiological

arousal in either group. However, given its design, this study could not provide insight into how
 ACCEPTED MANUSCRIPT

fear-relevant and fear-irrelevant stimulus exposure impacted extinction learning or longer-term

outcomes in the reduction of fear.

Another study that did include outcome data examined individuals with obsessive

PT
compulsive disorder (OCD) who had both checking rituals and significant fears of future

RI
disasters, assigning half the sample to two hours of in vivo exposure (i.e., real life exposure), and

the other half to 90 minutes of imaginal exposure to feared future disasters plus 30 minutes of in

SC
vivo exposure (Foa, Steketee, Turner, & Fischer, 1980). Assuming that specificity of exposure

NU
content was important, the authors hypothesized that those receiving imaginal exposure would

fare better than those receiving in vivo exposure only since imaginal exposure allowed for a
MA
better match to the participants’ core fears. The results revealed that both groups improved

significantly and to a similar degree. However, rate of relapse was significantly lower in the
D
TE

group receiving imaginal exposure plus in vivo exposure, which provides some support for the

hypothesis that the greater the match between the individual’s fear, the better the outcome.
P

Following this initial flurry of studies that ensued in animal and human populations in the
CE

decade following the published findings by Watson and Marks (1971), little empirical
AC

investigation into the importance of the relevance of exposure content has been conducted. One

exception is a recent small study of individuals with OCD that found that acquisition of emotion

regulation skills (prevention of emotional avoidance) in clinically-irrelevant contexts was

associated with decreases in OCD symptoms, and subsequent implementation of these skills in

clinically-relevant contexts were also associated with decreases in OCD. However, again, there

were significantly greater reductions in OCD symptoms when these skills were implemented in

clinically-relevant contexts as compared to the clinically-irrelevant contexts (Allen & Barlow,

2009). On the whole, there is evidence for the matching hypothesis, although the degree to which
 ACCEPTED MANUSCRIPT

the content of exposure is similar to, or matches, the feared structure may be important. This

factor needs more empirical examination to determine its utility in exposure therapy.

B. Fear activation as a mechanism of exposure

PT
The study by Watson and Marks (1971) implied that, regardless of the relevance of

RI
feared exposure material, activation of fear (as measured clinically, subjectively, and

physiologically) is a necessary component for subsequent extinction learning and reduction on

SC
these various fear indices. This idea has received support over the years, and there have been

NU
significant conceptual discussions about why such activation may serve as a crucial component

of later fear reduction and improved clinical outcomes. As mentioned previously, according to
MA
EPT, fear activation is conceptualized as one of the necessary conditions for successful recovery

from pathological fear, the other being incorporation of information that is incompatible with the
D
TE

pathological components of the fear structure. Other behavioral or learning theories related to

fear extinction have been less focused on the role of fear activation in impacting successful
P

treatment outcome.
CE

Typically, fear activation has been defined in both subjective and objective
AC

(physiological) terms. For subjective fear activation, this has been operationalized as peak (or

highest) patient-reported fear level (normally on a 0 to 100 or 0 to 10 scale), subtracting baseline

levels of subjective distress. Physiological fear activation (which often includes heart rate, skin

conductance, eye blink startle magnitude, and electromyogram) is measured similarly, by using

the difference between peak recordings on these measures and baseline physiological reactivity.

Empirical data. In line with subsequently developed theoretical models suggesting that

fear activation is a necessary mechanism of successful exposure and treatment outcome

(specifically, EPT), Watson and Marks (1971) found that increased physiological responsiveness
 ACCEPTED MANUSCRIPT

prior to the flooding of fear-relevant cues only was associated with better treatment outcome.

Similarly, other studies conducted around that time period found that increased heart rate during

initial exposure to the fearful stimulus in phobic individuals was associated with greater

PT
improvement in symptoms following systematic desensitization (Lang, Melamed, & Hart, 1970;

RI
Borkovec & Sides, 1979). Since then, many studies have examined the relationship between

increased physiological and subjective arousal during early confrontation to feared stimuli and

SC
treatment outcomes in anxiety-related disorders, some of which support the supposition that fear

NU
activation is a necessary, although not sufficient, condition for emotional processing to occur.

For example, Kozak, Foa & Steketee (1988) conducted a study with OCD patients who
MA
were treated with 15 sessions of imaginal and in vivo exposure therapy. The authors found that

greater subjective distress and higher physiological response (heart rate and electrodermal
D
TE

activity) during exposure predicted greater reductions in obsessional fear. In another small study

with female assault victims with PTSD, greater facial expression of fear (as coded by the Facial
P

Action Coding System by one of the reliably trained authors of the study) during the first
CE

imaginal exposure of prolonged exposure (PE) therapy was associated with greater improvement
AC

in treatment outcome (Foa, Riggs, Massie, & Yarczower, 1995). The study results revealed

significant associations between higher objectively measured fear activation and improved

outcome, and further found that fear activation appeared to mediate the relationship between

higher pre-treatment PTSD severity and better treatment outcome, implicating its importance in

impacting outcome.

Indirect evidence for the role of activation was found by Jaycox, Foa and Morral (1998),

who conducted cluster analyses using subjective distress ratings every five minutes during

imaginal exposure of PE therapy in female assault victims with PTSD. They found that patients
 ACCEPTED MANUSCRIPT

reporting higher subjective fear activation (or emotional engagement) and gradual between-

session habituation (discussed later) showed greater improvements in PTSD symptoms than the

other patients. Similarly, in a sample of individuals with simple phobia, social phobia and panic

PT
disorder, Lang, Bradley, and Cuthbert (1998) found that greater physiological arousal during

RI
imaginal exposure was associated with better treatment outcome.

Further, an examination with Vietnam veterans with PTSD who received flooding

SC
therapy (prolonged exposure to a traumatic memory without the processing component of PE)

NU
found increased subjective (self-reported anxiety and fear) and physiological (heart rate, skin

conductance, and electromyogram) activation during flooding (Pitman, Orr, Altmann, &
MA
Longpre, 1996). However, in contrast to the studies discussed above, only heart rate activation in

the first flooding session was associated with a decrease in PTSD symptoms at post-treatment
D
TE

(specifically, daily number of intrusive combat memories); the other measures of fear activation

were not associated with outcome. It is important to note that patients in this study also only
P

showed modest improvements in symptoms in comparison to previous studies that utilized PE

CE

for PTSD. The finding that heart rate was the only physiological measure of fear activation
AC

related to outcome is consistent with the findings reported by Watson and Marks (1971) with

fear-relevant cues.

