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Volume 8 – Number 5 CNS Spectrums - May 2003
373
FOCUS POINTS
• Cognitive-behavioral theory (CBT) suggests that patients’
distorted perceptions of social situations and their own
physical arousal lead to behaviors that enable them to
avoid anxiety-provoking situations in the short term, but
which act to generate and maintain disabling levels of
anxiety in social situations in the long term.
• CBT targets these beliefs in a variety of forms, including
exposure, cognitive restructuring, relaxation training, and
social skills training.
• Exposure therapy and cognitive restructuring have
tended to show results most comparable to pharma-
cotherapeutic interventions.
• Future research should continue to explore the effective-
ness of CBT and ways in which CBT and medication can
be partnered to achieve optimal outcomes for patients
with social anxiety disorder.
ABSTRACT
The present paper examines the role of cognitive-behav-
ioral therapy (CBT) in the treatment of social anxiety disor-
der (SAD). A cognitive-behavioral model of SAD is first
presented. Different modalities of CBT for SAD are then
described, including exposure, cognitive restructuring, relax-
ation training, and social skills training, and evidence sup-
porting their efficacy is reviewed. The comparative and
combined impact of CBT and pharmacotherapeutic interven-
tions is also explored. CBT appears to be an efficacious treat-
ment for SAD. However, the overall efficacy CBT may be
increased by closer examination of the active ingredients of
treatment. Such analyses may also enable more successful
integration of the different CBT techniques and of CBT and
pharmacotherapy in the treatment of SAD.
CNS Spectr 2003;8(5):373-381
THE IMPACT OF SOCIAL ANXIETY DISORDER
Social anxiety disorder (SAD) is the pathologic fear of
negative evaluation in one or more social or performance
situation(s).
1
Estimates of the 1-year prevalence of SAD
run as high as 8%,
2
although recent evidence suggests that
the rate of clinically significant SAD in the general popu-
lation is closer to 4%.
3
Despite its high prevalence, SAD
has only begun to receive substantial attention in the last
few years.
4
The social and personal consequences of SAD
are now known to be far-reaching. SAD disrupts an indi-
vidual’s relationships, resulting in fewer friendships,
greater difficulty getting along with friends, and less satis-
faction with one’s available network of social support.
5,6
Persons with SAD are also less likely to be married and
more likely to live alone than persons without mental dis-
order
7,8
and persons with other anxiety disorders.
9
Unemployment, underemployment (working at a level
below one’s abilities), reduced work productivity, and
increased dependence on public assistance are all charac-
teristic of individuals with SAD.
10-14
SAD also appears to
be a risk factor for other disorders and symptoms, includ-
ing major depression, alcoholism, and suicidal ideation.
8
Fortunately, pharmacologic interventions and cogni-
tive-behavioral therapy (CBT) have demonstrated efficacy
in treating this disorder and in helping patients reduce
their level of symptoms and disability and improve the
quality of their lives. This paper will focus on the impact
of CBT on the potentially catastrophic consequences of
SAD. We begin with a presentation of a cognitive-behav-
ioral model of SAD, which suggests how maladaptive pat-
terns of thought and behavior can maintain anxiety over
time and may be used to help explain how CBT can ame-
liorate anxiety in social situations. Next, we review the
major modalities of CBT for SAD, focusing on exposure,
cognitive restructuring, relaxation training, and social
skills training, as well as evidence in support of their effi-
cacy. Third, we examine the relationship between CBT
and pharmacologic interventions for SAD, first reviewing
research comparing the relative effectiveness of CBT and
medication and then considering the combined effects of
these two treatment approaches. Finally, we consider
future directions and current shortcomings in our under-
standing of the effectiveness of CBT for SAD.
Mr. Hambrick, Mr. Weeks, and Ms. Harb are all doctoral students in clinical psychology in the Department of Psychology at Temple University in
Philadelphia, Pennsylvania. Dr. Heimberg is professor of psychology, director of clinical training, and director of the Adult Anxiety Clinic in the
Department of Psychology at Temple University.
Disclosures: This work has been funded in part by a National Institute of Mental Health grant (44119) to Dr. Heimberg.
Acknowledgement: The authors wish to dedicate this article to the memory of Robert A. Gould, PhD.
Please direct all correspondence to: Richard G. Heimberg, PhD, Adult Anxiety Clinic of Temple University, Department of Psychology, Temple University,
Weiss Hall, 1701 North 13th Street, Philadelphia, PA 19122-6085; Tel: 215-204-1575, Fax: 215-204-5184; Email: heimberg@temple.edu.
Review Article
Cognitive-Behavioral Therapy for
Social Anxiety Disorder: Supporting
Evidence and Future Directions
By James P. Hambrick, MA, Justin W. Weeks, BA, Gerlinde C. Harb, MS
and Richard G. Heimberg, PhD
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374
THE COGNITIVE-BEHAVIORAL MODEL
OF SOCIAL ANXIETY DISORDER
A number of cognitive-behavioral models of SAD exist,
focusing on different aspects of how individuals with SAD
process social-evaluative information and how biases in infor-
mation processing may affect their emotional and behavioral
responses in social situations. The model discussed here was
first presented by Rapee and Heimberg
15
and later elaborated
by others.
16,17
The model is depicted in the Figure.
Rapee and Heimberg
15
argue that the experience of anxi-
ety in social situations is induced by the threat of a poten-
tially critical audience (ie, another person or persons
who may observe and evaluate the individual in the social
situation). An individual develops an image or mental rep-
resentation of him or herself as perceived by that audience,
reflecting a combination of memories or images of past
experiences in similar situations, appraisals of his or her
current physical state, and appraisal of negative or ambigu-
ous audience cues (eg, yawning or other displays of lack of
interest). This mental representation of the self as perceived
by the audience is compared to the person’s prediction of
audience expectations. That is, the person asks him or her-
self “Am I doing as well as the audience expects of me?”
The more negative the person’s response to this question,
the greater the perceived likelihood of negative evaluation
and cost of social failure. As shown in Figure 1, this judg-
ment subsequently gives rise to thoughts about how the per-
son is performing (particularly negative thoughts), physical
symptoms (eg, sweating, blushing, ormuscle tension), and
anxious behaviors (eg, social withdrawal or reduction of eye
contact). These thoughts, physiologic symptoms, and behav-
iors feed back into the person’s impressions of the situation,
driving the perception of the self as seen by the audience
downward, augmenting the person’s anxiety and reinforcing
his or her belief that he or she is performing poorly. The
channeling of the person’s attentional resources toward
signs of threat (eg, increasing physiologic arousal) instead of
sources of positive feedback (eg, displays of interest from
the audience) further exacerbates this process.
