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Cultural Considerations and
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Series in Anxiety and Related Disorders
Series Editor
Martin M. Antony
Professor, Department of Psychology
Ryerson University, Toronto, Ontario, Canada
For further volumes:
http://www.springer.com/series/6926
Michael W. Otto · Stefan G. Hofmann
Editors
Avoiding Treatment Failures
in the Anxiety Disorders
123
Editors
Michael W. Otto
Department of Psychology
Boston University
648 Beacon St.
Boston, MA 02215
USA
mwotto@bu.edu
Stefan G. Hofmann
Department of Psychology
Boston University
648 Beacon St.
Boston, MA 02215
USA
shofmann@bu.edu
ISBN 978-1-4419-0611-3
e-ISBN 978-1-4419-0612-0
DOI 10.1007/978-1-4419-0612-0
Springer New York Dordrecht Heidelberg London
Library of Congress Control Number: 2009938520
© Springer Science+Business Media, LLC 2010
All rights reserved. This work may not be translated or copied in whole or in part without the written
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Springer is part of Springer Science+Business Media (www.springer.com)
MWO: To my son, Jackson, for being who you are.
SGH: To Lukas, Benjamin, and Rosemary, for
making it easy to resolve life’s complications.
Preface
Over the last two decades, the field has witnessed dramatic advances in the conceptualization and treatment of anxiety disorders. Conditions, such as panic disorder,
that were once considered the domain of pharmacotherapy have now been shown
to be responsive to even ultra brief treatment protocols of cognitive-behavioral therapy (CBT). Indeed, the success of CBT across the anxiety disorders, and across the
diverse patients afflicted by these conditions, inspires confidence in both the principles of CBT and the models of the disorders on which they are based. Yet, in the
face of these clear advances, and the status of CBT as a first-line intervention for all
of the anxiety disorders, clinicians continue to be challenged by the persistence of
limited or poor treatment response among some patients. This volume is devoted to
addressing these challenges.
Authors of the chapters herein were responsible for integrating the latest in
empirical research on the nature and treatment of anxiety disorders with lessons
learned from actively working with patients in specialty clinic settings. The result
is a scholarly based, yet clinically applicable, discussion of issues of treatment nonresponse and the strategies used to address these clinical challenges. Interventions
that define empirically supported CBT for anxiety disorders are described in detail
and are complemented by novel clinical strategies and the variations in treatment
delivery that expert clinicians have applied with success. Accordingly, this volume
is designed to be of use to clinicians seeking to understand more about how CBT is
applied in the clinic as well as experienced clinicians seeking to find new strategies
to apply when standard interventions fail. This volume is also designed to provide a
state-of-the-art account of what is known and is not known about psychosocial treatment outcome for the anxiety disorders, thereby providing clinical researchers with
the latest evidence on principles of treatment, core intervention strategies, predictors
of nonresponse, and compensatory or novel interventions. By identifying treatment
complications and discussing strategies for resolving them, it is our hope that this
text will contribute to the further advancement of CBT for anxiety disorders.
Boston, Massachusetts
Michael W. Otto
Stefan G. Hofmann
vii
Contents
Part I
General Aspects of Treatment Complications
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Stefan G. Hofmann and Michael W. Otto
3
A Case Formulation Approach to Resolve Treatment Complications . .
Bethany A. Teachman and Elise M. Clerkin
7
Helping Exposure Succeed: Learning Theory Perspectives
on Treatment Resistance and Relapse . . . . . . . . . . . . . . . . . . .
Mark B. Powers, Bram Vervliet, Jasper A.J. Smits,
and Michael W. Otto
Therapeutic Alliance and Common Factors in Treatment . . . . . . . .
Daniella M. Halperin, Meara L. Weitzman, and Michael W. Otto
Combined Cognitive Behavioral and Pharmacologic Treatment
Strategies: Current Status and Future Directions . . . . . . . . . . . . .
Jasper A.J. Smits, Hannah E. Reese, Mark B. Powers, and Michael W. Otto
Cultural Considerations and Treatment Complications . . . . . . . . .
Stuart J. Spendlove, Carolyn T. Jackson, and Joaquin P. Borrego, Jr.
Part II
31
51
67
83
Avoiding Treatment Failures: Disorder-Specific Perspectives
Avoiding Treatment Failures in Panic Disorder . . . . . . . . . . . . . .
Heather W. Murray, R. Kathryn McHugh, and Michael W. Otto
103
Avoiding Treatment Failures in Obsessive Compulsive Disorder . . . . .
Luana Marques, Anne Chosak, Dieu-My Phan, Jeanne Fama,
Shana Franklin, and Sabine Wilhelm
125
Avoiding Treatment Failures in PTSD . . . . . . . . . . . . . . . . . . .
Claudia Zayfert and Jason C. DeViva
147
Avoiding Treatment Failures in Social Anxiety Disorder . . . . . . . . .
Stefan G. Hofmann, J. Anthony Richey, Anu Asnaani,
and Alice T. Sawyer
169
ix
x
Contents
Avoiding Treatment Failures in Generalized Anxiety Disorder . . . . .
Evelyn Behar and T.D. Borkovec
185
Avoiding Treatment Failures in Specific Phobias . . . . . . . . . . . . .
Georg W. Alpers
209
Part III Treatment Complications in Special Populations
Resolving Treatment Complications Associated with Comorbid
Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Christen M. Deveney and Michael W. Otto
231
Resolving Treatment Complications Associated with the
Presence of Comorbid Personality Disorders . . . . . . . . . . . . . . .
Matthew K. Nock, Tara L. Deliberto, and Michael Hollander
251
Resolving Treatment Complications Associated with Comorbid
Anxiety and Substance Use Disorders . . . . . . . . . . . . . . . . . . .
Elizabeth K. Reynolds, Matthew T. Tull, Idit Shalev, and C.W. Lejuez
271
Resolving Treatment Complications Associated with Comorbid
Eating Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Carolyn Black Becker, Claudia Zayfert, and Elizabeth M. Pratt
291
Resolving Treatment Complications Associated with Comorbid
Medical Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Joseph Greer, Jessica Graham, and Steven Safren
317
Resolving Treatment Complications in Children and Adolescents . . . .
Jamie A. Micco and Jill T. Ehrenreich
347
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
371
Contributors
Georg W. Alpers Department of Psychology, University of Würzburg, Germany;
Department of Psychology, University of Eichstätt, Eichstätt, Germany
J. Anthony Richey Department of Psychology, Boston University, Boston, MA,
USA
Anu Asnaani Department of Psychology, Boston University, Boston, MA, USA
Carolyn Black Becker Trinity University, San Antonio, TX, USA
Evelyn Behar University of Illinois, Chicago, IL, USA
T.D. Borkovec Penn State University, University Park, IL, USA
Joaquin P. Borrego Texas Tech University, Lubbock, TX, USA
Anne Chosak Department of Psychiatry, Massachusetts General Hospital and
Harvard Medical School, Boston, MA, USA
Elise M. Clerkin Department of Psychology, University of Virginia,
Charlottesville, VA, USA
Tara L. Deliberto Harvard University, Cambridge, MA, USA
Christen M. Deveney Department of Psychology, Boston University, Boston,
MA, USA
Jason C. DeViva Veterans Affairs Connecticut Health Care System, Newington,
CT, USA
Jill T. Ehrenreich Department of Psychology, University of Miami, Coral Gables,
FL, USA
Jeanne Fama Massachusetts General Hospital and Instructor at Harvard Medical
School, Boston, MA, USA
Shana Franklin OCD and Related Disorders Clinic, Massachusetts General
Hospital and Harvard Medical School, Boston, MA, USA
xi
xii
Contributors
Jessica Graham Department of Psychology, University of Massachusetts, Boston,
MA, USA
Joseph Greer Department of Psychology, Bronfman Science Center, Williams
College, Williamstown, MA, USA
Daniella M. Halperin Department of Psychology, Boston University, Boston,
MA, USA
Stefan G. Hofmann Department of Psychology, Boston University, Boston, MA,
USA
Michael Hollander Two Brattle Center, Cambridge, MA, USA
Carolyn T. Jackson Texas Tech University, Lubbock, TX, USA
C.W. Lejuez Center for Addictions, Personality, and Emotion Research,
Department of Psychology, University of Maryland, College Park, MD, USA
Luana Marques Department of Psychiatry, Massachusetts General Hospital and
Harvard Medical School, Boston, MA, USA
R. Kathryn McHugh Department of Psychology, Boston University, Boston,
MA, USA
Jamie A. Micco Massachusetts General Hospital and Harvard Medical School,
Cambridge, MA, USA
Heather W. Murray Department of Psychology, Boston University, Boston, MA,
USA
Matthew K. Nock Harvard University, Cambridge, MA, USA
Michael W. Otto Department of Psychology, Boston University, Boston, MA,
USA
Dieu-My Phan Body Dysmorphic Disorder Clinic, Massachusetts General
Hospital and Harvard Medical School, Boston, MA, USA
Mark B. Powers University of Amsterdam, Amsterdam, The Netherlands
Elizabeth M. Pratt Department of Psychology, Boston University, Boston, MA,
USA
Hannah E. Reese Harvard University, Cambridge, MA, USA
Elizabeth K. Reynolds Center for Addictions, Personality, and Emotion
Research, Department of Psychology, University of Maryland, College Park, MD,
USA
Steven Safren ABPP, Harvard Medical School; Behavioral Medicine, Department
of Psychiatry, Massachusetts General Hospital, Boston, MA, USA
Alice T. Sawyer Department of Psychology, Boston University, Boston, MA, USA
Contributors
xiii
Idit Shalev Department of Psychology, University of Maryland, College Park,
MD, USA
Jasper A.J. Smits Department of Psychology, Southern Methodist University,
Dallas, TX, USA
Stuart J. Spendlove Texas Tech University, Lubbock, TX, USA
Bethany A. Teachman Department of Psychology, University of Virginia,
Charlottesville, VA, USA
Matthew T. Tull Department of Psychiatry and Human Behavior, University of
Mississippi Medical Center, Jackson, MS, USA
Bram Vervliet University of Amsterdam, Amsterdam, The Netherlands
Meara L. Weitzman Department of Psychology, Boston University, Boston, MA,
USA
Sabine Wilhelm OCD and Related Disorders Clinic, Massachusetts General
Hospital and Harvard Medical School, Boston, MA, USA
Claudia Zayfert Dartmouth Hitchcock Medical Center, Lebanon, NH, USA
Part I
General Aspects of Treatment
Complications
Introduction
Stefan G. Hofmann and Michael W. Otto
Anxiety disorders are prevalent and disbling mental disorders. Although cognitivebehavioral therapy (CBT) is clearly effective, there is still room for improvement. In
this volume, the editors recruited a number of noted clinical researchers with extensive experience to contribute chapters covering the state-of-the-art CBT for anxiety
disorders, treatment complications encountered when applying these interventions
in clinical practice, and strategies for overcoming treatment failures when they are
encountered.