Indeed, several recent studies have found only partial or mixed results regarding the

relationship between fear activation during extinction learning (exposure) and treatment

outcome. van Minnen and Hagenaars (2002) categorized a group of patients with PTSD as either

responders (defined as those showing at least a 50% reduction in PTSD symptoms after 9

sessions of imaginal exposure), non-responders (for those not meeting the improvement

criterion), or as drop-outs from treatment (defined as anyone who did not complete the 9 sessions
 ACCEPTED MANUSCRIPT

of treatment, most of whom dropped out before session 2). The results were inconsistent. Overall

there were no differences between groups in mean and peak subjective anxiety ratings during the

first imaginal exposure. Contrast tests showed that the non-responders showed higher pre-

PT
imaginal ratings of subjective distress prior to starting their first imaginal exposure than those

RI
who improved over the course of treatment. On the other hand, the responder group showed a

greater increase (i.e., more fear activation) in subjective distress over the course of the first

SC
imaginal exposure compared to those who did not respond to the treatment. Only this latter

NU
finding is in line with the previous supporting studies of EPT. Initial or across-treatment

physiological measures of fear activation were not examined in this study.

MA
Another recent study examined several objective indices of fear activation (namely, heart

rate, carbon dioxide partial pressure, and respiration rate), as well as self-reported panic
D
TE

symptoms and subjective anxiety ratings, in patients with panic disorder and agoraphobia who

received three in vivo exposure sessions (Meuret, Seidel, Rosenfield, Hofmann, & Rosenfield,
P

2012). The results revealed that greater subjective anxiety, but not physiological measures of
CE

anxiety and panic during exposure were predictive of better improvement in panic symptoms.
AC

This finding for a significant relationship between subjective fear activation, and not

physiological activation, and treatment outcome is inconsistent with the previous findings by

Pitman et al., 1996, which found the opposite.

Related to this, Baker et al. (2010) utilizing an analogue sample of college students

scoring high on self-reported acrophobia, found no relationship between initial subjective

distress or initial heart rate activation and treatment outcome following two exposure sessions

conducted one week apart, or at two-week follow-up. Notably, these two more recent studies,

unlike the previous studies supporting the role of fear activation in improving treatment outcome,
 ACCEPTED MANUSCRIPT

utilized either less-than-optimal exposure protocols (only 2-3 exposures conducted over a short

space of time) or sub-clinical populations. On the other hand, these studies used more advanced

statistical approaches such as stepwise regression or multilevel modeling, while the previous

PT
examinations relied primarily on correlational analyses or simple t tests.

RI
Overall, a number of other studies conducted in both analogue and clinical samples over

the past few decades have found either no relationship between fear activation and outcome

SC
(Bluett, Zoellner, & Feeny, 2014; Rauch, Foa, Furr, & Filip, 2004; Tsao & Craske, 2000; Sloan

NU
& Telch, 2002; Telch, 2004), or even a negative relationship between fear activation and

outcome, with higher activation being associated with poorer outcome (Foa et al., 1983;
MA
Kircanski et al., 2012). Taken together with the other studies described above, these findings

suggest a mixed picture with regards to importance of fear activation in treatment outcome.
D
TE

C. Reduction of fear as proposed mechanism of successful treatment outcome

Watson and Marks (1971) discussed two hypothesized mechanisms through which
P

flooding may reduce pathological fear: 1) flooding works by blocking avoidance of the phobic
CE

stimuli and thereby permitting extinction to take place; 2) flooding works by allowing
AC

habituation1 of fear in general rather than the particular phobic fear. Watson and Marks plotted

the change in fear levels within and between exposure sessions and reported that earlier flooding

sessions were more anxiety-provoking for participants than were later sessions. They did not,

however, report on the significance of changes in anxiety within or between sessions, nor did

1
As mentioned previously, Watson and Marks used the terms “extinction” and
“habituation” somewhat interchangeably, while many researchers today generally consider the
term habituation inaccurate and argue that extinction more correctly connotes an active process
of new learning (see Bouton, 2004; Van Elzakker, Dahlgren, Davis, Dubois, & Shin, 2014). We
have therefore retained the terminology “extinction learning” to be consistent with both animal
and human models examining mechanisms of fear reduction.
 ACCEPTED MANUSCRIPT

they examine how these changes differed across conditions or related to treatment outcomes.

Nonetheless, in light of their finding that both the irrelevant and relevant flooding reduced fear to

a similar extent but had different prognostic correlates, the authors concluded that the irrelevant

PT
flooding may reduce fear through habituation to anxiety in general while relevant flooding may

RI
reduce fear through blocking avoidance and thereby permitting extinction, and that these

processes may not be mutually exclusive. Experimental research on flooding thrived in the

SC
decades following the Watson and Marks (1971) study. Flooding had emerged as a powerful

NU
clinical tool to treat a host of anxiety-related conditions and there was much interest in

delineating the mechanisms and optimal parameters of flooding. The reduction of subjective and
MA
physiological indices of anxiety during flooding was seen as a key mechanism.

In terms of the terminology frequently used to describe such reductions, the degree to
D
TE

which anxiety decreases during a single extinction trial or session of exposure therapy is referred

to as within-session extinction (WSE). The degree to which peak anxiety decreases across
P

extinction trials or sessions of exposure therapy is referred to as between-session extinction

CE

(BSE). To date, dozens of clinical and experimental studies have examined whether these
AC

processes are related to good outcomes following exposure therapy for anxiety-related conditions

(for a thorough review of WSE and BSE as potential mechanisms of exposure therapy, see

Craske et al., 2008). Both WSE and BSE have been measured by examining changes in

subjectively reported anxiety ratings using the subjective units of distress scale (SUDS), and

change in physiological measures of anxious arousal such as heart rate and skin conductance.

Empirical Data: Within-session extinction. Although anxiety typically declines from

the beginning to the end of an exposure session, the role of WSE in treatment outcomes has not

been well supported overall. A small number of studies have found some support for a direct
 ACCEPTED MANUSCRIPT

relationship between WSE and outcome. Foa et al. (1983) found that WSE of subjective fear was

associated with greater improvement at post-treatment and follow-up among participants

receiving EX/RP for OCD. With PTSD, the previously mentioned study by Pitman et al., (1996)

PT
found that of several subjective and physiological indices of anxiety measured, there was a non-

RI
significant trend for WSE in heart rate to correlate with the number of intrusions per day, which

was one of several PTSD-related outcomes examined. In addition, a more recent study by

SC
Norton, Hayes-Skelton, and Klenck (2011) found that WSE in subjective distress during group

NU
exposure therapy sessions for mixed anxiety disorders was associated with superior treatment

outcomes. Similarly, among contamination fearful undergraduates, Kircanski et al. (2012) found
MA
that WSE in subjective distress was associated with significantly lower obsession severity. On

the other hand, WSE in subjective distress was not related to compulsion severity or reported
D
TE

distress during a behavioral avoidance task and WSE in heart rate was not related to any

outcomes.
P

Support for the importance of WSE has also been found by two clinical studies and three
CE

non-clinical studies that have indirectly examined the relationship between WSE and outcomes.
AC