Although there is not a clear delineation between normal
shyness and SAD,
18
social anxiety may become more perva-
sive or extreme as a result of a number of factors. Biological
and temperamental factors can shape a person’s overall ten-
dencies to engage with or disengage from social situations.
These factors are reflected in Kagan and Snidman’s
19
find-
ings that infants who had initial difficulty engaging with new
stimuli (ie, new toys or unfamiliar people) tended to be more
shy later in life and more likely to meet criteria for a diagno-
sis of SAD,
20
and in twin studies finding evidence for the
heritability of shyness
21
and SAD.
22
Another potential factor in the development of SAD is
the distortion of the person’s self-image in long-term mem-
ory, sensitizing him or her to negative experiences in social
situations. Early or critical experiences can inform a per-
son’s image of him or herself, distorting the person’s
impression of his or her performance in the current
situation. Although data in support of distorted and biased
memory in SAD are mixed,
23
Hackmann and colleagues
24
showed that more than three-fourths of a sample of individ-
uals with SAD reported recurrent visual images of past
social catastrophes. These images were typically viewed
from the perspective of an outside observer rather than
through the eyes of the person and may be best described
as representations of the person’s worst fears of how they
appeared to others rather than accurate depictions of past
events. Importantly, these situations often occurred during
the period of onset of social anxiety and were sponta-
neously imaged in anticipation of current social situations.
Beliefs about the relative likelihood and potentially cata-
strophic consequences of failure in a social situation can
also have an impact on the person’s willingness to engage
with those situations. Foa and colleagues
25
found that prior
to CBT, individuals with SAD were much more likely to
make inaccurate assessments of the probability of negative
outcomes in social situations and to make dire predictions
about the consequences of social failures. CBT had some-
what of a normalizing effect on these evaluations.
If early experiences have an impact on current experi-
ence, then it stands to reason that current experiences will
have an impact on future experiences. Clark and Wells
26
Review Article
Volume 8 – Number 5 CNS Spectrums - May 2003
FIGURE. A MODEL OF THE GENERATION AND MAIN-
TENANCE OF ANXIETY IN SOCIAL/EVALU-
ATIVE SITUATIONS.
15
Reprinted with permission from Rapee RM, Heimberg RG. A cognitive-
behavioral model of anxiety in social phobia. Behav Res Ther. 1997;35:743.
Copyright by Elsevier Science Ltd. Used with permission of the publisher.
Hambrick JP, Weeks JW, Harb GC, Heimberg RG. CNS Spectr. Vol 8, No 5.
2003.
373-381_0503CNS_Hambrick 5/18/03 9:26 AM Page 374
375
point out that strategies the socially anxious person uses to
avoid the present situation may decrease anxiety in the short
term, but ultimately leave the person with an accumulation
of negative beliefs about the situation, as well as shame that
they were unable to perform as well as they hoped.
A full review of the evidence supporting this cognitive-
behavioral model is beyond the scope of this paper but is
available in the papers by Rapee and Heimberg,
15
Turk and
colleagues,
16
and Roth and Heimberg.
17
The model delin-
eates the interactive effect of physiologic arousal, interac-
tions with the environment, and distorted appraisals of the
impact and consequences of those experiences on the per-
son’s anxiety experience. In the next section, we discuss
how CBT attempts to address these aspects of SAD to lessen
the person’s distress in social situations.
COGNITIVE-BEHAVIORAL THERAPY
FOR SOCIAL ANXIETY DISORDER
Although there are differences among the CBT tech-
niques, they share a set of fundamental assumptions. CBT is
a time-limited and present-oriented approach that strives to
empower the patient to act as his or her own agent of
change.
27
In CBT, the therapist and patient work together as
a collaborative team. The therapist acts as observer and
coach, teaching coping skills and, in some types of CBT,
pointing out logical contradictions in the patient’s patterns
of thinking and behavior. The therapist’s roles as teacher
and coach vary according to the type of CBT being adminis-
tered and the relative emphasis of each on learning skills
versus encouragement to see situations in new ways and
permitting oneself to experience anxiety until it attenuates.
Meanwhile, the patient learns to move toward and engage
his or her anxiety and employs skills used in therapy to
cope with it on a daily basis between sessions. The four
modalities to be considered here are the most widely stud-
ied in the treatment of SAD: exposure, cognitive restructur-
ing, relaxation training, and social skills training.
Exposure to Feared Social Situations
Exposure to feared situations is essential for fear reduc-
tion. When the individual is exposed to the feared situation
but does not encounter the feared outcome (eg, outright
rejection in a social interaction), natural conditioning
processes involved in fear reduction (habituation and
extinction) take place. The individual is also confronted
with information that contradicts negative distorted beliefs.
The first stage of exposure treatment is the collaborative
development of a rank-ordered list of situations that provoke
anxiety for the patient (often referred to as the fear and
avoidance hierarchy). Patients put themselves into these
feared situations, starting with situations low on this rank-
ordered list. They are typically asked to engage the situation
fully (ie, maintaining a focus on the situation and all its vari-
ous aspects rather than attempting to filter the distressing
aspects of the situation from awareness or engage in some
other form of distraction). They are also asked to remain in
the situation until their anxiety naturally begins to subside.
As a sense of mastery in the lesser situation is obtained and
it no longer elicits distressing levels of fear, patients
approach increasingly more anxiety-evoking situations and
gradually work towards the social situations they find most
difficult. Exposure to feared situations may be administered
by means of imagery; role-play with the therapist or therapy
assistants; confronting feared situations in everyday life out-
side of session; or by a combination of these methods.
In addition, exposure protocols may differ in the amount
of therapist involvement (ie, self-exposure or clinician-
accompanied in vivo exposure), as well as the length, num-
ber, and interval between exposure sessions. Furthermore,
exposure is often combined with other treatment compo-
nents, such as applied relaxation or cognitive techniques.
Exposure exercises are most effective when patients’ psy-
chological engagement in the feared situation is maximized,
that is, when they pay full attention to the situation and
allow the inevitable rush of anxiety and arousal to occur.
28
However, anxious patients may try to distract themselves
from the feared situation as it unfolds, or their tendency to
focus attention on the threatening aspects of the situation
may prevent them from attending to what is actually hap-
pening. Therefore, instructions to maintain focus on the
feared situation are an important component of, and
increase the efficacy of, exposure techniques.
29
Cognitive Restructuring
Findings suggest that it is important for patients to exam-
ine thoughts related to feared situations and the beliefs that
underlie them. Indeed, current cognitive-behavioral models
of SAD
15,26
are based on the premise that the disorder devel-
ops due to inaccurate beliefs about potential dangers
encountered during social situations, negative outcome pre-
dictions of these situations, and biased perceptual process-
ing of events occurring within social situations. The goal of
cognitive restructuring is to help the patient evaluate feared
situations more realistically.