By definition, anxiety disorders are associated with significant distress or interference with the patient’s life and are associated with significant role disability. In
addition, anxiety disorders impose significant direct and indirect costs on the nation
in terms of medical resources as well as in reduced or lost productivity. In fact, it
is estimated that anxiety disorders are associated with greater economic costs than
any other mental disorder (DuPont, DuPont, & Rice, 2002).
Cognitive-behavioral therapy (CBT) is a gold standard treatment for the anxiety
disorders. Based on empirically supported models of the disorder, CBT provides a tailored set of interventions – often emphasizing exposure combined with
cognitive restructuring but also including other cognitive- and skill-based techniques (e.g., relaxation training or assertiveness training) – designed to modify the
self-perpetuating cycles that characterize the anxiety disorders.
CBT is clearly effective for anxiety disorders and offers direct benefits in terms
of symptom reduction, reduction in role disability, and enhancement of quality of
life, as demonstrated in numerous clinical trials. For example, a recent meta-analytic
review of randomized placebo-controlled CBT trials showed a mean effect size of
0.73 of CBT over psychosocial or pill placebo comparison conditions (Hofmann &
Smits, 2008). This body of work demonstrates that CBT strategies for anxiety disorders are more effective than the nonspecific effects of credible placebo interventions,
thus refuting the often-held belief that all psychotherapies are of equal effectiveness
with common (nonspecific) factors constituting the primary mechanism of action.
S.G. Hofmann (B)
Department of Psychology, Boston University, Boston, MA, USA
e-mail: shofmann@bu.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety Disorders,
Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_1,
C Springer Science+Business Media, LLC 2010
3
4
S.G. Hofmann and M.W. Otto
However, it is also clear that there is still considerable room for improvement to
help more patients achieve beneficial outcomes.
This book is designed to provide clinicians with detailed information on (1)
state-of-the-art CBT for anxiety disorders, (2) treatment complications encountered when applying these interventions in clinical practice, and (3) strategies
for overcoming treatment failures when they are encountered. This is achieved
by bringing together noted clinical researchers who have extensive experience
with CBT in the context of clinical practice, clinical supervision, and clinical
trials The chapters herein combine scholarly review of the literature with clinical experience and provides readers an empirically supported perspective that is
grounded in experience with providing targeted care to individuals in need. As
such, the text provides guidance useful for clinical practice as well as clinical
research.
The book is separated into three parts. Part I reviews the general aspects of
treatment complications. In order to facilitate the identification of treatment challenges, Teachman and Clerkin provide a case formulation approach in Chapter 2.
Powers, Vervliet, Smits, and Otto provide a learning theory perspective on treatment resistance and relapse in Chapter 3, and Halperin, Weitzman, and Otto discuss
therapeutic alliance and common treatment factors in Chapter 4. Issues of combined CBT and pharmacologic treatment are targeted by Chapter 5 by Smits,
Reese, Powers, and Otto. The contribution of cultural issues to treatment complications is examined by Spendlove, Jackson, and Borrego in the final chapter of
Part I.
Part II examines disorder-specific strategies for avoiding treatment failures.
Readers are provided with core strategies linked to case examples and accompanied by strategies to apply should treatment nonresponse be encountered. This
section opens with a focus on the treatment of panic disorder (Chapter 7 by
Murray, McHugh, and Otto), and is followed by chapters focused on the treatment of obsessive-compulsive disorder (Chapter 8 by Marques, Chosak, Phan,
Fama, Franklin, and Wilhelm), post-traumatic stress disorder (Chapter 9 by Zayfert
and DeViva), social anxiety disorder (Chapter 10 by Hofmann, Richey, Asnaani, and
Sawyer), generalized anxiety disorder (Chapter 11 by Behar and Borkovec), and
specific phobias (Chapter 12 by Alpers).
A special feature of the book is Part III on special populations, which covers the common problems of anxiety disorders that are comorbid with depression
(Chapter 13 by Deveney and Otto), personality disorders (Chapter 14 by Nock,
Deliberto, and Hollander), substance use disorders (Chapter 15 by Reynolds, Tull,
Shalev, and Lejuez), eating disorders (Chapter 16 by Becker, Zayfert, and Pratt),
medical conditions (Chapter 17 by Greer, Graham, and Safren), and treatment
complications specific to children and adolescents (Chapter 18 by Micco and
Ehrenreich).
Our hope is that this text will provide the CBT practitioner with useful clinical
guidance to overcoming obstacles and impasses when treating some of the most
debilitating and costly mental health problems.
Introduction
5
References
DuPont, R. L., DuPont, C. M., & Rice, D. R. (2002). The economic costs of anxiety disorders. In
D. J. Stein & E. Hollander (Eds.), Textbook for anxiety disorders (pp. 475–483). Washington,
DC: American Psychiatric Press, Inc.
Hofmann, S. G., & Smits, J. A. J. (2008). Cognitive-behavioral therapy for adult anxiety disorders:
A meta-analysis of randomized placebo-controlled trials. Journal of Clinical Psychiatry, 69,
621–632.
Kessler, R. C., Berglund, P. A., Demler, O., Jin, R., & Walters, E. E. (2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the national comorbidity survey
replication (NCS-R). Archives of General Psychiatry, 62, 593–602.
Kessler, R. C, Chiu, W. T., Demler, O., Merikangas, K. R., & Walters, E. E. (2005). Prevalence,
severity, and comorbidity of 12-month DSM-IV disorders in the national comorbidity survey
replication. Archives of General Psychiatry, 62, 617–627.
A Case Formulation Approach to Resolve
Treatment Complications
Bethany A. Teachman and Elise M. Clerkin
There is a tendency to think of case formulation as an activity that occurs at the
outset of therapy to guide initial clinical decision-making, but which plays little role
once therapy is underway. However, we believe that case formulation is most useful when viewed as a dynamic, iterative process that invites frequent revisiting of
hypotheses as new client data become available. As Eells describes in her influential
handbook, “A psychotherapy case formulation is a hypothesis about the causes, precipitants, and maintaining influences of a person’s psychological, interpersonal, and
behavioral problems. A case formulation helps organize information about a person, particularly when that information contains contradictions or inconsistencies in
behavior, emotion, and thought content.” (Eells, 2007, p. 4). By viewing case formulation as an animate hypothesis-testing enterprise, the process becomes very useful
for resolving treatment complications. In particular, it helps with identifying potential “stuck points” by generating alternative approaches and possible explanations
for treatment stagnation.
In the current chapter, we consider some of the many ways that case formulations
can help enhance treatment outcome for anxiety disorders. We will focus predominantly on case formulation from a cognitive behavioral perspective because this
approach reflects the dominant treatment perspective for anxiety disorders (see list
of empirically supported treatments; e.g., Chambless & Ollendick, 2001). However,
we also consider recommendations from alternate therapeutic orientations. In particular, underlying the proposals we offer is a perspective borrowed from Motivational
Interviewing (Miller & Rollnick, 2002), which suggests that apparent “resistance”
in therapy is better understood as ambivalence about making changes. Moreover,
ambivalence is expected when we ask clients to give up well-established (albeit maladaptive) ways of thinking, behaving, and relating to others. Thus, complications in
treatment present puzzles for therapists and clients to investigate, rather than purposeful defiance on the client’s part. Case formulation is a valuable tool that can
help put the pieces of the puzzle (back) together when a treatment is floundering.
B.A. Teachman (B)
Department of Psychology, University of Virginia, Charlottesville, VA, USA
e-mail: bteachman@virginia.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_2,
C Springer Science+Business Media, LLC 2010
7
8
B.A. Teachman and E.M. Clerkin
We will outline the seven steps advocated by Persons and Tompkins (2007) for
clinicians to follow to develop an effective cognitive behavioral therapy (CBT) case
formulation. These include (1) creating a problem list, (2) assigning DSM diagnoses, (3) selecting a primary diagnosis, (4) applying an empirically supported,
nomothetic formulation, (5) integrating individual client characteristics, (6) hypothesizing about mechanisms maintaining the disorder, and (7) considering antecedents
for the current onset of illness. Our goal in outlining these steps is not to espouse
one “correct” way for devising a case formulation. Rather, we use these steps as a
springboard to evaluate the multiple ways that case formulation can help identify
problems and potential solutions to aid in treatment planning and implementation.