Beckham, Vrana, May, Gustafson, & Smith (1990) found that flying phobia participants who

showed greater WSE in heart rate during an in vivo exposure session were more likely to elect to

fly in the subsequent 8 weeks than those who showed less WSE in heart rate. van Minnen and

Hagenaars (2002) found that responders to PE for PTSD showed greater WSE in subjective

distress than non-responders, although this was only true for imaginal exposures completed for

homework; there were no differences in WSE between responders and non-responders during

sessions. In a nonclinical sample of snake fearful women, Lang, Melamed and Hart (1970) found

that participants who achieved greater fear reduction following systematic desensitization
 ACCEPTED MANUSCRIPT

showed greater WSE in heart rate than those with less post-treatment fear reduction. In their non-

clinical sample of speech phobic undergraduates, Borkovec and Sides (1979) found that

participants who received systematic desensitization showed greater WSE in subjective distress

PT
and superior post-treatment outcomes than participants who received either exposure with or

RI
without contiguous relaxation, or exposure only. Using a similar non-clinical sample, Chaplin

and Levine (1981) found that participants who received continuous exposure demonstrated

SC
greater WSE than those who received interrupted exposure, and that the continuous exposure

NU
group demonstrated lower anxiety on two of three post-treatment outcomes. Oliver and Page

(2003) found that blood-injection fearful participants who engaged in a distracting conversation
MA
during exposure showed greater WSE in subjective distress than those who engaged in a

conversation focused on the phobic stimuli during exposure or those who received exposure
D
TE

alone (with no conversation) and were also more likely to show superior outcomes at post-

treatment and follow-up.

P

A larger number of studies have failed to find any support for the relationship between
CE

WSE and clinical outcomes. Jaycox et al. (1998) found that WSE in self-reported anxiety was
AC

unrelated to PE treatment outcome among sexual assault survivors. In a small sample of PTSD

participants, Sripada and Rauch (2015) found that WSE in subjective distress was unrelated to

both symptom change and treatment responder status following PE for PTSD. In a

nonrandomized study by van Minnen and Foa (2006), participants with PTSD who received 60-

minutes of imaginal exposure evidence significantly greater WSE than those who received 30-

minutes. However, there were no differences between groups in terms of post-treatment PTSD

outcomes. This finding was replicated in a small RCT showing that WSE was greater for

participants with PTSD who received 40-minutes of imaginal exposures versus 20-minutes, but
 ACCEPTED MANUSCRIPT

again, there were no differences in outcome between the two groups (Nacasch et al., 2015).

These latter studies indicate that although length of exposure does influence the degree of WSE,

it appears that WSE is unrelated to outcome.

PT
Null results have also been found in studies of exposure therapy for OCD and panic

RI
disorder. In a study designed to evaluate the role of attention versus distraction during exposure

for OCD, Grayson, Foa, and Steketee (1982) found that WSE in heart rate and subjective anxiety

SC
was evident in both treatment conditions, but was unrelated to return of subjective fear at the

NU
beginning of the next session. Kozak et al. (1988) found that WSE in subjective anxiety, heart

rate, and electrodermal activity were all unrelated to any of the clinical outcomes assessed
MA
among participants receiving EX/RP for OCD. There was also a trend for BSE in subjective

anxiety to predict improvement in rated fear and avoidance. Among panic disorder participants
D
TE

receiving exposure-based CBT plus either a low or moderate dose of alprazolam, Riley et al.

(1995) found that WSE of physiologic measures was unrelated to responder status at post-
P

treatment. Similarly, Meuret et al. (2012) found that neither WSE in physiological or subjective
CE

anxiety was related to clinical outcomes among panic disorder participants receiving exposure
AC

therapy.

Many studies with non-clinical samples have also failed to support the WSE-outcome

relationship. Among their sample of height-fearful participants, Baker et al. (2010) found that

WSE in subjective distress and heart rate during the in vivo exposure sessions were both

unrelated to behavioral or self-report acrophobia outcomes. Culver, Stoyanova, and Craske

(2012) found that WSE in neither subjective anxiety nor heart rate was related to self-report,

physiologic, or behavioral outcomes at 2-week follow-up among participants fearful of public-

speaking. Moreover, greater WSE in subjective anxiety was related to worse outcomes on a
 ACCEPTED MANUSCRIPT

behavioral avoidance task. Results from non-clinical studies examining the relationship between

WSE and outcomes indirectly are consistent with the above null findings. In a sample of height-

fearful undergraduates, Lang and Craske (2000) found that although WSE in heart rate was

PT
greater among participants who received constant versus varied exposure, there were no

RI
differences in treatment outcomes between groups. Similarly, Kamphuis and Telch (2000) found

that undergraduates with claustrophobia fears who received one session of exposure with guided

SC
threat reappraisal showed superior fear reduction than those who received exposure with a

NU
distraction task, despite the fact that WSE was equal across groups. Using a similar sample,

Sloan and Telch (2002) compared exposure with guided reappraisal to exposure with safety-
MA
seeking behavior. Once again, WSE was equal across groups, but the reappraisal condition was

superior to the comparison condition at post-treatment and follow-up. Finally, among

D
TE

undergraduates with public-speaking anxiety, Tsao and Craske (2000) found that those who

received spaced exposure had superior follow-up outcomes than those who received massed
P

exposure, despite the fact that significant WSE in heart rate or subjective fear was not observed
CE

in either group.
AC

Empirical Data: Between-session extinction. In contrast to WSE, BSE has been shown

to predict exposure therapy outcomes more consistently. Several studies of PTSD have found

that extinction between imaginal exposure sessions is related to lower PTSD severity at post-

treatment. Among 69 participants with PTSD receiving PE, Rauch et al. (2004) found that

greater BSE in subjective distress over the course of six imaginal exposure sessions was

associated with more reduction in PTSD symptoms at post-treatment. In contrast to the null

findings on WSE, van Minnen and Foa (2006) found that BSE was significantly related to PTSD

symptoms at post-treatment among participants with PTSD, regardless of whether they received
 ACCEPTED MANUSCRIPT

sessions with 60- or 30-minutes of imaginal exposure. Also in contrast to null WSE findings,

Sripada and Rauch (2015) found that BSE in subjective distress was related to both symptom

change and treatment responder status in participants receiving PE for PTSD.