The first step in cognitive restructuring is the identifica-
tion of negative thoughts that occur prior to, during, or after
a confrontation with feared situations. Next, the patient and
therapist evaluate the accuracy of these thoughts using evi-
dence obtained from Socratic dialogue and/or from planned
“behavioral experiments.”
30
The goal is to develop evalua-
tions based on data that is more objective and rational than
the patient’s anxiety-driven perceptions.
By utilizing these rational thoughts in lieu of their cus-
tomary negative interpretations in exposures to anxiety-pro-
voking situations, patients are provided with a
cognitive-coping strategy, which, over time and repetition,
will allow them to modify their habitual negative beliefs
about social situations.
Most cognitive approaches to the treatment of social
anxiety are closely tied to exposure. Exposure to anxiety-
provoking situations is central to cognitive restructuring, for
helping patients access their negative thoughts and to
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376
obtain evidence to evaluate these thoughts. Behavioral
experiments are designed to provide patients with opportu-
nities to treat their thoughts as hypotheses and test whether
their beliefs (eg, “I will not be able to speak” or “Everyone
will laugh at me”) are realistic appraisals.
Behavioral experiments may require patients to enter
anxiety-provoking situations without engaging in their usual
“safety behaviors.”
31,32
Patients often hold erroneous beliefs
that engaging in safety behaviors allows him or her to man-
age their anxiety successfully and that the implementation
of safety behaviors will prevent feared catastrophes.
For example, individuals with SAD may attempt to con-
trol shaking of their arms in anxiety-provoking encounters
by stiffening muscles or by tightly holding on to objects.
Other individuals may be reticent in social situations and
choose not to contribute to conversations for fear of saying
the wrong thing and being criticized by others. Thereafter,
she or he may believe that they “survived” the feared situa-
tion only because they engaged in the safety behavior.
However, they may have denied themselves the opportunity
to learn that they could have managed the situation ade-
quately without doing so. Safety behaviors often interfere
with the execution of competent social behaviors and inad-
vertently lead to the very negative consequences that
patients seek to avoid.
31
The socially anxious individuals who speak little in
social situations, fearing they might say the wrong words if
they fully engage the conversation, are likely to evoke nega-
tive reactions in their conversation partners and thus miss
opportunities for future positive social interactions and the
development of meaningful relationships. It is therefore
important to design behavioral experiments that require the
abandonment of these behaviors in order to give patients the
opportunity to be exposed to corrective information about
their false beliefs.
Thus, most cognitive techniques include an exposure
component and are rarely purely cognitive. In fact, several
treatment protocols have combined exposure with other
treatment components, most notably, cognitive-behavioral
group therapy (CBGT).
33
In CBGT, groups of 4–7 patients,
balanced with regard to age and sex, are led by male and
female cotherapists and typically meet for 12 weekly
2.5-hour sessions. The first two sessions are devoted to pro-
viding patients with a cognitive-behavioral model of SAD
and to introducing the concepts of exposure, homework, and
cognitive restructuring. Structured exercises are used to
teach patients the concepts and procedures involved in the
identification, logical analysis, and disputation of negative
automatic thoughts. During the remaining 10 sessions, ther-
apists plan graduated individualized exposure role-plays for
patients that allow them to examine and modify their nega-
tive thoughts before, during, and after exposure to feared
situations. Therapist-directed cognitive-restructuring exer-
cises and coaching are integrated with exposure to feared
situations to provide opportunities for testing the veracity
of patients’ negative thoughts. Furthermore, homework
assignments are developed for each patient at the end of each
session; these usually consist of exposures to real-life situa-
tions. When approaching feared situations outside of group
sessions, patients are encouraged to utilize cognitive-restruc-
turing skills before, during, and after the homework event.
Relaxation Training
Individuals with SAD often experience excessive physio-
logic arousal when confronted with, or in anticipation of,
feared social situations, and this arousal may interfere with
optimal social performance. Effective relaxation strategies
provide patients with a means of coping with these physio-
logic manifestations of social anxiety.
Current approaches to relaxation training are derived
from the work of Wolpe,
34
Bernstein and Borkovec,
35
and
Bernstein and colleagues,
36
and involve exercises aimed at
the relaxation of different muscle groups (both in-session and
as homework assignments). Progressive muscle relaxation
practices involve focusing on particular muscle groups, tens-
ing for 5–10 seconds, releasing the tension, and noticing the
difference between sensations accompanying tension and
relaxation. Progressive muscle relaxation begins by working
on 16 muscle groups, Its focus is on progressively larger
muscle groups in order to achieve relaxation rapidly. Further,
patients may be taught cue-controlled relaxation, which
involves the repeated pairing of a word (eg, “relax”) with a
relaxed bodily state, and then using the word as a cue to
achieve a relaxed state during everyday activities. These
relaxation strategies are most effective in the treatment of
SAD if ultimately applied in feared social situations.
Applied relaxation involves three skills to be acquired in
treatment: recognition of the early sensations of anxiety and
physiologic arousal; proficiency in achieving a relaxed state
quickly while engaging in daily activities; and use of relax-
ation strategies in anxiety-provoking situations. Applied
relaxation for socially anxious individuals combines relax-
ation techniques with exposure to feared situations.
37
Social Skills Training
Social skills training for SAD is based on the premise
that socially anxious patients exhibit behavioral deficien-
cies (eg, poor eye contact, poor conversation skills) that
elicit negative reactions from others, thereby causing social
interactions to be punishing and anxiety-inducing for the
patient. Social skills training is comprised of several tech-
niques designed to reduce these deficiencies. These tech-
niques include therapist modeling, behavioral rehearsal,
corrective feedback, social reinforcement, and homework
assignments. Research on this phenomenon has produced
conflicting results, with some studies finding performance
deficits among socially anxious persons
38,39
and others fail-
ing to do so.
40,41
It is important to note that any therapeutic efficacy of
social skills training is not necessarily attributable to the
remediation of deficiencies in the patient’s repertoire of
social skills, although this possibility is equally viable.
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Alternatively, social skills training may yield therapeutic
effects due to the training aspects (eg, repeated practice of
feared social behaviors), the exposure aspects (eg, con-
frontation of feared situations) or the cognitive elements (eg,
corrective feedback about the adequacy of one’s social
behavior) inherent in the instruction of such skills.
Regardless, social skills training may be easily combined
with other techniques, such as cognitive restructuring or
exposure. For instance, Social Effectiveness Training
42
is a
multicomponent treatment package that combines exposure
with social skills training and education in a mixture of
group and individual formats.