We will close the chapter by discussing the use of different modalities of case formulation and alternative treatment strategies to resolve typical complications that
arise in therapy.
Using Cognitive Behavioral Case Formulation to Resolve
Treatment Complications
Just as there is not a single cognitive behavioral treatment for anxiety disorders,
there is not a single CBT case formulation. Those working from a primarily cognitive orientation are likely to form hypotheses about a client’s maladaptive beliefs
that contribute to the development and maintenance of their disorder. For instance,
clinicians providing cognitive therapy for obsessive compulsive disorder (OCD) will
emphasize a client’s unhealthy interpretations about the meaning of their intrusive
thoughts (see Frost & Steketee, 2002; Rachman, 1998). Analogously, a therapist
working from cognitive models of social phobia will highlight the onset of fears of
negative evaluation and beliefs that one will fall short of an expected standard (see
Clark & Wells, 1995; Rapee & Heimberg, 1997). On the other hand, when working
primarily from a behavioral perspective, maladaptive behaviors and environmental
contingencies, such as reinforcements for avoidance, will likely feature prominently
in case formulation.
Notwithstanding the many varieties of possible content in CBT case formulations, Persons and Tompkins (2007) outline a series of seven steps that are common
to developing effective formulations. As we outline, each of these seven steps
provide opportunity for the clinician to re-evaluate a case that is not proceeding
smoothly.
Problem List
It is critical to compile a comprehensive biopsychosocial problem list that characterizes the range of different problem areas in a client’s life. Although it is unlikely that
all of the different problems will be targeted in treatment, having this list (and updating it throughout treatment) will help ensure that a feasible approach to treatment is
A Case Formulation Approach to Resolve Treatment Complications
9
selected, and can help both the client and the therapist anticipate barriers to change.
In addition to assessing the difficulties associated with the presenting clinical
problems, Woody, Detweiler-Bedell, Teachman, and O’Hearn (2002) recommend
evaluating the following domains as a start to creating the problem list: Injurious
Behavior (e.g., suicidal ideation or actions), School/Occupational Functioning (e.g.,
job or school stability, financial status), Family Functioning (e.g., relationships with
key family members, parenting skills), Other Interpersonal Functioning (e.g., frequency and quality of social supports), Behavioral Health (e.g., medical history
and physical fitness), Risky Behaviors (e.g., alcohol abuse, legal difficulties), and
Culture, Spirituality, and Moral Development (e.g., involvement with religious institutions, level of acculturation). In addition, evaluation of motivational factors, such
as readiness for change, can be useful for anticipating therapy-interfering behaviors.
It is often tempting to skip doing a full assessment of functioning across different life domains when treating an anxiety disorder because there are clear and
effective treatments available for most anxiety diagnoses; thus, the full problem list
may seem superfluous if therapists feel they already know what type of treatment
they will provide. However, not being aware of the broader picture of a client’s
functioning can easily sabotage a treatment. For instance, it is common for wellintentioned therapists to suggest all manner of creative exposures that turn out
not to be viable because of financial problems (attending movies for clients with
agoraphobia and taking long excursions for persons with driving phobias are common examples of impractical exposures for clients with limited means). Similarly,
identifying challenges related to diversity issues is critical, whether tied to cultural background and difficulties related to acculturation or concerns stemming from
prejudice tied to physical challenges, religion, ethnicity, social status, or sexual orientation (see Hays, 1995). By referring to the problem list and recognizing how
these other life challenges may impact implementation of standard CBT strategies,
homework adherence can often be greatly enhanced.
Using the problem list component of case formulation is also very useful for
recognizing complications in treatment that follow from difficult interpersonal relationships. We see this frequently in the context of OCD and generalized anxiety
disorder (GAD) where couples may develop an unhealthy dyad with one individual
repeatedly requesting reassurance from their partner. Changing this reassuranceseeking ritual is often important for success in treatment, but without some
knowledge about the relationship dynamics (including those with a partner, parent,
teacher, friend, or other “support” person), interpersonally oriented interventions
can easily backfire.
As a general guideline, when treatment is not proceeding as planned, especially
when adherence to treatment recommendations is low, returning to the problem
list and considering other problems that may be operating as barriers to strategy
implementation is an easy and often fruitful first step to resolving the impasse.
Additionally, it is important to check if new problems have arisen since the last
evaluation or if any major domains were not evaluated. This list can also help clinicians determine if one reason for a stalled treatment is that the wrong problems
were prioritized. One of the challenges when working with complicated clients who
10
B.A. Teachman and E.M. Clerkin
have high levels of comorbidity and related impairments in functioning is making
an educated guess about a good place to start when forming an initial treatment
plan. The problem list and its role in case formulation are helpful in this regard by
highlighting how one problem area may fuel another, and in turn, how change in
one area may alleviate difficulties in another.
Five-Axis DSM Diagnoses
Once the problem list has been compiled, DSM diagnoses are assigned along the
five axes (Axis I: clinical disorders, including major mental disorders; Axis II: pervasive or personality conditions; Axis III: medical conditions; Axis IV: psychosocial
and environmental factors; Axis V: Global Assessment of Functioning). Often it is
not feasible to complete a full, structured Axis II personality disorder evaluation. In
this case, it can still be beneficial to note difficult personality dimensions that may
interfere with treatment because they may be helpful when returning to the case
formulation to generate hypotheses about why treatment may be stalled. Common
situations where this arises in anxiety treatment concern clients with an overly
dependent personality (who may then want the therapist to directly give advice and
make decisions for them), or clients with an avoidant personality style (who have
few social relationships and, in some cases, limited social skills). Recognizing that
change in personality disorders tends to occur more slowly than change in Axis I
problems is important.
Similarly, even though a complete medical evaluation for Axis III rarely coincides with a mental health intake evaluation, asking about medical problems is
critical for treatment planning. For instance, we frequently learn about medical
conditions, such as asthma or neck pain, that influence the type of interoceptive
exposures (exercises that bring on physical sensations relevant to anxiety and panic)
we recommend for individuals with panic attacks. This is also the time where clients
will often discuss upcoming medical interventions that may interfere with treatment
attendance.
Psychosocial and environmental difficulties outlined on Axis IV, such as unemployment, and the more general assessment of functioning on Axis V are useful
for setting realistic goals for different stages of therapy. It is not unusual for clients
(and new therapists) to feel discouraged about progress in therapy because they had
unreasonable expectations about the extent and speed of recovery related to the focal
disorder (e.g., that a client with OCD would become free of obsessions; that symptoms of panic would never again come out of the blue). Clients sometimes imagine
that change in one area of functioning will miraculously solve all other problems.
Expectations for a reasonable pace of change are essential for keeping both the client
and therapist motivated. Having some idea about other areas of limited functioning
will help determine the resources the person has available to aid with the hard work
necessary for progress in treatment. Along these lines, it is helpful to get an evaluation of premorbid functioning (i.e., a sense of a client’s skills and lifestyle before
onset of the disorder).
A Case Formulation Approach to Resolve Treatment Complications
11
Primary Diagnosis
Persons and Tompkins (2007) advocate that the therapist should select a primary
or “anchoring” diagnosis at this point in CBT case formulation. Frequently this
is determined by the diagnosis that causes the most distress for the individual or
contributes to the most difficulties on the problem list. This is ideally a collaborative
decision so that the client and therapist are working toward similar goals in therapy.
The selection of the primary diagnosis is used to guide which nomothetic template
will be used as the basis for the individual formulation.
Challenges with this step of the process that can contribute to later treatment
complications include: (1) disagreement between the therapist and client about the
appropriate diagnosis to prioritize, (2) selection of a diagnosis that is not primary
or sufficiently important to the individual’s overall functioning, or (3) other comorbid diagnoses interfering with progress on the selected diagnosis. When problems
emerge in therapy where the therapist feels like the therapy is repeatedly being
pulled off-track because the client regularly wants to work on issues unrelated to
the selected focus, it is worth revisiting the case formulation to consider whether
one of the above difficulties with selecting the primary diagnosis has occurred.
In the case of complications due to disagreement about the appropriate diagnostic focus, we recommend a careful functional analysis for the client and therapist
to evaluate how the different problems are related. For instance, a client may wish
to focus on panic attacks even though they occur very infrequently and seem secondary (according to the therapist’s perspective) to social anxiety that is limiting
social interactions on a daily basis. In this case, the client and therapist might consider how avoidance due to fear of future panic versus avoidance due to fear of
negative evaluation from others is most impairing. Did one versus the other lead to
missed opportunities at work, or to more conflict with a spouse? When problems are
highly connected, as in this example, it is often difficult to tease apart which anxiety
problem is contributing most to the overall impairment (e.g., a promotion at work
might be passed up because it would involve public speaking where the individual
feared having a panic attack). Nevertheless, in the area of anxiety disorders (unlike
other problem areas, such as substance abuse), we find that it is usually not very
difficult for the client and therapist to come to agreement about an order in which
they will tackle different problems so long as the decision is made collaboratively.