PT
Several clinical studies provide support for the role of BSE on some, but not all indices of

RI
BSE or across outcomes. In OCD patients, Kircanski et al. (2012) found that BSE in heart rate

was associated with lower obsession severity and lower reported distress during a behavioral

SC
avoidance task (but not compulsion severity). In this study, BSE in subjective distress was not

NU
related to any outcomes. Kozak et al. (1988) showed that BSE in heart rate (but not

electrodermal activity) between session 2 and session 6 of EX/RP predicted improvement in

MA
rated fear and avoidance (but not rituals). There was also a non-significant trend for BSE in

subjective anxiety to predict improvement in rated fear and avoidance. Among OCD patients
D
TE

receiving EX/RP, Foa et al. (1983) found that greater BSE in subjective anxiety was associated

with superior outcomes at post-treatment, but not at follow-up. In a non-clinical sample, Baker et
P

al. (2010) found that BSE in subjective distress (but not heart rate) across two in vivo exposure
CE

sessions was related to lower reported distress during a behavioral avoidance task (but not to
AC

self-reported fear of heights) at post-treatment among height-fearful participants. As previously

noted, Pitman et al. (1996) found null results for several process variables and most of the

subjective and physiological indices of anxiety measured, however, there was a non-significant

trend for BSE in heart rate to correlate with the number of intrusions per day.

A larger number of studies provide indirect support for the relationship between BSE and

exposure therapy outcomes by showing that those who show greater BSE also tend to have

superior outcomes. The cluster analysis conducted in the study by Jaycox et al. (1998) found that

sexual assault survivors with PTSD fit one of three different patterns of change during prolonged
 ACCEPTED MANUSCRIPT

exposure therapy: 1) high initial fear activation and gradual BSE, 2) high fear activation and no

BSE, and 3) moderate fear activation and no BSE. Providing indirect support for the relationship

between BSE and outcome, participants in the first group showed greater improvement than

PT
those in the other two groups. van Minnen and Hagenaars (2002) found that responders to PE

RI
showed greater BSE in subjective distress compared to non-responders. However, in this study,

BSE was only measured between the first two sessions of prolonged exposure; change in

SC
subjective distress over all nine sessions of imaginal exposure was not assessed. In an RCT

NU
testing the effects of adding d-cycloserine (DCS) to virtual reality exposure therapy for

acrophobia, Ressler et al. (2004) showed that compared to those who received a placebo, those
MA
who received DCS had greater BSE in subjective anxiety and BSE in spontaneous fluctuations in

skin conductance, and showed significantly greater improvement at post-treatment and 3-month
D
TE

follow-up. In a large sample of PTSD patients receiving PE therapy, Bluett et al. (2014) showed

that the minority of participants (35.3%) who exhibited a reliable change in distress (i.e., reliable
P

BSE) across sessions had lower PTSD severity at post-treatment compared to those who
CE

exhibited a lack of reliable BSE. However, given that both groups of participants made marked
AC

improvements during treatment and there were no differences in PTSD diagnostic status, the

authors concluded that BSE is not necessary to achieve good PTSD outcomes.

Several studies examining the role of attentional processes on extinction with non-clinical

samples also provide some indirect support for the relationship between BSE and outcome.

Kamphuis and Telch (2000) found that participants with claustrophobia fears who received one

session of exposure with guided threat reappraisal showed greater fear reduction and less return

of fear than those who received exposure with a distraction task, their combination, or exposure

alone. Partial indirect support was found for the BSE-outcome relationship by the finding that
 ACCEPTED MANUSCRIPT

BSE in subjective anxiety was significantly greater in those who received exposure with guided

threat reappraisal, either with or without a cognitive load task. In a related study, Sloan and

Telch (2002) found that participants who received exposure with guided reappraisal showed

PT
greater BSE in subjective anxiety and had superior outcomes on several measures at post-

RI
treatment (but not at follow-up) compared to those who received exposure with safety-seeking

behavior or exposure alone. In a non-clinical sample of blood-injection fearful participants,

SC
Oliver and Page (2003) found that those who engaged in distraction during exposure showed

NU
greater BSE in subjective distress relative to those who focused on the phobic stimuli during

exposure or those who received exposure alone. Compared to the other two groups, participants
MA
in the exposure plus distraction condition showed superior outcomes at post-treatment and

follow-up. Finally, Telch et al. (2004) found that claustrophobic participants who engaged in a
D
TE

distraction task during exposure had worse outcomes and less BSE in subjective fear than those

who engaged in a threat-focused task or a neutral control group.

P

In contrast to the above findings, some studies have failed to find support for the
CE

relationship between BSE and outcomes. In participants with PTSD receiving PE, Nacasch et al.
AC

(2015) found that although BSE was greater for those who received 40-minutes of imaginal

exposures versus 20-minutes and greater BSE in the overall sample was significantly correlated

to greater reduction in PTSD symptoms, there were no differences in outcome between the

groups that received shorter or longer duration of imaginal exposure. Meuret et al. (2012) found

that despite significant BSE in measures of physiological and subjective anxiety over the course

of exposure therapy for panic disorder, none of the indices of BSE were associated with clinical

outcomes. Similarly, Riley et al. (1995) found that BSE of physiologic measures was unrelated

to whether panic disorder patients were classified as responders at post-treatment.

 ACCEPTED MANUSCRIPT

The role of BSE was also examined indirectly in several analogue studies by Craske and

colleagues. Rowe and Craske (1998) found that spider-fearful participants who were exposed to

varying spider stimuli showed greater BSE in subjective anxiety prior to and during approach to

PT
a novel spider than those exposed to the same spider. Despite this difference in BSE, there were

RI
no group differences in outcome at post-assessment, and those exposed to varying stimuli

showed superior outcomes during the 3-week follow-up. However, exposure in this study

SC
consisted of seven short exposure trials completed in a single experimental session, and therefore

NU
the results may not generalize to a typical course of exposure therapy.

Tsao and Craske (2000) compared four trials of exposure delivered in a single session
MA
(massed exposure), over an equal number of intervening days (uniformly-spaced exposure), and

over increasing number of intervening days (expanding-spaced exposure) among participants

D
TE

fearful of public speaking. Although BSE in subjective anxiety was equal across groups and BSE

in heart rate was not observed in any group, the expanding-spaced exposure group showed
P

superior outcomes at the post-treatment follow up. Among height-fearful participants, Lang and
CE

Craske (2000) examined twelve 5-minute exposure trials delivered in a massed versus expanding
AC

spaced schedule as well as constant versus varied exposure. Participants who received massed

and constant exposure showed greater BSE than those who received expanding and varied

exposure; however, there were no consistent differences in outcomes across groups. Results of

these latter two studies are consistent with those of Chaplin and Levine (1981), who compared

continuous versus interrupted exposure for public speaking anxiety and found that continuous

exposure was associated with superior outcomes, despite the fact that both groups demonstrated

significant BSE.
 ACCEPTED MANUSCRIPT

Distress tolerance as an alternative mechanism. One possible explanation for the

inconsistent findings, particularly with regard to BSE, is that the relevant mechanism is not fear

reduction, but rather, increased tolerance to fear or distress during phobic situations. Indeed,

PT
Craske et al. (2008), among others, have suggested that the ability to engage in goal-directed

behavior despite experiencing distress, and being able to tolerate one’s anxiety during exposure,

RI
ensures that extinction learning will occur, regardless of reduction in fear. Several empirical

SC
studies have found significant associations between distress tolerance and degree of anxiety