EFFICACY OF COGNITIVE-BEHAVIORAL
THERAPY FOR SOCIAL ANXIETY DISORDER
A large number of outcome studies have been conducted
in the last 2 decades. In order to evaluate the efficacy of
CBT for SAD, meta-analytic strategies have been increas-
ingly used to examine this large and growing literature.
Meta-analyses reduce the results of each study to a common
quantitative metric, the effect size (ES). The within-group
ES (also referred to as “uncontrolled”) denotes the number
of standard deviation units of improvement for patients
within a particular treatment group. An average within-
group ES of 1.0 for a specific treatment method signifies an
average improvement of one standard deviation unit for
patients in all studies who received a particular treatment.
These ESs should be interpreted with caution, however,
because they do not control for the influence of non-specific
factors or sample differences which may affect treatment.
43
In contrast, between-group ESs, also known as controlled
ESs, index the degree to which patients who receive a par-
ticular treatment improve more than patients in a control
condition, expressed in standard deviation units. An aver-
age between-group ES of 1.0 indicates that the treatment
group improved one standard deviation unit more than the
control group. Guidelines for the interpretation of the mag-
nitude of ESs are provided by Cohen,
44
who states that 0.20,
0.50, and 0.80 correspond to small, medium, and large
effects, respectively.
Five meta-analytic investigations have examined the effi-
cacy of CBT for SAD
43,45-48
and have provided very promising
findings. The overall within-group ES for CBT has been large.
For example, Chambless and Hope
45
meta-analyzed 8 con-
trolled CBT studies that compared the relative efficacies of
CBGT, exposure and anxiety management, and applied relax-
ation training. CBT demonstrated an average within-group ES
of 0.94. Thus, patients receiving CBT demonstrate substantial
improvement in social anxiety symptoms after treatment.
Furthermore, in comparison with control groups, CBT
appears to be an effective treatment, more beneficial than
placebo, supportive counseling, and wait-list control groups
(average within-group ES of 0.3). The overall controlled ES
for CBT was reported to be 0.74 by Gould and colleagues.
47
CBT has not only been found efficacious in the short-
term but also in follow-up investigations. Uncontrolled pre-
treatment to follow-up ESs indicate that treatment gains are
maintained after CBT ends (average ESs ranging from
0.78–1.31 for various types of CBT, with average follow-up
intervals ranging from 3.65–4.75 months).
43,45,46,48
These ESs
are generally larger than pre- to posttreatment ESs, suggest-
ing that most patients either maintained their gains or made
additional improvements. The one uncontrolled ES calcu-
lated for change between posttreatment and follow-up
(0.23)
47
supports this assertion, indicating a small effect for
additional improvement during follow-up.
CBT appears to be an efficacious treatment for SAD in
both the short- and long-term. However, the aforementioned
analyses do not speak to the relative efficacy of the variety
of CBT types. Many CBT treatments are comprised of het-
erogeneous procedures, often including more or less focus
on behavioral techniques (eg, exposure, relaxation, social
skills training), and/or cognitive strategies. Research has
attempted to elucidate what components may be important
in achieving treatment success, that is, which types of CBT
may be more or less important than others.
All five meta-analyses have addressed this question by
comparing the average ESs of different types of CBT. In a
meta-analysis of 24 studies, Feske and Chambless
43
investi-
gated the differential effects of treatments combining expo-
sure with cognitive restructuring and treatments using only
exposure. Mean uncontrolled ESs were generally indicative
of large treatment effects and were similar for the two groups
of treatments (exposure and combined, 0.99 and 0.90,
respectively); controlled ESs, however, suggested a better
treatment response for exposure-only treatments (1.06 and
0.38, respectively). The combined treatments, however,
were compared with more stringent control groups than the
exposure treatments. Of the seven combined treatment stud-
ies, two included placebo and educational support group
control conditions, whereas exposure-only treatments were
all compared with wait-list control groups. Thus, this differ-
ence in control conditions may have attenuated controlled
ESs for the combined treatment group. The authors of this
meta-analysis excluded several studies supportive of the
use of cognitive techniques in combination with exposure,
and thus, the results may be somewhat skewed toward
greater efficacy of exposure-only treatments.
In contrast to Feske and Chambless,
43
Gould and col-
leagues
47
meta-analyzed 27 trials of CBT and found the
largest controlled ESs for both exposure therapy (0.89) and
the combination of exposure and cognitive restructuring
(0.80). Treatments involving cognitive restructuring alone
(0.60) and social skills training (0.60) were moderately effi-
cacious. Similarly, among psychological treatments for SAD
recently meta-analyzed by Fedoroff and Taylor,
46
combined
(cognitive restructuring and exposure) therapy, cognitive
restructuring alone, social skills training, and applied relax-
ation demonstrated significant effects at posttreatment (the
average within-group ESs were 0.84, 0.72, 0.64, and 0.51,
respectively). For studies of exposure treatment alone, the
average ES (1.08) was large, but there was a great deal of
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variability among studies, and the confidence interval
around this figure overlapped with zero, suggesting a non-
significant average treatment effect.
Finally, Taylor
48
examined the relative efficacy of cogni-
tive restructuring, exposure therapy, combined cognitive
restructuring and exposure, and social skills training in a
meta-analysis of 42 treatment-outcome trials for SAD. For
all active CBT treatments, improvements in social anxiety
were similar and superior to those of wait-list control
groups. However, when compared with placebo-controlled
groups (pill placebo or attention placebo), only the treat-
ments combining cognitive restructuring and exposure were
significantly better.
Thus, these results suggest that combined and pure expo-
sure treatments do not consistently result in different treat-
ment outcomes, and the addition of cognitive techniques
may neither deter nor increase the efficacy of exposure
treatments. Analyses of follow-up data show that all active
treatments result in maintenance of gains. In the meta-
analysis by Feske and Chambless,
43
improvements were
maintained in both exposure-only and combined treatments,
resulting in similar average within-group ESs for both
groups at follow-up (1.04 and 1.10, respectively). Fedoroff
and Taylor
46
report that there were no differences between
the four reviewed CBT treatments (exposure, cognitive-
restructuring, combined exposure and cognitive restructur-
ing, and social skills training) at follow-up.
In summary, while research clearly supports CBT as an
efficacious treatment for SAD, the question of which vari-
eties of CBT are most beneficial has not been resolved.
Evidence points to exposure and treatments using both cog-
nitive strategies and exposure as the most efficacious. Social
skills training or relaxation training do not appear to be
indicated for every patient and may have less impact on the
patient who is socially facile or who reports little physiologic
arousal, respectively. However, the question of whether the
addition of cognitive strategies increases treatment gains
above those achieved by exposure alone is still unresolved.