Deciding on a phase approach to therapy (see Woody et al., 2002), where problems will be broken down and then undertaken in sequence can make this decision
process easier. Clearly, some agreement on the treatment plan is needed if “collaborative empiricism” and willingness to try exposures (in a non-coercive environment)
is to succeed.
At times, the therapist and client readily agree on an anchoring diagnosis, but
they make a poor choice so treatment does not produce the expected gains. This can
frequently occur when issues of differential diagnosis are challenging. For instance,
in the panic disorder versus social phobia example above, it is not unusual to assume
that the presence of panic attacks warrants panic disorder treatment. Frequent panic
attacks are without question incredibly distressing, but these can often occur as part
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of the presentation of another anxiety disorder, which is in fact primary. Individuals
with specific and social phobias, for example, sometimes have panic attacks (or fear
they will) when encountering their feared situation. Yet, while there are important
overlapping components in the treatments for phobias and for panic disorder, there
are also critical differences (in required exposures, catastrophic cognitions, etc.)
that may need a targeted treatment. There are numerous challenging differential
diagnoses in the context of anxiety disorders: body dysmorphic disorder symptoms
can overlap with social phobia, depression symptoms can overlap with GAD, rituals associated with eating disorders can look similar to OCD, to name just a few.
When a treatment is not progressing well, considering whether the right treatment
targets have been selected is an important step in the problem-solving process, and
reconsidering the links between the selected diagnosis and the problem list is a good
place to look for solutions.
Re-evaluating the selected primary diagnosis is also useful when a client has
other disorders comorbid with the anxiety diagnosis. This is the norm rather than
the exception, but the field is still at early stages in terms of research to guide how
to select treatment goals with complex clients who have multiple diagnoses. One
obvious issue to consider is whether the presence of an additional diagnosis is possibly interfering with the anxiety treatment. This occurs frequently in the context
of substance abuse, eating disorders (especially in anorexia nervosa when starvation greatly impairs cognitive processing), psychotic disorders, and severe mood
disorders (where lethargy and retardation, unmanaged manic symptoms, or suicidal
ideation can all interfere with the ability to engage in treatment). In these cases,
it may be necessary to focus on the interfering diagnosis first before returning to
treatment for the anxiety problem.
Nomothetic Formulation
Selecting the anchoring diagnosis provides a useful focal point so that the therapist
can then turn to the research literature to determine whether a group-level, nomothetic formulation exists for that diagnosis. While many disorders do not yet have such
formulations, there are a number of choices that have a strong empirical foundation
for anxiety disorders. This does not mean there will be a readily available formulation to exactly match your particular client; for instance, the field sorely needs
formulations for anxiety disorders that recognize cultural differences. These include
adaptations of standard CBT formulations that take into account unique treatment
needs related to age, race and ethnicity, religious affiliation, sexual orientation, etc.
Notwithstanding, there are many useful sources to draw upon even when no exact
match exists – imagine, for example, that you want to develop a formulation for a
client who is 79 years old and has social phobia as the primary diagnosis. There are
multiple CBT formulations for social phobia, including the highly influential models by Clark and Wells (1995) and by Rapee and Heimberg (1997). However, these
are not geared toward conceptualizing elderly clients, so if this is likely to be central to the case formulation, seeking out a further nomothetic template that includes
A Case Formulation Approach to Resolve Treatment Complications
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an aging focus would be helpful. While we are unaware of such a template specific to social phobia, valuable models exist for anxiety problems in general among
elderly persons (see Beck & Stanley, 1997; McCarthy, Katz, & Foa, 1991; Sheikh
& Salzman, 1995, among others) and for some specific anxiety disorders, such as
GAD (see Ayers, Sorrell, Thorp, & Wetherell, 2007), which can then be modified to
reflect social anxiety concerns.
The purpose of selecting the nomothetic formulation is that it serves as the
template for developing hypotheses about the psychological mechanisms that are
maintaining the disorder, which can then be targeted in treatment. In the case of
social phobia, the nomothetic formulation would likely lead to hypotheses about
how fears of negative evaluation result in maladaptive avoidance of social situations
(the avoidance relieves anxiety in the short-term, but worsens it in the long-term). In
panic disorder with agoraphobia, the formulation might highlight how catastrophic
misinterpretations of benign bodily sensations and one’s ability to tolerate anxiety
contribute to a “fear-of-fear” cycle and avoidance of situations where panic sensations might occur (e.g., drinking caffeine). In OCD, a cognitive formulation would
emphasize the misinterpretation of unwanted thoughts as being meaningful or personally significant, while a more behavioral formulation would focus on the impact
of doing rituals to reduce the anxiety caused by obsessions. As evident from these
examples, the nomothetic formulation is particular to the disorder, but is generic
in the sense that it is thought to apply to most individuals who have the disorder,
regardless of whether OCD involves hand-washing or checking locks, or whether
social phobia involves public speaking or dating fears. It is in the next step that the
formulation is adapted to the individual client.
The nomothetic formulation incorporates a number of valuable components for
helping resolve treatment complications. In particular, it brings a wealth of empirical support for a given conceptualization and subsequent treatment approach. Using
the research literature to understand what approaches have worked well – and
equally importantly, worked poorly – saves the clinician an amazing amount of time
and trial and error. Notwithstanding, it is difficult to anticipate how an approach
that works well for people on average will work for a given individual, particularly when a case is complex and the client may not match the clinical population
used in the research studies on some critical variable (e.g., pattern of comorbidity, ethnic background). To date, there is not sufficient data to guide therapists in
deciding when to individually tailor a treatment versus when to adhere closely to
an empirically supported treatment (see discussions in Persons & Tompkins, 2007;
Schulte, Kunzel, Pepping, & Schulte-Bahrenberg, 1992). We recommend trying the
empirically supported approach first but monitoring progress regularly so that a
treatment that is not moving ahead is recognized quickly (see Woody et al., 2002).
In this way, an unhelpful intervention will not continue unchecked and a change
of course can be considered (see discussion of alternate treatment options at the
end of this chapter). Thus, individual client-level data should be collected throughout therapy regardless of whether an empirically supported or individually tailored
plan is implemented. In this sense, all formulations and treatment plans can be
evidence-based.
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Perhaps the most useful lesson from this step of case formulation with regards
to addressing a stagnant or deteriorating therapy is the focus on empiricism. It is
well known that clinicians, like all humans, are vulnerable to biases that distort our
memory and interpretations so that we tend to “see what we want to see” (see Garb,
1997; Fiske & Taylor, 1984; Lopez, 1989). This is why including objective measures
of progress is so critical. Being an empiricist can occur both at the level of selecting
a formulation with compelling research support and at the level of collecting data
from the individual client. In turn, these data are often the key to identifying the
barriers that are blocking advances in treatment.
Individualize the Formulation
The next step is to take the nomothetic formulation and apply it to a particular
individual, taking into account his or her particular problem list and the posited
relationships among the problems. As noted, cognitive behavioral formulations for
anxiety tend to be diagnosis-based in that there is a model to guide the conceptualization and treatment of a given disorder. While this model has enormous utility and
predictive validity, treatment complications can readily ensue if formulation stops
at the level of the diagnosis. Knowing that a person meets criteria for post traumatic
stress disorder (PTSD), social phobia, or GAD allows one to make an educated
guess about a first line of treatment to try (based on the research literature), but it
does not explain how the model is a fit or mismatch for that specific person. As
Wilson (1998) noted, “Empirically-supported, manual-based treatments are good,
but not good enough” (p. 367).
One does not have to be in practice for long before encountering seeming mismatches. There is the client with OCD who reports no awareness of obsessions
tied to his compulsions, or who does not see the compulsions as anxiety-reducing.
There is the individual with panic disorder who denies experiencing any catastrophic
(mis)interpretations of her bodily sensations. Even when the disorder-based model
does readily fit, it details a process but does not explain why or how that particular person came to make those catastrophic misinterpretations, experience those
obsessions, etc.
Case formulation can help translate the group-level treatment approach to a given
client, and this translation can guide critical decision points in treatment when a
standard strategy does not appear to be working. One important place to start is
to consider how the various difficulties on the problem list might be inter-related.
For instance, a recent client seeking treatment at our clinic for GAD was receiving a standard worry control treatment protocol, but progress was incredibly slow.
At first, this was puzzling to the therapist because the client, Steve, a 27-year-old
recently married man of Korean descent, appeared highly motivated and committed
to the therapy. He was early for each session and not only completed his homework, but had assembled a color-coded binder in which he kept his session notes.
Moreover, he had inquired about and purchased self-help books to use as adjuncts
to his weekly therapy session. It would be hard to imagine a more “perfect” client.
A Case Formulation Approach to Resolve Treatment Complications
15
Not surprisingly (in retrospect!), this turned out to be the very problem that was
interfering with the client making progress.
When the therapist returned to the problem list, she was reminded of the client’s
perfectionistic thinking and how this had caused considerable impairment in Steve’s
job and even in his marriage, because he was so easily discouraged by small setbacks. The clinician had initially missed how this same pattern was playing out in
therapy because it had been so pleasurable to work with the client who was clearly
trying to please the therapist. Once the clinician recognized the relationship between
Steve’s perfectionism and his response to treatment, she was able to talk to Steve
about his tendency to try to implement the techniques he was learning so rigidly that
he felt like a failure whenever he experienced quite minor stumbling blocks (e.g., a
single day with increased worry). This was creating a vicious cycle, whereby Steve
would experience more worry and then try even more rigidly to follow the program.