NU
symptoms (e.g., Schmidt, Richey, & Fitzpatrick, 2006; Marshall-Berenz, Vujanovic, Bonn-

Miller, Bernstein, & Zvolensky, 2010), but the role of distress tolerance as a potential moderator
MA
or mechanism of outcome in exposure therapy has been less explored than the other mechanisms

examined here.
D
TE

One study by McHugh et al. (2014) found that for patients in a partial hospitalization

CBT program, increases in distress tolerance were associated with lower anxiety symptoms (not
P

specific to a particular diagnosis) at post-treatment. However, this study did not examine anxiety
CE

symptoms specific to a particular anxiety disorder and did not appear to routinely utilize
AC

exposures. On the basis of their findings, Bluett et al. (2014) suggested that while distress/fear

reduction was not associated with outcome in individuals receiving exposure therapy for PTSD,

better treatment outcome may be associated with increase in distress tolerance (as evidenced by

continued willingness to engage in exposure throughout treatment). However, as the authors

note, this study did not measure distress tolerance directly. In a community sample of individuals

who scored low on a measure of distress tolerance, Macatee and Cougle (2015) introduced a

two-week computerized intervention directly aimed at improving distress tolerance. The

intervention successfully improved distress tolerance in the active condition compared to the
 ACCEPTED MANUSCRIPT

waitlist control condition, and this improvement in distress tolerance mediated urges to

neutralize intrusive thoughts (mental compulsions). A potential shortcoming of this study was

the use of an analogue sample of participants who were not necessarily high in OCD symptoms;

PT
given the possibility that distress tolerance is more central to the maintenance of anxiety

RI
pathology, such an intervention would need to be tested further to determine whether it shows

similar effects in clinical populations. Overall, distress/fear tolerance as a mechanism of

SC
exposure therapy shows promise. However, given that the methods by which distress tolerance is

NU
acquired and adequately measured are still largely unknown, considerable additional theoretical

and empirical work is needed to fully understand how distress tolerance fits in with animal and
MA
human models of fear extinction.
D

Summary of Findings
TE

Relevance of specificity of content to extinction learning. The theoretical

developments and the empirical evidence examining the importance of specificity of content in
P
CE

extinction learning since the Watson and Marks (1971) article was published taken together

suggest that: (1) the field generally veered away from the findings by Watson and Marks (1971),
AC

and continued to test protocols that included exposure content that is relevant to core fears of the

patients being tested; and (2) in fact, beyond a decade after their paper, the interest in examining

the impact of fear irrelevant content on treatment outcome was abandoned .

From a review of developments in the field since this time, it is not clear why this issue

was not pursued further, but it is likely because it was not in line with the forefront theories (e.g.,

EPT, bioinformational theory) about extinction learning that emerged after this study, which as

described previously, outline how important it is to tap into the relevant core fear in order to

affect meaningful fear reduction. Again, it is worth noting that the study by Watson and Marks
 ACCEPTED MANUSCRIPT

(1971) arguably did not actually employ fear stimuli that were totally irrelevant to the

individual’s pathological fear structure, which extant theories of fear extinction would posit

might have led to some extinction effects since even with these irrelevant stimuli there was some

PT
degree of matching to the underlying fear structure (Foa & Kozak, 1986; Lang et al., 1977).

RI
Exploring the utility of tapping into irrelevant fears (more strictly defined than what was

done in the Watson and Marks study) may be a fruitful avenue to explore further. Such an

SC
endeavor would certainly be in line with the more recent transdiagnostic approaches being

NU
adopted for preliminary clinical efficacy trials (Farchione et al., 2012; Craske, 2012), which calls

for the use of assessment and intervention strategies that cut across diagnoses and specific fear
MA
domains. For example, the theory underlying one such transdiagnostic treatment (the Unified

Protocol, UP; Barlow et al., 2011) posits that there are more similarities in the etiology and latent
D
TE

structures (e.g. underlying common factors such as neuroticism and behavioral inhibition) of

various anxiety and mood disorders than there are differences. Thus, this treatment approach
P

focuses overall on increasing tolerance to strong emotions (not just specific fears) and correcting
CE

maladaptive emotion regulation strategies. However, without more vigorous and systematic
AC

empirical investigation, the utility of exposures to generally distressing stimuli that do not

specifically aim to match participants’ core fears is unclear, and currently unsupported.

Fear activation as a mechanism of exposure. Despite the many strides made by the

theoretical models discussed above in helping us understand how fear activation impacts

treatment outcome, there are many questions that have not been sufficiently examined, and doing

so may explain some of the inconsistencies found in the empirical evidence regarding the

relationship between fear activation and treatment outcome. For instance, Foa, Hembree, and

Rothbaum (2007) coined the terms over-engagement and under-engagement, suggesting that
 ACCEPTED MANUSCRIPT

both too little activation and too much activation hinder emotional processing and therefore

treatment outcome. That is, it is possible that over-activation might actually hinder the corrective

learning and disconfirmation needed to result in successful reduction of fear. Similarly, McNally

PT
(2007) has suggested that there is an optimal level of fear activation required for fear extinction.

RI
To this end, distraction can be viewed as a means of titrating the level of fear activation, at least

in certain anxiety disorders (e.g., phobic-stimulus-irrelevant conversation with spider phobic

SC
patients during exposure was shown to result in superior outcome, particularly in those reporting

NU
higher levels of initial baseline fear; Johnstone & Page, 2004). Indeed, Foa et al. (2006) modified

the original EPT to incorporate such findings and suggest that distraction may serve as a helpful
MA
way to moderate level of fear activation in certain anxiety disorders (such as specific phobias)

and as a maladaptive cognitive form of avoidance in other disorders (such as agoraphobia), but
D
TE

this area deserves additional empirical attention.

Other researchers (e.g., Craske et al., 2008) have noted that roughly an equal number of
P

studies have either supported or refuted the notion that fear activation (particularly initial fear
CE

activation in the first exposure session) meaningfully predicts treatment outcome across a range
AC

of fear-based disorders, thus its status as a mechanism of outcome is still unclear. The

methodological and assessment differences across these studies have also been purported to

account for the observed inconsistencies in findings; for example, some studies utilize

physiological indices of fear activation while others do not, different lengths and spacing of

exposures, use of clinical versus subclinical samples (Craske et al., 2008). In addition, it is

important to acknowledge that many of the earlier studies done on this area utilized smaller

samples (under 20 participants), although this is not unusual for initial studies examining

mechanisms of psychopathology, and effects of fear activation on outcome were noted even with
 ACCEPTED MANUSCRIPT

these small sample sizes. Taken together, while the impact of adequate fear activation during

extinction learning on subsequent fear reduction is still in flux, it is crucial that this potential

mechanism is studied more systematically and vigorously. Indeed, the implications for exposure

PT
treatment of anxiety-related disorders are considerable based on the determination of whether

RI
fear activation is necessary for successful treatment outcomes.