Several possible explanations have been suggested for the
general lack of difference in comparisons of exposure and
combined treatments. First, it is possible that these overall no-
difference results are due to the actual implementation of
exposure and combined interventions overlap. For example,
exposure treatments often include therapist feedback about
the patient’s performance or the (lack of) visibility of anxiety
symptoms.
49
Such interventions may not be labeled as cogni-
tive, yet they share common features with cognitive interven-
tions, which may increase the frequency of no-difference
findings. Second, those studies that have found an added ben-
efit of cognitive procedures may reflect chance findings.
50
Finally, it is possible that, for some patients, exposure-only
treatments are sufficient to produce significant improvements,
whereas other individuals may require the addition of cogni-
tive-restructuring to achieve optimal outcomes. Unfortunately,
it is not yet known which variables may identify those groups
of patients.
51
Whether or not cognitive techniques are shown to
be necessary in the treatment of SAD, it appears that individu-
als who demonstrate more cognitive change (as assessed with
measures of rational thinking, positive and negative self-state-
ments, or thought listing procedures after behavior tests and
the like) show greater improvements in social anxiety.
52,53
Although cognitive change is an important or even necessary
part of reduction in social anxiety, it is not clear whether
changes in maladaptive thinking require the use of cognitive
techniques. Furthermore, the correlational nature of the rela-
tionship between cognitive and clinical change leaves open
the possibility that greater cognitive change may either lead to
or be a consequence of clinical improvement.
45
COGNITIVE-BEHAVIORAL THERAPY
AND PHARMACOTHERAPY FOR
SOCIAL ANXIETY DISORDER
A number of medications have demonstrated superiority
to placebo in at least one published double-blind study of
the treatment of SAD, including the selective serotonin
reuptake inhibitors paroxetine, sertraline, and fluvoxamine;
the monoamine oxidase inhibitor phenelzine; the reversible
inhibitors of monoamine oxidase brofaromine; the high-
potency benzodiazepine clonazepam; and the anticonvul-
sant gabapentin.
54
Few studies have directly compared the
relative efficacy of CBT and pharmacotherapy for SAD.
However, many published studies have examined either the
efficacy of CBT or the efficacy of pharmacotherapy. Thus,
we turn again to the meta-analyses that summarized and
compared these treatment methods statistically.
Two of the meta-analyses discussed earlier also examined
the relative efficacy of CBT and pharmacotherapy for SAD.
Gould and colleagues
47
reported similar controlled effect
sizes for cognitive-behavioral (0.74) and pharmacologic
(0.62) interventions on measures of social anxiety. Federoff
and Taylor,
46
however, report superior effect sizes for acute
pharmacotherapy. Benzodiazepines were superior to most
cognitive-behavioral interventions, but this was not the case
for either the monoamine oxidase inhibitors or selective sero-
tonin reuptake inhibitorss. It was not possible to examine
whether pharmacotherapy was associated with maintenance
of gains as reported earlier for CBT because these data were
not generally reported for medication treatments.
As previously mentioned, there are few studies directly
investigating the relative efficacy of medication and CBT
approaches. Of the few studies which have been conducted to
date, two used medication treatments, buspirone and atenolol,
which have not demonstrated superiority to placebo in con-
trolled trials.
55,56
Other studies included specific instructions
to engage in exposure to feared situations for patients receiv-
ing medication or placebo, making results difficult to inter-
pret.
57,58
One of these studies found that both clonazepam with
exposure instructions and CBGT produced significant and
similar improvements on clinician-rated measures.
58
In this
study, some self-report measures indicated greater improve-
ment for the medication/exposure condition among treatment
completers, but not in intent-to-treat analyses.
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Heimberg and colleagues
59
compared the relative effi-
cacy of group CBT and phenelzine with two control condi-
tions in a sample of 133 patients with SAD. The first was a
pill placebo, the second an educational supportive therapy
designed to resemble group CBT in credibility and genera-
tion of positive outcome expectations. In a conservative
analysis of the impact of the treatments, individuals who
dropped out of treatment were counted as nonresponders.
After 12 weeks of treatment, 58% of the patients treated
with group CBT and 65% of those patients treated with
phenelzine were classified as responders by independent
assessors, not significantly different from each other, but
significantly better than the placebo conditions. Individuals
on phenelzine typically responded faster, but showed much
greater rates of relapse after 6 months of maintenance treat-
ment and a 6-month follow-up period than did individuals
treated with group CBT.
60
Finally, we examine whether combining CBT and pharma-
cotherapy increases treatment gains. There are at least three
possible outcomes of combining medication and CBT: syner-
gistic effects on improvements, preservation of an equivalent
treatment response, or reduced efficacy. Synergistic effects
might occur if the combination of treatments increases an
individual’s likelihood for a positive response or it increases
the magnitude of improvements across individuals. There
would be little benefit to combining treatments if both med-
ication and CBT target the same aspects of SAD. The combi-
nation of interventions may result in decreased treatment
efficacy if patients receiving both medication and CBT
believe that the medication is the primary agent of change
and they consequently invest less in the activities involved in
CBT. This phenomenon has been studied in patients with
agoraphobia who received the combination of alprazolam and
exposure or relaxation treatment.
61
In this investigation,
patients who attributed improvements more to medication
than to their own efforts and who felt less confident in coping
without medication after 8 weeks of treatment showed higher
relapse rates and more withdrawal symptoms during drug
taper and follow-up periods.
Although common in clinical practice of the treatment of
SAD, empirical investigations of a combined treatment
strategy are lacking. Two published studies that have exam-
ined this issue used medications which were not superior to
placebo in controlled studies.
55,62
In another study,
63
expo-
sure combined with sertraline was not more efficacious than
sertraline and placebo. The follow-up investigation of the
Heimberg-Liebowitz collaborative study
64
includes a
phenelzine/CBGT combination condition. Preliminary
results show some evidence of superior treatment response
in the combined treatment. However, knowledge in this area
of research on the treatment of SAD is still lacking.
In summary, research supports the efficacy of both phar-
macotherapy and CBT for SAD. Pharmacotherapy may show
somewhat greater acute efficacy and may be associated with
quicker response. CBT may confer greater protection
against relapse. The evidence is also extremely limited for
how CBT and pharmacotherapeutic interventions might
work together in the treatment of SAD.
FUTURE DIRECTIONS IN TREATMENT
FOR SOCIAL ANXIETY DISORDER
Stein
65
has made a case for “cognitive-behaviorally
informed pharmacotherapy,” emphasizing the best possible
integration of resources to produce the best possible level of
care for the patient. Looking at how medication and therapy
respectively contribute to improvement can inform which
patients benefit from which intervention, and even if both
modalities are necessary. It should not be automatically
assumed that a combination of two effective treatments is
better than one intervention alone. However, we know little
about the specific characteristics of the patient that will
allow us to make this prediction. We also need to keep in
mind that not all cognitive-behavioral techniques may com-
bine equally well with medications and may do so better
with some medications than others. For instance, medica-
tions that inhibit the experience of anxiety, such as benzodi-
azepines or β-blockers, may be relatively poorer candidates
for combination with exposure techniques.