He became increasingly sensitive to his perceived failings and worried excessively
about “screwing up treatment.” The therapist suggested Steve put away his binder
of session notes and self-help books for a while, and actually do less typical therapy
homework for a few weeks. He was encouraged to focus on enhancing the quality of
his life versus working on treatment assignments so rigidly. Ironically, by stepping
back and reducing his focus on the usual worry control assignments, Steve was able
to make far more progress. Of course, Steve was still doing homework for the therapy – the focus of the homework had simply shifted from closely monitoring anxiety
and explicitly re-evaluating negative automatic thinking to considering what Steve
truly valued in his life and focusing on promoting those goals.
As this case illustrates, the individual’s intra- and interpersonal circumstances –
and how these interact with the focal diagnosis and its treatment – need to be
considered to understand how to apply the nomothetic formulation to help a particular person. This does not mean that clinicians should abandon the evidence-based
treatment plan at the first sign of a treatment complication. Instead, it suggests consideration of how the relations among a client’s strengths and weaknesses can lead
to more effective application of an intervention. Further, the decision to advocate for
less standard CBT homework (e.g., keeping thought records) in order to challenge
perfectionist beliefs highlights the importance of focusing on the principle behind a
given strategy, as opposed to rigidly following a script when adapting a formulation
to a particular individual.
Hypotheses About the Basis of Mechanisms
Maintaining the Disorder
Once the nomothetic formulation has been adapted for the specific individual, the
next stage is to develop hypotheses about the origins of the mechanisms that are
thought to maintain the disorder. This involves evaluating the client’s social and
family history (both in terms of family psychiatric history and information about
the client’s upbringing). Relevant information for a person with social phobia might
include early life experiences with parents and teachers that contributed to fears of
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being evaluated negatively by authority figures. In GAD, one might inquire about
the development of beliefs that the world is an unpredictable and dangerous place, or
that the client is somehow vulnerable and unable to cope. For someone with OCD,
were there religious teachings that emphasized the importance of purity of thought?
More generally, when did the individual start avoiding situations that made him
anxious, and in what ways was this avoidance behavior reinforced?
Ideally, one would generate multiple hypotheses about the etiology of the maladaptive ways of thinking, behaving, and relating to others. Considering more than
one hypothesis is important down the line for helping the therapist and client see
more than one avenue for intervention. The goal of generating ideas about how the
problem developed is not to figure out the “cause” of a disorder – this is rarely
definable – but to assist with treatment planning. These hypotheses can help the
client develop some kind of narrative about the onset of their problems. In turn, this
narrative can make the treatment approach more comprehensible and credible, in
part by helping clients appreciate the need to identify and then alter maladaptive
patterns that maintain the disorder.
For example, Lily, a 43-year-old woman with PTSD (following a rape that
occurred when she was in her 20s), recognized that she was trained at a young age
to avoid confrontation at all costs. As a result, she developed a pattern of avoiding
all interactions that might elicit negative affect, especially anger (either in herself or
in others). Upon considering this explanation for the development of her avoidance
behavior, and consequent maintenance of her PTSD, Lily was far more willing to
consider prolonged exposures in treatment. At the same time, the client discussed
her mother’s constant warnings as she was growing up about the need to be vigilant
around men because “they were only after one thing.” Although Lily had enjoyed
dating in her teens and early 20s, following the rape she became extremely distrustful of all men who were not family, even ending close male friendships that had
been quite supportive. Again, once these early warnings and ensuing beliefs were
recognized, the client was able to engage in cognitive restructuring to re-evaluate
her over-general conclusions about the dangerousness of men.
This step of the case formulation is often helpful when treatment is stuck because
the generation of multiple hypotheses about how the disorder developed (or mechanisms maintaining it) can point to a variety of potential targets for intervention. This
is not to say that the solution for a disorder has to be rectifying some factor that contributed to its development; after all, aspirin can help a headache, but the absence
of aspirin was not the cause of the headache. However, identifying factors that contributed to the development of a disorder can be motivating for clients when they
recognize that the disorder was not predetermined. If they learned dysfunctional
ways of thinking or behaving, they also have the ability to learn more adaptive
approaches. Analogously, this stage of hypothesis generation can help clients see
their role in the onset of a problem; this is not done to assign blame but to empower
clients by helping them see that they have choices in how they respond to the events
in their lives.
For instance, clients with social phobia will often talk about being teased in
childhood, and feel this contributed to the development of their fears. While this
A Case Formulation Approach to Resolve Treatment Complications
17
hypothesis is certainly reasonable, it is likely incomplete. Most people experience
teasing in childhood to some degree, so the individual is challenged to consider why
their fears of negative evaluation grew and persisted. This may lead to hypotheses
about a parent who was overly critical and emphasized the need to “put on a good
face”, which in turn contributed to the development of a core belief of inadequacy.
By recognizing that others might not have accepted the teasing as valid (i.e., as a
sign of their inadequacy), the client then has a choice to consider other ways of
responding to criticism.
This step of the case formulation can be a powerful one when treatment is going
poorly because it can help the client better understand why their problems developed, and show them that they can now work towards a different way of responding
to the world.
Precipitants of Illness
The final step in CBT case formulation involves considering possible precipitants
for the current period of illness. As with the previous step, the goal is not to figure
out the cause of the illness, but to recognize possible triggers and activating situations so clients can learn how to minimize these situations in the future. When
antecedents are recognized, clients also learn that seemingly unpredictable anxiety
reactions can often be understood more fully (and seem more predictable and controllable). Further, this step can be helpful when a treatment feels stuck because it
allows the client and therapist to consider whether the same triggers are still in place
and may explain the difficulty in breaking old patterns and alleviating symptoms.
For instance, discovering that increased fighting in the marriage preceded a surge
in panic attacks can allow the client to work on changing his interpersonal environment (e.g., consider couple’s counseling to reduce the marital conflict) while
simultaneously using the conflict trigger as an opportunity for exposures to elicit
panic symptoms.
Each of these seven steps in CBT case formulation can play a valuable role in
resolving treatment complications. In particular, as noted by Eells (2007), the formulation can help make sense of seeming inconsistencies in a client’s presentation
across thoughts, feelings, and behaviors. To illustrate how the formulation can be
used, we introduce a case example that highlights a common inconsistency; the discrepancy between a client’s stated treatment goals and her behavior. The “yes, but”
refrain in response to one treatment recommendation after another can be frustrating
for even the most experienced clinician. By returning to (and potentially reconsidering) the posited origins, mechanisms, and precipitants of the anxiety problem,
it often becomes clear why an apparent discrepancy is occurring. Once a possible
explanation has been identified, paths to resolve the impasse are much easier to
identify.
Case example. Kelly was a 51-year-old mother of two college-aged daughters
who contacted our clinic after seeing an advertisement for one of our research studies, which provided free treatment for panic disorder. Upon calling, she reported that
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she had a 10-year history of occasional panic attacks but that they had significantly
worsened following September 11, 2001. She felt a strong sense of loss of control
following 9/11, and was terrified that her college-aged daughters, who no longer
lived in their home town, might come to harm. Despite this terror, she rarely spoke
of her concerns, wanting to maintain her reputation among her friends as a “woman
who had it together.” Her panic attacks typically occurred in the evenings and were
triggered by small signs of gastrointestinal distress, which escalated into fears that
she might lose bladder control and make a fool of herself.
The initial case formulation focused on the standard nomothetic one for panic
attacks following Clark’s (1986) model – that she was catastrophically misinterpreting changes in bodily sensations, resulting in a rapidly worsening fear-of-fear
cycle. At the idiographic level, the fears tied to 9/11 were emphasized as a precipitant for the worsening of symptoms, and her fears about losing control were thought
to be critical maintaining factors. At the outset of the treatment, Kelly appeared
highly engaged, asking questions during the initial psychoeducation component and
commenting frequently that she was so glad to be “helping with a research study”
because one of her daughters was working in a research lab at college.
However, when it came time to start doing exposures to elicit panic sensations, Kelly regularly had reasons why a given exposure was not likely to help her.
For instance, she initially denied any avoidance behaviors, but subsequent probing revealed that she would not drink caffeine because of the jittery sensations
and occasional upset stomach it brought on, and would not eat a full meal after
6:00 pm because of concerns that she would have indigestion. When Kelly was
encouraged to consider trying these activities, she suggested that caffeine was not
good for you and eating large meals at night was unhealthy because her metabolism
worked more slowly then. All the while, she kept reiterating that she was very
happy to be in treatment because she believed research was important, and was
glad to be contributing. After numerous circular discussions and unsuccessful brainstorming about alternate exposure options, the therapist felt stuck. Kelly regularly
said she was happy to be in the study and even agreed that exposures were likely
very helpful for reducing panic, but rejected all suggestions for personally tailored
exposures.
At this stage, the therapist revisited the case formulation and hypothesized that
the critical link that she had been missing was the common denominator that tied
together the client’s secrecy about her fears amongst her friends (in order to appear
“together”) and her insistence that she was participating in treatment to help with
the research study. The therapist tried focusing less on fears of losing control tied
to bodily changes or harm coming to others (e.g., the fears related to 9/11), and
reconceptualized the problem around the client’s difficulties admitting to a weakness. Just as Kelly had not wanted others to know of her fears about her family
or about her panic attacks, she also did not want to think of herself as someone
who needed therapy. Focusing on the research component of her treatment participation was interfering with her engaging in the therapy as someone who actually
needed help. With this new hypothesis, the therapist was then able to understand the
client’s seeming resistance and use cognitive restructuring techniques to help the
A Case Formulation Approach to Resolve Treatment Complications
19
client re-evaluate her beliefs about the unacceptability of needing help. With this
revised case formulation, the client eventually recognized that she was participating
to get help for panic as well as to help with research, and became more willing to
try exposures.