WSE and BSE as mechanisms of treatment outcome. In terms of the role of WSE, it

SC
seems that while a small number of studies have found evidence that WSE is related to exposure

NU
therapy outcomes, the majority of studies do not support the idea that WSE is necessary for good

outcomes. Some researchers have suggested that null findings may be due to a limited range on
MA
this process variable, given that WSE occurs for most patients. However, this interpretation is

inconsistent with studies that find good reduction in symptoms from pre-to post-treatment in the
D
TE

absence of significant WSE. Thus, although patients may experience WSE during exposure

sessions, the degree of WSE is not a consistent predictor of outcome.

P

In contrast to findings on WSE, BSE has been associated with superior outcomes with
CE

some consistency. To date, however, the majority of supporting studies has not examined the
AC

relationship between BSE and outcome directly, but have instead examined whether group

differences in BSE match with group differences in outcome. For both WSE and BSE studies,

methodological differences in how process variables are measured (e.g., subjective ratings vs.

physiological), types of outcomes examined (e.g., reported, behavioral, physiological) and

schedule of exposure sessions significantly complicates comparisons across studies.

In light of the somewhat mixed findings described above, the necessity of WSE and BSE

has been the subject of much debate. In the most recent update to EPT, Foa et al. (2006) reported

that most studies do not find a direct relationship between WSE and treatment outcomes and
 ACCEPTED MANUSCRIPT

suggest that WSE may not, in fact, be a reliable indicator of emotional processing. Researchers

such as Craske et al. (2008) and others have called to question the necessity of WSE as well as

BSE for therapeutic recovery. Craske et al. proposed that fear tolerance, defined as the ability to

PT
engage in goal-directed behavior despite experiencing distress is a more important clinical

RI
concept than fear reduction (i.e., WSE or BSE), and that as long as the participant is able to

tolerate their anxiety during exposure, extinction learning will occur regardless of change in

SC
distress levels. Indeed, modern learning theories of extinction (e.g., Bouton, 2004) propose that

NU
fear tolerance promotes extinction learning which has been considered a key mechanism of

exposure therapy, and this is deemed a fruitful avenue to examine further.

MA
D
P TE
CE
AC
 ACCEPTED MANUSCRIPT

References

Allen, L. B., & Barlow, D. H. (2009). Relationship of exposure to clinically irrelevant emotion

cues and obsessive-compulsive symptoms. Behavior Modification, 33(6), 743-762.

PT
http://dx.doi.org/10.1177/0145445509344180

RI
Baker, A., Mystkowski, J., Culver, N., Yi, R., Mortazavi, A., & Craske, M. G. (2010). Does

habituation matter? Emotional processing theory and exposure therapy for acrophobia.

SC
Behaviour Research and Therapy, 48(11), 1139-1143.

NU
http://dx.doi.org/10.1016/j.brat.2010.07.009

Barlow, D. H., Farchione, T. J., Fairholme, C. P., Ellard, K. K., Boisseau, C. L., Allen, L. B., &
MA
Ehrenreich-May, J. (2011). Unified protocol for transdiagnostic treatment of emotional

disorders: Therapist guide. New York, NY, US: Oxford University Press.
D
TE

Baum, M., & Leclerc, R. (1974). Irrelevant stress vs response prevention (flooding) interpolated

between avoidance acquisition and extinction in rats. Journal of Psychiatric Research,

P

10(3-4), 307-314. http://dx.doi.org/10.1016/0022-3956(74)90012-0

CE

Beckham, J. C., Vrana, S. R., May, J. G., Gustafson, D. J., & Smith, G. R. (1990). Emotional
AC

processing and fear measurement synchrony as indicators of treatment outcome in fear of

flying. Journal of Behavior Therapy and Experimental Psychiatry, 21(3), 153-162.

http://dx.doi.org/10.1016/0005-7916(90)90002-3

Bluett, E. J., Zoellner, L. A., & Feeny, N. C. (2014). Does change in distress matter?

Mechanisms of change in prolonged exposure for PTSD. Journal of Behavior Therapy

and Experimental Psychiatry, 45(1), 97-104.

http://dx.doi.org/10.1016/j.jbtep.2013.09.003

Borkovec, T. D., & Sides, J. K. (1979). The contribution of relaxation and expectancy to fear
 ACCEPTED MANUSCRIPT

reduction via graded, imaginal exposure to feared stimuli. Behaviour Research and

Therapy, 17(6), 529-540. http://dx.doi.org/10.1016/0005-7967(79)90096-2

Bouton, M. E. (2004). Context and behavioral processes in extinction. Learning & Memory,

PT
11(5), 485-494. http://dx.doi.org/10.1101/lm.78804

RI
Bouton, M. E., & Swartzentruber, D. (1991). Sources of relapse after extinction in Pavlovian and

instrumental learning. Clinical Psychology Review, 11(2), 123-140.

SC
http://dx.doi.org/10.1016/0272-7358(91)90091-8

NU
Chaplin, E. W., & Levine, B. A. (1981). The effects of total exposure duration and interrupted

versus continuous exposure in flooding therapy. Behavior Therapy, 12(3), 360-368.

MA
http://dx.doi.org/10.1016/S0005-7894(81)80124-4

Craske, M. G. (2012). Transdiagnostic treatment for anxiety and depression. Depression and
D
TE

Anxiety, 29(9), 749-753. http://dx.doi.org/10.1002/da.21992

Craske, M. G., Kircanski, K., Zelikowsky, M., Mystkowski, J., Chowdhury, N., & Baker, A.
P

(2008). Optimizing inhibitory learning during exposure therapy. Behaviour Research and
CE

Therapy, 46(1), 5-27. http://dx.doi.org/10.1016/j.brat.2007.10.003

AC

Culver, N. C., Stoyanova, M., & Craske, M. G. (2012). Emotional variability and sustained

arousal during exposure. Journal of Behavior Therapy and Experimental Psychiatry,

43(2), 787-793. http://dx.doi.org/10.1016/j.jbtep.2011.10.009

Farchione, T. J., Fairholme, C. P., Ellard, K. K., Boisseau, C. L., Thompson-Hollands, J., Carl, J.

R., . . . Barlow, D. H. (2012). Unified protocol for transdiagnostic treatment of

emotional disorders: A randomized controlled trial. Behavior Therapy, 43(3), 666-678.

http://dx.doi.org/10.1016/j.beth.2012.01.001

Foa, E. B., Grayson, J. B., Steketee, G. S., Doppelt, H. G., Turner, R. M., & Latimer, P. R.
 ACCEPTED MANUSCRIPT

(1983). Success and failure in the behavioral treatment of obsessive-compulsives. Journal

of Consulting and Clinical Psychology, 51(2), 287-297. http://dx.doi.org/10.1037/0022-

006X.51.2.287

PT
Foa, E. B., Hembree, E. A., & Rothbaum, B. O. (2007). Prolonged exposure therapy for PTSD:

RI
Emotional processing of traumatic experiences: Therapist guide. New York, NY: Oxford

University Press.