Future investigators of the combination of CBT and med-
ication may need to think outside the box when considering
how best to combine these two treatment modalities.
27
We
should not automatically think of the simultaneous adminis-
tration of both treatments. It would be of great interest to
know the relative efficacy of different methods of starting
and sequencing these aspects of treatment. For instance,
one might start a patient on medication first to take the edge
off his or her fears and promote quicker entry into feared sit-
uations. The medication might be phased out as the patient
learns cognitive-behavioral skills for coping with anxious
arousal. Cognitive-behavioral interventions might also be
used to help patients with SAD discontinue medications on
which they have become psychologically or physically
dependent, as has been done quite successfully with panic
disorder patients.
66
A similar strategy might be utilized with
patients who have used medications successfully but who
may be likely to relapse on medication discontinuation.
CBT might also be used to augment gains in partial respon-
ders to pharmacotherapy.
CONCLUSION
SAD is a prevalent, often debilitating fear of participating
in one or more social or performance situations. Cognitive-
behavioral models of SAD suggest that it is based, in part,
on distorted, catastrophic appraisals of the consequences of
physiologic and behavioral reactions to social situations.
Both CBT and pharmacologic interventions have been
shown to have efficacy in the treatment of SAD. What is less
clear is the active mechanisms of change in these cases and
how these treatments can be most effectively integrated to
provide the patient the best quality care. As yet, little is
known about the ways in which specific CBT techniques are
best combined with specific pharmacotherapies. In fact,
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380
there remains much to learn about the best methods of com-
bining the different techniques of CBT. These are clearly
important agenda for future research.
REFERENCES
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed.. Washington, DC: American Psychiatric Press, Inc.; 1994.
2. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence
of DSM-III-R psychiatric disorders in the United States: results from the
National Comorbidity Survey. Arch Gen Psychiatry. 1994;51:8-19.
3. Narrow WE, Rae DS, Robins LR, Regier DA. Revised prevalence estimates of
mental disorders in the United States: using a clinical significance criterion to
reconcile 2 surveys’ estimates. Arch Gen Psychiatry. 2002;59:115-123.
4. Weiller E, Bisserbe J-C, Boyer P, Lepine JP, Lecrubier Y. Social phobia in gen-
eral health care: an unrecognized, undertreated, disabling disorder. Br J
Psychiatry. 1996;168:169-174.
5. Whisman M, Sheldon C, Goering P. Psychiatric disorders and dissatisfaction
with social relationships: does type of relationship matter? J Abnorm Psychol.
2000;109:803-808.
6. La Greca AM, Lopez N. Social anxiety among adolescents: linkages with peer
relations and friendships. J Abnorm Child Psychol. 1998;26:83-94.
7. Wittchen H, Fuetsch M, Sonntag H, Muller N, Liebowitz M. Disability and
quality of life in pure and comorbid social phobia-findings from a controlled
study. Eur Psychiatry. 1999;14:118-131.
8. Schneier FR, Johnson J, Hornig CD, et al. Social phobia. Comorbidity and mor-
bidity in an epidemiologic sample. Arch Gen Psychiatry. 1992;49:282-288.
9. Lelliott P, McNamee G, Marks I. Features of agora, social, and related phobias
and validation of the diagnoses. J Anxiety Disord. 1991;5:313-322.
10. Ballenger J, Davidson J, Lecrubier Y, et al. Consensus statement on social
anxiety disorder from the International Consensus Group on Depression and
Anxiety. J Clin Psychiatry. 1998;59(suppl. 17):54-60.
11. Stein M, McQuaid J, Laffaye C, et al. Social phobia in the primary medical
care setting. J Fam Pract. 1999;49:514-519.
12. Mannuzza S, Schneier F, Chapman T, et al. Generalized social phobia.
Reliability and validity. Arch Gen Psychiatry. 1995;52:230-237.
13. Olfson M, Fireman B, Weissman M, et al. Mental disorders and disability
among patients in a primary care group practice. Am J Psychiatry.
1997;154:1734-1740.
14. Schneier F, Heckelman L, Garfinkel R, et al. Functional impairment in social
phobia. J Clin Psychiatry. 1994;55:322-331.
15. Rapee RM, Heimberg RG. A cognitive-behavioral model of anxiety in social
phobia. Behav Res Ther. 1997;35:741-756.
16. Turk CL, Lerner J, Heimberg RG, Rapee RM. An integrated cognitive-behav-
ioral model of social anxiety. In: Hofmann SG, DiBartolo PM, eds. From Social
Anxiety to Social Phobia: Multiple Perspectives. Needham Heights, Mass:
Allyn & Bacon; 2001:281-303.
17. Roth DA., Heimberg RG. Cognitive-behavioral models of social anxiety disor-
der. In: Schneier FR, ed. Psychiatric Clinics of North America: Social Anxiety
Disorder. vol. 24. New York, NY: W. B. Saunders Company; 2001:753-771.
18. Rapee, RM. Descriptive psychopathology of social phobia. In: Heimberg RG,
Liebowitz MR, Hope DA, Schneier FR, eds. Social Phobia: Diagnosis,
Assessment, and Treatment. New York, NY: Guilford Press; 1995:41-66.
19. Kagan J, Snidman N. Infant predictors of inhibited and uninhibited profiles.
Psychol Science. 1991;2:40-44.
20. Schwartz CE, Snidman N, Kagan J. Adolescent social anxiety as an outcome of
inhibited temperament in childhood. J Am Acad Child Adolesc Psychiatry.
1999;38:1008-1015.
21. Matheny A Jr. Children’s behavioral inhibition over age and across social situ-
ations: genetic similarity for a trait during change. J Pers. 1989;57:215-235.
22. Kendler KS, Neale MC, Kessler RC, et al. The genetic epidemiology of pho-
bias in women. The interrelationship of agoraphobia, social phobia, situation-
al phobia, and simple phobia. Arch Gen Psychiatry. 1992;49:273-281.
23. Coles ME, Heimberg RG. Memory biases in the anxiety disorders: current sta-
tus. Clin Psychol Review. 2002;22:587-627.
24. Hackmann A, Clark DM, McManus F. Recurrent images and early memories
in social phobia. Behav Res Ther. 2000;38:601-610.