The following dialog illustrates the therapist and client working together to try to
connect the seemingly discrepant components of her presentation:
Therapist: I am wondering how to make sense of the different things you’re
telling me. On the one hand, you’ve repeatedly said that you want to be in
the group and that you agree that exposures are likely helpful for panic. On
the other hand, it feels like whenever we suggest trying an exposure, you
have a reason why it won’t work for you.
Kelly: I just really want to support the research you’re doing, and I’ve told my
daughter all about the study.
Therapist: That’s great that you’ve shared your experience with your daughter
and that she has been supportive. I’ve noticed that you keep referring to our
work here as a research study, rather than as therapy. While it’s certainly true
that we’re conducting research, the goal is also to provide you with treatment for your panic disorder. What do you think it would be like to tell your
daughter that you are in therapy, instead of in a research study?
Kelly: Then she would think something was wrong with me.
Therapist: I see how that could be difficult, but why would it be bad for her to
find out that you needed some help right now?
Kelly: I’m the Mom.
Therapist: And what does it mean for you to be the Mom?
Kelly: It means I should be the one who is always in control.
Therapist: That’s quite a tough standard to meet. Is that also the standard you
set for yourself with your friends? You told me that you try not to share your
problems with them either, and that they don’t know about your fears for
your family or about your panic attacks.
Kelly: I guess so, although it’s not something I really think much about. I suppose I’ve just always prided myself on being the one who everyone else can
count on. It scares me to be the one who has a problem – I’ve always been
the one who fixed other people’s problems. Who will they turn to if I’m all
screwed up?
Therapist: I understand that acknowledging your own problems can be very
scary. I wonder, though, whether having a problem like panic attacks really
means that you’re “all screwed up” and can no longer help other people. . .
As this case illustrates, revisiting the formulation to look for clues about seeming
inconsistencies – in this case, the discrepancy between the client’s apparent engagement in treatment yet unwillingness to try exposures – can highlight patterns and
likely explanations for treatment barriers that might not be apparent without the
formulation’s guideposts.
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Using Different Modalities of Case Formulation to Resolve
Treatment Complications
The above discussion has focused on CBT formulation, but case formulation can
take many forms. In some traditions, formulation is done primarily at the outset of
therapy (e.g., interpersonal psychotherapy where a focal problem area is selected
early on; Markowitz & Swartz, 2007), while for other orientations the formulation
occurs later in treatment (e.g., emotion-focused therapy where critical information
is not thought to emerge without experience in the “safe context of the therapeutic
environment”; Greenberg & Goldman, 2007). Regardless, in all instances the formulation is assumed to be a dynamic hypothesis. As we have outlined, in the case
of anxiety disorders, a disorder-specific nomothetic formulation usually serves as
the starting point. While this formulation is determined at the outset of therapy as
soon as a primary diagnosis is selected, the refining of this formulation to include
client-specific data should occur and recur throughout treatment. Moreover, using a
DSM disorder-based, nomothetic formulation is not the only approach. For example, the substantial rates of comorbidity across mood and anxiety problems have
led to recent advances that focus on treating “negative affect syndrome,” rather
than isolating single disorders (see Barlow, Allen, & Choate, 2004). Others have
advocated focusing on more general, underlying emotional processing difficulties
that emerge during therapy, such as fear of abandonment, rather than emphasizing
specific disorders at the outset of treatment (e.g., Greenberg & Goldman, 2007).
Another important distinction across different case formulation traditions
includes adherence to a categorical versus dimensional model. The categorical
approach follows the so-called medical model, which views disorders as “discrete
pathological entities” with predictable causes and prognoses (Eells, 2007, p. 9). In
contrast, the dimensional approach focuses less on classification, instead viewing
psychopathology on a continuum from normal to pathological. CBT formulations
for anxiety typically follow a categorical approach, emphasizing a particular disorder to understand a person’s problems. This approach is very useful for selecting
a treatment plan that corresponds with the categorical decision, but can reify the
category (treating an abstract concept, like a disorder, as though it were a concrete
entity) and can leave out important non-categorical influences on the origin and
course of the disorder. For instance, intra- and interpersonal dimensions, such as
openness to experience and ability to form alliances with others, do not fit into neat
categories (until you reach the Axis II personality disorders, and even then the categorical nature of these disorders is controversial; Widiger, 1992), but undoubtedly
influence treatment outcome (see Martin, Garske, & Davis, 2000).
Related to the focus on dimensions versus categories, case formulation
approaches also vary in their emphasis on a person’s weaknesses versus strengths
and on change versus acceptance (e.g., cognitive-behavioral and interpersonal
formulations focus more on fixing problems and skill deficits, relative to more
humanistic approaches, such as an emotion-focused therapy formulation). While
CBT approaches make some reference to the value of acceptance, this is far more
explicit in other approaches, such as case formulation in dialectical behavior therapy
A Case Formulation Approach to Resolve Treatment Complications
21
(DBT; see Koerner, 2007). This focus on working to accept some distress and
negative circumstances can be extremely valuable with anxiety-disordered clients,
particularly when perfectionist tendencies lead to overly rigid applications of change
strategies (as the earlier case example with Steve’s GAD treatment illustrated). The
recent emphasis on mindfulness strategies (see later section) attests to these potential benefits. In fact, many of the dialectics outlined in DBT case formulation can be
extremely useful for generating hypotheses to understand treatment complications
in anxiety disorders. For example, recognizing both sides of the emotional vulnerability dialectic – inability or unwillingness to regulate emotions during emotional
extremes versus attempts to deny or ignore vulnerability – can help make sense of
clients’ inconsistencies in their readiness to confront avoidance behaviors in anxiety.
Similarly, being aware of the active–passive dialectic, where the individual oscillates between passive, acting incompetent behaviors versus trying to appear overly
together, can aid in catching over- or under-predictions of fear that can interfere with
successful learning during exposures.
Thus, while we advocate starting with a cognitive and/or behavioral case formulation for most anxiety problems because of the extensive research base supporting
these treatment modalities, we also note the importance of drawing upon other
case formulation approaches when clients are not making the expected progress.
Analogously, when starting with an alternate treatment approach (e.g., a recent clinical trial suggests non-CBT approaches, such as psychodynamic therapy, may also
be efficacious in the treatment of panic disorders; Milrod et al., 2007), the clinician
is advised to consider CBT or other case formulation steps to revise a floundering
treatment.
Using Case Formulation to Decide to Add or Change
Treatment Strategies
Before closing, we would like to comment on a number of additional treatment
strategies that are not explicit components of most standard CBT approaches,
which may help address some of the common difficulties that case formulation can
reveal. Unfortunately, matching data that indicate specific treatment alternatives to
use based on unique client characteristics are limited, both generally (see Project
MATCH Research Group, 1993) and for specific anxiety problems (see Clarkin
& Levy, 2004; Dusseldorp, Spinhoven, Bakker, Van Dyck, & Van Balkom, 2007).
Thus, it is unclear at this point whether these suggested alternatives will ultimately
garner empirical support as effective treatment matches for the presenting complications. However, the following suggestions address the theoretical mechanisms
thought to underlie the given treatment complication, so are a reasonable place to
start. It is important to note that this list is by no means exhaustive, but is included
as an initial guide to respond to common problems that can arise in the treatment
of anxiety disorders. For further information on combined treatment strategies, see
Chapter 5.
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Treatment Complication 1: Lack of Motivation or Difficulty
with Follow-Through
One of the biggest challenges in psychotherapy is working with clients who
have difficulty following through on treatment plans and homework assignments,
who have many prior failed treatments, or who experience hopelessness about
their ability to change. This problem can sometimes be recognized early in
the case formulation process by either learning about a long history of unsuccessful past treatments (especially multiple cases of dropping out of treatment),
or by giving a mini-homework assignment and evaluating whether or not this
is completed between sessions. We frequently ask clients to spend some time
between the first couple of sessions thinking about their specific goals for therapy and trying to identify concrete ways their life would be different if treatment
were effective. Whether and how this assignment is completed may give early
clues about whether motivation and follow-through are likely to be treatment
barriers.
Fortunately, there are a number of specialized treatment approaches that have
been developed to address these difficulties. For instance, Motivational Interviewing
(MI) (Miller & Rollnick, 2002) is a widely used technique that draws from the
transtheoretical model of change (Prochaska & DiClemente, 1992) to highlight the
differences between clients’ goals and their current behavior, and tries to reduce
these discrepancies. Motivational Interviewing has achieved considerable success
in helping clients overcome difficult motivational problems in order to profit from
treatment, particularly within the realm of substance abuse (Burke, Arkowitz, &
Dunn, 2002). Recent evidence indicates that Motivational Interviewing may be
beneficial for clients with anxiety problems as well. For example, Westra and
Dozois (2006) found that individuals with a principal anxiety diagnosis displayed
greater benefits from CBT if they first participated in Motivational Interviewing
sessions.