SC
Foa, E. B., Huppert, J. D., & Cahill, S. P. (2006). Emotional processing theory: An update. In B.

NU
O. Rothbaum (Ed.), Pathological anxiety: Emotional processing in etiology and

treatment (pp. 3-24). New York, NY: Guilford Press.

MA
Foa, E. B., & Kozak, M. J. (1986). Emotional processing of fear: Exposure to corrective

information. Psychological Bulletin, 99(1), 20-35. http://dx.doi.org/10.1037/0033-

D
TE

2909.99.1.20

Foa, E. B., McNally, R. J., & Williams, L. (1996). Mechanisms of change in exposure therapy.
P

In R. M. Rapee (Ed.), Current controversies in the anxiety disorders (pp. 329-343). New
CE

York, NY: Guilford Press.

AC

Foa, E. B., Riggs, D. S., Massie, E. D., & Yarczower, M. (1995). The impact of fear activation

and anger on the efficacy of exposure treatment for posttraumatic stress disorder.

Behavior Therapy, 26(3), 487-499. http://dx.doi.org/10.1016/S0005-7894(05)80096-6

Foa, E. B., Steketee, G., Turner, R. M., & Fischer, S. C. (1980). Effects of imaginal exposure to

feared disasters in obsessive-compulsive checkers. Behaviour Research and Therapy,

18(5), 449-455. http://dx.doi.org/10.1016/0005-7967(80)90010-8

Grayson, J. B., Foa, E. B., & Steketee, G. (1982). Habituation during exposure treatment:

Distraction vs attention-focusing. Behaviour Research and Therapy, 20(4), 323-328.

 ACCEPTED MANUSCRIPT

http://dx.doi.org/10.1016/0005-7967(82)90091-2

Jaycox, L. H., Foa, E. B., & Morral, A. R. (1998). Influence of emotional engagement and

habituation on exposure therapy for PTSD. Journal of Consulting and Clinical

PT
Psychology, 66(1), 185-192. http://dx.doi.org/10.1037/0022-006X.66.1.185

RI
Johnstone, K. A., & Page, A. C. (2004). Attention to phobic stimuli during exposure: The effect

of distraction on anxiety reduction, self-efficacy and perceived control. Behaviour

SC
Research and Therapy, 42(3), 249-275. http://dx.doi.org/10.1016/S0005-7967(03)

NU
00137-2

Kamphuis, J. H., & Telch, M. J. (2000). Effects of distraction and guided threat reappraisal on
MA
fear reduction during exposure-based treatments for specific fears. Behaviour Research

and Therapy, 38(12), 1163-1181. http://dx.doi.org/10.1016/S0005-7967(99)00147-3

D
TE

Kircanski, K., Mortazavi, A., Castriotta, N., Baker, A. S., Mystkowski, J. L., Yi, R., & Craske,

M. G. (2012). Challenges to the traditional exposure paradigm: Variability in exposure

P

therapy for contamination fears. Journal of Behavior Therapy and Experimental

CE

Psychiatry, 43(2), 745-751. http://dx.doi.org/10.1016/j.jbtep.2011.10.010

AC

Kozak, M. J., Foa, E. B., & Steketee, G. (1988). Process and outcome of exposure treatment with

obsessive-compulsives: Psychophysiological indicators of emotional processing.

Behavior Therapy, 19(2), 157-169. http://dx.doi.org/10.1016/S0005-7894(88)80039-X

Lang, A. J., & Craske, M. G. (2000). Manipulations of exposure-based therapy to reduce return

of fear: A replication. Behaviour Research and Therapy, 38(1), 1-12.

http://dx.doi.org/10.1016/S0005-7967(99)00031-5

Lang, P. J. (1977). Imagery in therapy: An information processing analysis of fear. Behavior

Therapy, 8(5), 862-886. http://dx.doi.org/10.1016/S0005-7894(77)80157-3

 ACCEPTED MANUSCRIPT

Lang, P. J. (1979). A bio-informational theory of emotional imagery. Psychophysiology, 16(6),

495-512. http://dx.doi.org/10.1111/j.1469-8986.1979.tb01511.x

Lang, P. J., Bradley, M. M., & Cuthbert, B. N. (1998). Emotion, motivation, and anxiety: Brain

PT
mechanisms and psychophysiology. Biological Psychiatry, 44(12), 1248-1263.

RI
http://dx.doi.org/10.1016/S0006-3223(98)00275-3

Lang, P. J., Levin, D. N., Miller, G. A., & Kozak, M. J. (1983). Fear behavior, fear imagery, and

SC
the psychophysiology of emotion: The problem of affective response integration. Journal

NU
of Abnormal Psychology, 92(3), 276-306. http://dx.doi.org/10.1037/0021-843X.92.3.276

Lang, P. J., Melamed, B. G., & Hart, J. (1970). A psychophysiological analysis of fear
MA
modification using an automated desensitization procedure. Journal of Abnormal

Psychology, 76(2), 220-234. http://dx.doi.org/10.1037/h0029875

D
TE

Macatee, R. J., & Cougle, J. R. (2015). Development and evaluation of a computerized

intervention for low distress tolerance and its effect on performance on a neutralization
P

task. Journal Of Behavior Therapy And Experimental Psychiatry, 48, 33-39.

CE

doi:10.1016/j.jbtep.2015.01.007
AC

Marshall-Berenz, E. C., Vujanovic, A. A., Bonn-Miller, M. O., Bernstein, A., & Zvolensky, M.

J. (2010). Multimethod study of distress tolerance and PTSD symptom severity in a

trauma-exposed community sample. Journal Of Traumatic Stress, 23(5), 623-630.

doi:10.1002/jts.20568

McHugh, R. K., Kertz, S. J., Weiss, R. B., Baskin-Sommers, A. R., Hearon, B. A., &

Björgvinsson, T. (2014). Changes in distress intolerance and treatment outcome in a

partial hospital setting. Behavior Therapy, 45(2), 232-240.

doi:10.1016/j.beth.2013.11.002
 ACCEPTED MANUSCRIPT

McNally, R. J. (2007). Mechanisms of exposure therapy: How neuroscience can improve

psychological treatments for anxiety disorders. Clinical Psychology Review, 27(6), 750-

759. http://dx.doi.org/10.1016/j.cpr.2007.01.003

PT
Meuret, A. E., Seidel, A., Rosenfield, B., Hofmann, S. G., & Rosenfield, D. (2012). Does fear

RI
reactivity during exposure predict panic symptom reduction? Journal of Consulting and

Clinical Psychology, 80(5), 773-785. http://dx.doi.org/10.1037/a0028032

SC
Mineka, S. (1976). Effects of flooding an irrelevant response on the extinction of avoidance

NU
responses. Journal of Experimental Psychology: Animal Behavior Processes, 2(2), 142-

153. http://dx.doi.org/10.1037/0097-7403.2.2.142
MA
Nacasch, N., Huppert, J. D., Su, Y., Kivity, Y., Dinshtein, Y., Yeh, R., & Foa, E. B. (2015). Are

60-minute prolonged exposure sessions with 20-minute imaginal exposure to traumatic

D
TE

memories sufficient to successfully treat PTSD? A randomized noninferiority clinical

trial. Behavior Therapy, 46(3), 328-341. http://dx.doi.org/10.1016/j.beth.2014.12.002

P

Norton, P. J., Hayes-Skelton, S., & Klenck, S. C. (2011). What happens in session does not stay
CE

in session: Changes within exposures predict subsequent improvement and dropout.