25. Foa EB, Franklin ME, Perry KJ, Herbert JD. Cognitive biases in generalized
social phobia. J Abnorm Psychol. 1996;105:433-439.
26. Clark DM, Wells A. A cognitive model of social phobia. In: Heimberg RG,
Liebowitz MR, Hope DA, Schneier FR, eds. Social Phobia: Diagnosis,
Assessment, and Treatment. New York, NY: Guilford Press; 1995:69-93.
27. Heimberg RG. Cognitive-behavioral therapy for social anxiety disorder: cur-
rent status and future directions. Biol Psychiatry. 2002;51:101-108.
28. Foa EB, Kozak MJ. Emotional processing of fear: exposure to corrective infor-
mation. Psychol Bull. 1986;99:20-35.
29. Wells A, Papageorgiou C. Social phobia: effects of external attention on anxi-
ety, negative beliefs, and perspective taking. Behav Ther. 1998;29:357-370.
30. Beck AT, Rush J, Shaw BF, et al. Cognitive Therapy of Depression. New York,
NY: Guilford Press; 1987.
31. Wells A, Clark DM, Salkovskis P, et al. Social phobia: the role of in-situation
safety behaviors in maintaining anxiety and negative beliefs. Behav Ther.
1995;26:153-161.
32. Morgan H, Raffle C. Does reducing safety behaviours improve treatment response
in patients with social phobia? Aust N Z J Psychiatry. 1999;33:503-510.
33. Heimberg RG, Becker RE. Cognitive-Behavioral Treatment for Social Phobia:
Basic Mechanisms and Clinical Strategies. New York, NY: Guilford Press; 2002.
34. Wolpe J. Psychotherapy by Reciprocal Inhibition. Stanford, Calif: Stanford
University Press; 1958.
35. Bernstein DA, Borkovec TD. Progressive Relaxation Training: A Manual for
the Helping Professions. Champaign, Ill: Research Press; 1973.
36. Bernstein DA, Borkovec TD, Hazlett-Stevens H. New Directions in Progressive
Relaxation Training: A Guidebook for Helping Professionals. Westport, CT:
Praeger Publishers/Greenwood Publishing Group, Inc.; 2000.
37. Ost LG. Applied relaxation: description of a coping technique and review of
controlled studies. Behav Res Ther. 1987;25:397-409.
38. Halford K, Foddy M. Cognitive and social skills correlates of social anxiety. Br
J Clin Psychol. 1982;21:17-28.
39. Stopa L, Clark DM. Cognitive processes in social phobia. Behav Res Ther.
1993;31:255-267.
40. Glasgow RE, Arkowitz H. The behavioral assessment of male and female
social competence in dyadic heterosexual interactions. Behav Ther.
1975;6:488-498.
41. Rapee RM, Lim L. Discrepancy between self- and observer ratings of perfor-
mance in social phobics. J Abnorm Psychol. 1992;101:728-731.
42. Turner SM, Beidel DC, Cooley MR, et al. A multicomponent behavioral treat-
ment for social phobia: social effectiveness therapy. Behav Res Ther.
1994;32:381-390
43. Feske U, Chambless DL. Cognitive behavioral versus exposure only treatment
for social phobia: a meta-analysis. Behav Ther. 1995;26:695-720.
44. Cohen J. Statistical Power Analysis for the Sciences. New York, NY: Academic
Press; 1977.
45. Chambless DL, Hope DA. Cognitive approaches to the psychopathology and
treatment of social phobia. In: Salkovskis PM, ed. Frontiers of Cognitive
Therapy. New York, NY: Guilford Press; 1996:345-382.
46. Fedoroff IC, Taylor S. Psychological and pharmacological treatments of social
phobia: a meta-anlaysis. J Clin Psychopharmacol. 2001;3:311-324.
47. Gould RA, Buckminster S, Pollack MH, et al. Cognitive-behavioral and phar-
macological treatment for social phobia: a meta-analysis. Clin Psychol: Sci
Prac. 1997;4:291-306.
48. Taylor S. Meta-analysis of cognitive-behavioral treatments for social phobia.
J Behav Ther Exp Psychiatry. 1996;27:1-9.
49. Newman MG, Hofmann SG, Trabert W, et al. Does behavioral treatment of
social phobia lead to cognitive changes? Behav Ther. 1994;25:503-517.
50. Scholing A, Emmelkamp PM. Exposure with and without cognitive therapy for
generalized social phobia: effects of individual and group treatment. Behav
Res Ther. 1993;31:667-681.
51. Scholing A, Emmelkamp PM. Treatment of generalized social phobia: results
at long-term follow-up. Behav Res Ther. 1996;34:447-452.
CNS
Review Article
Volume 8 – Number 5 CNS Spectrums - May 2003
373-381_0503CNS_Hambrick 5/18/03 9:26 AM Page 380
381
52. Mattick RP, Peters L. Treatment of severe social phobia: effects of guid-
ed exposure with and without cognitive restructuring. J Consult Clinl
Psychol. 1988;56:251-260.
53. Mattick RP, Peters L, Clarke JC. Exposure and cognitive restructuring
for social phobia: a controlled study. Behav Ther. 1989;20:3-23.
54. Blanco C, Antia SX, Liebowitz, MR. Pharmacotherapy of social anxiety
disorder, Biol Psychiatry. 2002;51:109-120.
55. Clark DB, Agras WS. The assessment and treatment of performance
anxiety in musicians. Am J Psychiatry. 1991;148:598-605.
56. Turner SM Beidel, DC, Jacob RG. Social phobia: a comparison of behav-
ior therapy and atenolol. J Consult Clin Psychol. 1994;62:350-358.
57. Gelernter CS, Uhde TW, Cimbolic P, et al. Cognitive-behavioral and
pharmacological treatments of social phobia. A controlled study. Arch
Gen Psychiatry. 1991;48:938-945.
58. Otto MW, Pollack MH, Gould RA, Worthington JJ 3rd, McArdle ET,
Rosenbaum JF. A comparison of the efficacy of clonazepam and cogni-
tive-behavioral group therapy for the treatment of social phobia.
J Anxiety Disorders. 2000;14:345-358.
59. Heimberg RG, Liebowitz MR, Hope DA, et al. Cognitive behavioral
group therapy vs. phenelzine therapy for social phobia: 12-week out-
come. Arch Gen Psychiatry. 1998;55:1133-1141.
60. Liebowitz MR, Heimberg RG, Schneier FR, et al. Cognitive-behavioral
group therapy versus phenelzine in social phobia: long-term outcome.
Depress Anxiety. 1999;10:89-98.
61. Basoglu M, Marks IM, Kilic C, Brewin CR, Swinson RP. Alprazolam
and exposure for panic disorder with agoraphobia. Attribution of
improvement to medication predicts subsequent relapse. Br J
Psychiatry. 1994;164:652-659.