Readiness Treatment (VanDyke & Pollard, 2005) is another promising method
for working with individuals who have failed to respond to at least one firstline treatment approach. The basic principle underlying Readiness Treatment is
that treatment-interfering behaviors (TIBs; i.e., behavior patterns incompatible with
successful participation in treatment) may have disrupted therapy. Common TIBs
include failure to acknowledge having a problem, difficulty following the treatment
plan, or frequently coming late to treatment sessions. Thus, cognitive interventions
are primarily designed to focus on readiness for treatment and beliefs associated
with the TIBs, as opposed to focusing on beliefs directly related to the anxiety disorder. Ideally, the TIBs should be added to the problem list and become an active
part of the case formulation. Originally developed for OCD, initial pilot data suggest
that Readiness Treatment may be effective in reducing TIBs so that clients can more
fully engage in treatment (VanDyke & Pollard, 2005). At this point, future research
is needed to more fully establish the efficacy of Readiness Treatment for anxiety
problems more broadly.
A Case Formulation Approach to Resolve Treatment Complications
23
Treatment Complication 2: Interpersonal Problems
Interpersonal issues often disrupt treatment, and may need to be addressed to begin
making progress in therapy or to restart a “stuck” treatment. This is part of why it
is imperative to create a full biopsychosocial problem list at the outset of treatment,
which can help to identify interpersonal problems early on. Additionally, there are
times when maladaptive relationship patterns may contribute to the client’s anxiety
disorder. Frequent reassurance-seeking was one example mentioned earlier. We also
sometimes see interpersonal conflict arise when the client starts to make progress in
therapy and their dependence on others is reduced as avoidance behaviors diminish. This often requires redefining roles in the relationship, and can dramatically
change power dynamics in the relationship. Although the progress in therapy is
clearly positive, treatment can stall if these new relationship demands mean that
avoidance behavior (rather than exposure) is being reinforced. In these cases, therapists will want to identify interpersonal problem areas that seem thematically or
temporally related to the client’s anxiety disorder and incorporate them into the
case formulation.
Applying techniques from interpersonal psychotherapy (IPT; Weissman,
Markowitz, & Klerman, 2000) is one approach to handling these problems.
Although IPT focuses on identifying and changing interpersonal problems implicated in the development of depressive episodes, these same types of problem areas
are often important in pathological anxiety. Traditionally, these include unresolved
grief, disputes with friends or relatives, difficulties forming or maintaining relationships, and problems coping with a life transition (e.g., leaving home for college,
getting married, having a baby, etc.). Notably, IPT is an empirically supported treatment for both depression (Weissman et al., 2000) and bulimia nervosa (Fairburn,
Jones, Peveler, Hope, & O’Connor, 1993), two disorders that share a high rate of
comorbidity with anxiety problems. Further, initial pilot studies indicate that IPT
may be an effective alternative for treating anxiety problems, including social phobia (Lipsitz, Markowitz, & Cherry, 1999), PTSD (Bleiberg & Markowitz, 2005),
and panic disorder (Lipsitz, Gur, & Miller, 2006). Additionally, Crits-Christopher,
Gibbons, and Narducci (2005) suggest that clients suffering from GAD may particularly benefit from interpersonally oriented therapy given that relational fears are
the predominant worry domain in GAD (Roemer, Molina, & Borkovec, 1997).
Treatment Complication 3: Emotion Regulation Difficulties
There are a variety of ways that severe emotion regulation difficulties may impact
treatment of anxiety problems. For instance, early exposure exercises, ratings of
automatic thoughts, or mood evaluations may indicate that a client uses only
extreme ends of rating scales, reporting either exceptionally low or high anxiety,
regardless of the provocation. This is useful information for the case formulation
because it may indicate that the client has trouble feeling or expressing gradations in
24
B.A. Teachman and E.M. Clerkin
emotions, and is experiencing the world in a very all-or-nothing fashion. Similarly,
clients may have difficulty identifying a range of different emotions, using anxiety
as a default response when the situation may be eliciting sadness, disgust, anger, or
other forms of negative affect. We often find this pattern will emerge early in the
case formulation process if therapists inquire about triggers for the current episode.
In other cases, emotion regulation difficulties present later in treatment, and can then
be used to revise the case formulation. For example, we occasionally see clients who
reliably over- and then under-predict the fear they expect to experience in various
situations, contributing to a recycling pattern of excessive avoidance and lack of
self-efficacy, followed by disappointment over a perceived failed exposure.
Fortunately, a number of treatment approaches have been developed to enhance
emotion regulation skills, including those specific to treatment-resistant anxiety disorders (see Mennin, 2006). Also, dialectical behavior therapy (DBT) (Linehan,
1993), an empirically supported treatment for Borderline Personality Disorder,
includes multiple emotion regulation strategies. Although we are not aware of clinical trials evaluating the efficacy of DBT specific to treating anxiety, there is evidence
that integrating aspects of DBT may be useful. For example, Cloitre, Koenen, and
Cohen (2002) found that individuals with PTSD benefited from the inclusion of
DBT strategies focused on emotion regulation skills prior to exposure work.
When incorporating DBT, clients are taught to observe and describe their current emotional state (without judgment), placing a particular emphasis on separating
descriptions of how one is feeling from descriptions of the actions that led up to that
emotion. DBT techniques include helping clients to identify the precipitating events
for emotional reactions, instructing clients to observe ongoing cognitive, physiological, and nonverbal behavior responses, and focusing on what other people might
feel in similar situations (Linehan, 1993). For example, the client who consistently
fails to predict how fearful she will be in a given situation may be instructed to
imagine what others would feel when encountering a similar challenge. Meanwhile,
an anxious client who has difficulty identifying a range of emotions may be taught
to pay attention to physiological and behavioral reactions for “cues” that highlight
the complexity of his or her emotions.
Treatment Complication 4: Difficulties with Relaxation
and Acceptance
It is not uncommon for the case formulation to reveal difficulties with acceptance of
negative affect and arduous life circumstances, or problems with relaxation. During
the assessment and initial case formulation phase, clients often report having difficulty relaxing. Alternatively, this problem becomes apparent if the therapist asks
how the client spends his or her leisure time. Some individuals may not actually do
anything to relax, and many anxious persons are unaware that they lack pleasurable
activities in their life designed just for fun. In our experience, it is less common for
clients to directly report that they have problems with acceptance; yet, this may also
A Case Formulation Approach to Resolve Treatment Complications
25
constitute a treatment complication in pathological anxiety. This often emerges during case formulation when a client repeatedly talks about an issue that they cannot
seem to “let go” of (e.g., an old relationship or perceived slight). In some cases,
the difficulty focuses on rumination over an incident that the client sees as tied to
the onset of the anxiety problem, such as an experience of childhood bullying that
contributed to excessive worry or fears of negative evaluation. Although difficulties
with relaxation and acceptance clearly differ, similar treatments may be helpful for
both when standard relaxation techniques that are part of many CBT formulations
are not successful at resolving the impasse.
In particular, Mindfulness (e.g., Kabat-Zinn, 1990) and Acceptance and
Commitment Therapy (ACT; Hayes, Strosahl, & Wilson, 1999) may be useful approaches to target problems with relaxation or acceptance. For example,
Mindfulness, a type of awareness stemming from Eastern traditions, focuses on
relaxation techniques, developing an awareness of different possibilities, and altering habitual ways of responding (Martin, 1997). Demonstrating its potential utility,
a group intervention based on mindfulness meditation led to significant reductions
in anxiety among people with generalized anxiety and panic disorders (Miller,
Fletcher, & Kabat-Zinn, 1995). Roemer and Orsillo (2002) advise that when incorporating mindfulness into traditional CBT, clinicians should focus on enhancing
awareness of patterns of anxious responding. For instance, they suggest teaching
clients to contrast typical patterns of avoidance with mindfulness techniques, such
as “noticing and letting go” of tension during progressive muscle relaxation.
ACT, another technique to address difficulties with relaxation and acceptance,
has received preliminary empirical support for treating a variety of problems (Hayes,
Follette, & Linehan, 2004), including anxiety disorders (Twohig, Masuda, Varra, &
Hayes, 2005). ACT is premised on the idea that trying to eliminate the occurrence
of negative thoughts and feelings may be counterproductive (Hayes et al., 1999);
instead ACT focuses on altering the ways that difficult private experiences function
mentally. Researchers stress that a so-called “negative thought” or “negative emotion” that is mindfully observed may no longer function in a negative way, even if it
might in other contexts (Hayes, Luoma, Bond, Masuda, & Lillis, 2006). Thus, ACT
may be particularly useful for addressing acceptance concerns in anxiety given that
a core goal of the treatment is to facilitate acceptance and a sense of “psychological flexibility” (Hayes et al., 2004). However, it should be noted that other authors
have questioned the claim that ACT is uniquely different from CBT (Hofmann &
Asmundson, 2008) and questioned the empirical support for ACT (Öst, 2008).
Treatment Complication 5: Information Processing Biases
and Rigid Thinking
Cognitive models of anxiety disorders have increasingly relied on information
processing paradigms to better understand the maintenance and development of
maladaptive anxiety and avoidance (Beck & Clark, 1997). These paradigms suggest that reductions in the tendency to preferentially process potentially threatening
26
B.A. Teachman and E.M. Clerkin
information may decrease anxiety symptoms (see Williams, Watts, MacLeod, &
Mathews, 1997). Not surprisingly, biases in the ways clients attend to, interpret, and
recall threat cues often figure prominently in case formulation, and can be detected
in a variety of ways. For instance, during the initial assessment, accounts of prior
fear-relevant interactions can be challenged to examine the rigidity with which a
client clings to overly negative interpretations of the encounters.