AC

Journal of Anxiety Disorders, 25(5), 654-660.

http://dx.doi.org/10.1016/j.janxdis.2011.02.006

Oliver, N. S., & Page, A. C. (2003). Fear reduction during in vivo exposure to blood-injection

stimuli: Distraction vs. attentional focus. British Journal of Clinical Psychology, 42(1),

13-25. http://dx.doi.org/10.1348/014466503762841986

Pavlov, I. (1927). Conditioned reflexes. New York, NY: Oxford University Press.

Pitman, R. K., Orr, S. P., Altman, B., & Longpre, R. E. (1996). Emotional processing and

outcome of imaginal flooding therapy in Vietnam Veterans with chronic posttraumatic

 ACCEPTED MANUSCRIPT

stress disorder. Comprehensive Psychiatry, 37(6), 409-418.

http://dx.doi.org/10.1016/S0010-440X(96)90024-3

Rauch, S. A. M., Foa, E. B., Furr, J. M., & Filip, J. C. (2004). Imagery vividness and perceived

PT
anxious arousal in prolonged exposure treatment for PTSD. Journal of Traumatic Stress,

RI
17(6), 461-465. http://dx.doi.org/10.1007/s10960-004-5794-8

Rescorla, R. A., & Wagner, A. R. (1972). A theory of Pavlovian conditioning: variations in the

SC
effectiveness of reinforcement and nonreinforcement. In A. H. Black & W. F. Prokasy

NU
(Eds.), Classical conditioning II: current research and theory (pp. 64-99). New York:

Appleton-Century-Crofts.
MA
Ressler, K. J., Rothbaum, B. O., Tannenbaum, L., Anderson, P., Graap, K., Zimand, E., . . .

Davis, M. (2004). Cognitive enhancers as adjuncts to psychotherapy: Use of D-

D
TE

cycloserine in phobic individuals to facilitate extinction of fear. Archives of General

Psychiatry, 61(11), 1136-1144. http://dx.doi.org/10.1001/archpsyc.61.11.1136

P

Riley, W. T., McCormick, M. G. F., Simon, E. M., Stack, K., Pushkin, Y., Overstreet, M. M., . . .
CE

Magakian, C. (1995). Effects of alprazolam dose on the induction and habituation

AC

processes during behavioral panic induction treatment. Journal of Anxiety Disorders,

9(3), 217-227. http://dx.doi.org/10.1016/0887-6185(95)00003-7

Rowe, M. K., & Craske, M. G. (1998). Effects of varied-stimulus exposure training on fear

reduction and return of fear. Behaviour Research and Therapy, 36(7-8), 719-734.

http://dx.doi.org/10.1016/S0005-7967(97)10017-1

Schmidt, N. B., Richey, J. A., & Fitzpatrick, K. K. (2006). Discomfort intolerance: Development

of a construct and measure relevant to panic disorder. Journal Of Anxiety Disorders,

20(3), 263-280. doi:10.1016/j.janxdis.2005.02.002

 ACCEPTED MANUSCRIPT

Skinner, B. F. (1938). The behavior of organisms: An experimental analysis. Oxford, England:

Appleton-Century-Crofts.

Sloan, T., & Telch, M. J. (2002). The effects of safety-seeking behavior and guided threat

PT
reappraisal on fear reduction during exposure: An experimental investigation. Behaviour

RI
Research and Therapy, 40(3), 235-251. http://dx.doi.org/10.1016/S0005-7967(01)

00007-9

SC
Sripada, R. K., & Rauch, S. A. M. (2015). Between-session and within-session habituation in

NU
prolonged exposure therapy for posttraumatic stress disorder: A hierarchical linear

modeling approach. Journal of Anxiety Disorders, 30, 81-87.

MA
http://dx.doi.org/10.1016/j.janxdis.2015.01.002

Telch, M. J., Valentiner, D. P., Ilai, D., Young, P. R., Powers, M. B., & Smits, J. A. J. (2004).
D
TE

Fear activation and distraction during the emotional processing of claustrophobic fear.

Journal of Behavior Therapy and Experimental Psychiatry, 35(3), 219-232.

P

http://dx.doi.org/10.1016/j.jbtep.2004.03.004
CE

Tsao, J. C. I., & Craske, M. G. (2000). Timing of treatment and return of fear: Effects of massed,
AC

uniform-, and expanding-spaced exposure schedules. Behavior Therapy, 31(3), 479-497.

http://dx.doi.org/10.1016/S0005-7894(00)80026-X

Van Elzakker, M. B., Dahlgren, M. K., Davis, F. C., Dubois, S. & Shin, L. M. (2014). From

Pavlov to PTSD: The extinction of conditioned fear in rodents, humans, and anxiety

disorders. Neurobiology of Learning and Memory, 113, 3–18.

van Minnen, A., & Foa, E. B. (2006). The effect of imaginal exposure length on outcome of

treatment for PTSD. Journal of Traumatic Stress, 19(4), 427-438.

http://dx.doi.org/10.1002/jts.20146
 ACCEPTED MANUSCRIPT

van Minnen, A., & Hagenaars, M. (2002). Fear activation and habituation patterns as early

process predictors of response to prolonged exposure treatment in PTSD. Journal of

Traumatic Stress, 15(5), 359-367. http://dx.doi.org/10.1023/A:1020177023209

PT
Watson, J. P., & Marks, I. M. (1971). Relevant and irrelevant fear in flooding: A crossover study

RI
of phobic patients. Behavior Therapy, 2(3), 275-293. http://dx.doi.org/10.1016/S0005-

7894(71)80062-X

SC
NU
MA
D
P TE
CE
AC
 ACCEPTED MANUSCRIPT

Highlights:

 Many theoretical and empirical developments have occurred since Watson & Marks
(1971).
 The match between the underlying fear and exposure content seems to be important.
 Role of fear activation in outcome is mixed and needs more investigation.

PT
 Within-session extinction is a limited predictor of outcome.
 Between-session extinction has more, but still mixed, support as mechanism in

RI
extinction.

SC
NU
MA
D
P TE
CE
AC