62. Falloon IR, Lloyd GG, Harpin RE. The treatment of social phobia.
Real-life rehearsal with nonprofessional therapists. J Nerv Ment Dis.
1981;169:180-184.
63. Blomhoff S, Haug TT, Hellström K, et al. Randomised controlled gener-
al practice trial of sertraline, exposure therapy, and combined treatment
in generalised social phobia. Br J Psychiatry. 2001;179:23-30.
64. Heimberg RG. The understanding and treatment of social anxiety: what
a long strange trip it’s been (and will be). Presidential address present-
ed at: Annual Meeting of the Association for Advancement of Behavior
Therapy; November 15-17, 2002; Reno, Nev.
65. Stein MB. Is the combination of medication and psychotherapy better
than either alone? Paper presented at: Annual Meeting of the Anxiety
Disorders Association of America; March 21-24, 2002; Austin, Tex.
66. Otto MW, Pollack MH, Sachs GS, et al. Discontinuation of benzodi-
azepine treatment: efficacy of cognitive-behavioral therapy for patients
with panic disorder. Am J Psychiatry. 1993;150:1485-1490.
Review Article
Volume 8 – Number 5 CNS Spectrums - May 2003
2. Foa EB, Franklin ME, Kozak MJ. Psychosocial treatments for obsessive-com-
pulsive disorder: literature review. In: Swinson RP, Antony MM, eds.
Obsessive-Compulsive Disorder: Theory, Research, and Treatment. New York,
NY: Guilford Press; 1998:258-276.
3. Franklin ME, Foa EB. Cognitive-behavioral treatment of obsessive-compul-
sive disorder. In: Nathan PE, Gorman JM, eds. A Guide to Treatments That
Work. New York, NY: Oxford University Press; 1998:339-357.
4. Rauch SL, Jenike MA. Pharmacological treatment of obsessive-compulsive
disorder. In: Nathan PE, Gorman JM, eds. A Guide to Treatments That Work.
New York, NY: Oxford University Press; 1998:358-376.
5. Greist J, Chouinard G, DuBoff E, et al. Double-blind parallel comparison of
three dosages of sertraline and placebo in outpatients with obsessive-compul-
sive disorder. Arch Gen Psychiatry. 1995;52:289-295.
6. Goodman WK, Price LH, Rasmussen SA, Delgado PL, Heninger GR, Charney
DS. Efficacy of fluvoxamine in obsessive-compulsive disorder. A double-blind
comparison of fluvoxamine and placebo. Arch Gen Psychiatry. 1989;46:36-40.
7. Wheadon DE, Bushnell WD, Steiner M. A fixed-dose comparison of 20, 40 or
60 mg paroxetine to placebo in the treatment of OCD. Paper presented at:
Annual Meeting of the American College of Neuropsychopharmaclogy;
December 7-11, 1993; Honolulu, Hawaii.
8. Tollefson G, Birkett M, Koran L, Genduso L. Continuation treatment of OCD:
double-blind and open-label experience with fluoxetine. J Clin Psychiatry.
1994;55:69-78.
9. Foa EB, Kozak MJ. Psychological treatment for obsessive-compulsive disor-
der. In: Mavissakalian MR, Prien RF, eds. Long-term Treatment of Anxiety
Disorders. Washington, DC: American Psychiatric Press; 1996:285-309.
10. Ravizza L, Maina G, Bogetto F, Albert U, Barzega G, Bellino S. Long-term
treatment of obsessive-compulsive disorder. CNS Drugs. 1998;10:247-255.
11. Zohar J, Sasson Y, Chopra M, Amital D, Iancu I. Pharmacological treatment of
obsessive-compulsive disorder: a review. In: Maj M, Sartorius N, Okasha A,
Zohar J, eds. Obsessive-Compulsive Disorder. New York, NY: John Wiley &
Sons, Inc.; 2000:43-92.
12. Leonard H, Swedo S, Lenane M, et al. A double-blind desipramine substitu-
tion during long-term clomipramine treatment in children and adolescents
with obsessive-compulsive disorder. Arch Gen Psychiatry. 1991;48:922-927.
13. Marks IM, Lelliott P, Basoglu M, et al. Clomipramine, self-exposure and ther-
apist-aided exposure for obsessive-compulsive rituals. Br J Psychiatry.
1988;152:522-534.
14. O’Sullivan G, Noshirvani H, Marks I, Monteiro W, Lelliott P. Six-year follow-
up after exposure and clomipramine therapy for obsessive-compulsive disor-
der. J Clin Psychiatry. 1991;52:150-155.
15. deHaan E, van Oppen P, van Balkom AJLM, Spinhoven P, Hoogduin CAL, van
Dyck R. Prediction of outcome and early versus late improvement in OCD
patients treated with cognitive behaviour therapy and pharmacotherapy. Acta
Psychiatr Scand. 1997;96:354-362.
16. Cottraux J, Mollard E, Bouvard M, Marks I. Exposure therapy, fluvoxamine, or
combination treatment in obsessive-compulsive disorder: one-year follow-up.
Psychiatry Res. 1993;49:63-75.
17. Baer L, Ricciardi J, Keuthen N, et al. Discontinuing obsessive-compulsive
disorder medication with behavior therapy. Am J Psychiatry. 1994;151:1842.
18. American Psychiatric Association. Diagnostic and Statistical Manual of
Mental Disorders. 3rd ed rev. Washington, DC: American Psychiatric
Association; 1987.
19. Goodman WK, Price LH, Rasmussen SA, et al. The Yale-Brown Obsessive-
Compulsive Scale (Y-BOCS): past development, use, and reliability. Arch Gen
Psychiatry. 1989;46:1006-1016.
20. Foa EB, Grayson JB, Steketee GS, et al. Success and failure in the behavioral
treatment of obsessive-compulsives. J Consult Clin Psychol. 1983;51:287-297.
21. Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatry.
1960;23:56-62.
22. Hedlund J, Vieweg B. The Hamilton Rating Scale for Depression: a compre-
hensive review. J Operating Psychiatry. 1979;10:149-165.
23. Foa EB, Kozak MJ, Goodman WK, Hollander E, Jenike MA, Rasmussen SA.
DSM-IV field trial: obsessive-compulsive disorder. Am J Psychiatry.
1995;152:90-94.
24. Pato MT, Zohar-Kadouch R, Zohar J, Murphy DL. Return of symptoms after
discontinuation of clomipramine in patients with obsessive-compulsive disor-
der. Am J Psychiatry. 1988;145:1521-1525.
Hembree continued from page 290
373-381_0503CNS_Hambrick 5/18/03 9:26 AM Page 381