When the case formulation reveals a rigid pattern of selectively processing threat
material, an experimental treatment approach known as “information processing
training” may be considered. During information processing training, researchers
are attempting to reduce anxiety by literally “re-training” biases in interpretation of
and attention to danger cues. Although still preliminary, results are promising that
these techniques may effectively shift processing biases in healthy (see MacLeod,
Rutherford, Campbell, Ebsworthy, & Holker, 2002; Mathews & MacLeod, 2005)
and anxious populations (e.g., Amir, Weber, Beard, Bomyea, & Taylor, 2008;
Teachman & Addison, 2008). Further, information processing training may be used
to augment existing, empirically supported approaches to help clients consolidate
their treatment gains more rapidly. Note, though, that the ultimate impact of these
types of interventions for reducing anxiety symptoms is not yet known.
Treatment Complication 6: Low Self-Efficacy and Losing
Treatment Gains
In some instances, an empirically supported treatment is showing signs of progress,
but the gains are painfully slow, suggesting additional treatment may be necessary. If
the case formulation reveals that a client has extremely low self-efficacy (e.g., about
the ability to implement treatment strategies), or the client is regularly losing gains
between sessions or having trouble practicing on his or her own, more intensive
treatment may be indicated. Whenever possible, decisions about enhanced treatment
should be made collaboratively by the client and therapist. Further, more intensive
treatment should be framed as additional support as opposed to a failure on the
client’s part.
Introducing more intensive treatment can be as simple as adding a few “booster”
sessions, or increasing sessions from once to twice a week. For certain clients, particularly those whose issues are most salient in their homes, adding home visits may
also be helpful. OCD clients with hoarding problems, for example, may greatly benefit from having a therapist come to their house to help begin the exposure exercises
necessary to get rid of excessive belongings. Alternatively, when pathology is so
severe that significant treatment gains are unrealistic in a standard setting, inpatient
care may be recommended. This more intensive form of treatment offers several
advantages over traditional outpatient care, including enhanced structure, support,
and therapeutic contact (VanDyke & Pollard, 2005). For example, Abramowitz, Foa,
and Franklin (2003) found that, although treatment effects for twice-weekly outpatient (versus inpatient) work were similar for clients with OCD, there was a trend
for clients in the more intensive setting to show greater symptom improvement.
A Case Formulation Approach to Resolve Treatment Complications
27
Conclusion
In this chapter, we have outlined just a sampling of the myriad ways that case formulation can help rejuvenate a flailing anxiety treatment. While the chapter focused
mainly on the steps used to develop a CBT case formulation and ways that these
steps can aid in identifying potential treatment complications early on, it is clear
that case formulation across many different treatment modalities can help manage
difficulties in anxiety disorder treatments. In most cases, CBT case formulation will
initially be matched with CBT approaches. However, we have tried to show that
when these first-line approaches are not successful, alternative treatment options
may be helpful. Case formulation is especially useful for highlighting likely treatment barriers early in the evaluation and therapy process, so that minimal time
is wasted on strategies that are not likely to bear fruit. Further, because case formulation involves generating multiple hypotheses about the factors that led to the
development and maintenance of the mechanisms fueling the disorder, the process
naturally leads to multiple, creative solutions to address problems. Case formulation is a dynamic process that encourages clinicians to be similarly dynamic in their
treatment planning. When case formulation becomes stagnant, so too will treatment.
Whether using CBT or another modality, case formulation is most successful in
helping to resolve treatment complications when it encourages therapists to think
outside the box and truly use collaborative empiricism – iteratively trying and then
evaluating new ideas to move therapy forward.
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Helping Exposure Succeed: Learning Theory
Perspectives on Treatment Resistance
and Relapse
Mark B. Powers, Bram Vervliet, Jasper A.J. Smits, and Michael W. Otto
Exposure-based interventions are core to the psychosocial treatment of anxiety
disorders. Protocols utilizing these elements are associated with some of the highest
effect sizes in the anxiety treatment literature (e.g., Hofmann & Smits, 2008). These
interventions rely on the use of experience to aid the learning of safety in relation to
the core fears underlying anxiety disorders; yet, the efficacy of these interventions
may be limited by a number of contextual and procedural challenges. This chapter provides a review of studies of these procedures and parameters and provides a
conceptual overview of a heuristic for guiding exposure interventions. Relative to
this heuristic, we attend to the stimulus properties, duration, spacing, gradation, and,
particularly, context of exposure interventions.
Exposure Is New Learning
Perhaps the most important concept in helping clinicians arrange effective exposure
is the evidence that extinction learning is new learning rather than the weakening
of previous associative learning (Bouton, Woods, & Pineno, 2004; Rescorla, 2001).
Because the old learning remains intact, the new learning of safety competes with
the old fear learning (Bouton, 2002). Successful treatment results when the new
learning becomes the dominant association to the once-feared cues (e.g., an expectant audience in the case of social anxiety disorder). Said differently, after exposure
treatment, the meaning of fear cues becomes ambiguous, with both anxiety-relevant
and safety meanings associated with the cue. The task of the cognitive behavior
therapist is to ensure that safety learning dominates this competition between the
memories, so that cues once core to the anxiety disorder no longer elicit anxiety
and avoidance when encountered. As such, the question for the clinician is how to
arrange exposure so that a patient best learns that the phobic cues underlying the
disorder are safe.
M.B. Powers (B)
University of Amsterdam, Amsterdam, The Netherlands
e-mail: mpowers@fmg.uva.nl
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_3,
C Springer Science+Business Media, LLC 2010
31
32
M.B. Powers et al.
To help achieve this aim, clinicians need to consider how to link the feared cues
with memories of successful exposure. As will be reviewed below, this is done by
completion of exposures across the range of the most salient cues and contexts, and
the use of as many recall and generalization cues as possible. In short, the more
salient that the extinction learning can be made to the patient around the most relevant cue (“this is exactly what I have been fearing; I expected a bad outcome, but
it did not occur”) the more relevant the learning. Also, the more that a patient can
rehearse and remember this learning, the better this learning will be available for
recall. Our own heuristic for achieving these ends are drawn richly from the animal learning research and experimental studies discussed below. Nonetheless, it is
important to note that the result of the heuristic is similar to those derived from a
cognitive perspective that seeks to use experience from “behavioral experiments” to
provide unambiguous opportunities to change beliefs underlying anxiety disorders
(e.g., Wells et al., 1995). Indeed, when extinction is considered appropriately as new
learning, and when a variety of retention and recall aids are adopted for this new
learning (including accurate cognitive cues, “I can do this” “these situations are no
longer bothersome”) much of the distinction between behavioral experiments used
in cognitive therapy and exposure interventions plus cognitive generalization cues
is rendered moot.
In arranging exposure therapy for anxiety patients, we believe clinicians have
three central tasks: (1) helping the patient identify the core fears underlying the
anxiety disorder, (2) arranging exposure interventions to disconfirm those fears by
providing the patient with direct experiences with their ability to safely confront and
cope adequately with the feared cues, and (3) demonstrate this ability to themselves
in enough diverse contexts so that this ability is strongly remembered for application in the future. Concerning the identification of the core fears, we recommend
careful evaluation of the individual patient in relation to the likely patterns identified by psychopathology research. For example, psychopathology research provides
strong evidence that panic disorder is characterized by fears of and catastrophic
interpretations of anxiety and panic symptoms, whereas social anxiety disorder is
characterized by fears of and catastrophic interpretations of humiliation or embarrassment (Barlow, 2002). Nonetheless, despite the commonality of these core fears
among individuals with these disorders, there are important individual variations on
how these core fears are experienced. For example, in panic disorder, individuals
fear different anxiety sensations and have different catastrophic interpretations of
these sensations. Targeting exposure to the exact fears experienced by the patient
will provide the most relevant learning of safety by elucidating the exact contingencies to be broken by the exposure (non-occurrence of aversive outcomes). For
example, a concern about symptoms of dizziness in panic disorder, due to fears of
fainting, may be linked to any of a number of additional concerns such as the fear of
falling, fears of scrutiny (e.g., “I will look stupid if I am woozy”), or fears of being
incapacitated (“others would take my wallet if I faint”). Elucidation of the specific
concern, for example with a traditional “downward arrow” questioning technique
(Burns, 1980), is helpful in specifying the correct conditions for targeted exposure.
Although the induction of dizziness with interoceptive exposure (e.g., headrolling or spinning in a chair) would be a core intervention for panic disorder
Helping Exposure Succeed
33
(Barlow & Craske, 2007), but it would be delivered differently to address the core
concerns of a specific patient. For example, for core fears linked to falling, interoceptive exposure to dizziness while standing may be especially relevant; for fears of
scrutiny, performance of a social task while dizzy may be important; and for fears
of being incapacitated, induction of dizziness around strangers may be the exposure of choice. In all these instances, the goal is to provide therapeutic learning
by showing the patient that no aversive outcome follows exposure to the fear cues.
Exposure exercises need not start with this bull’s eye target, but it will be important
for the therapist to work toward this top-of-the-hierarchy set of cues to achieve full
extinction of the core fear.
As part of the task of honing exposure toward core fears, consideration of the
additive property of fear cues is important. For example, exposure to memories
of an assault in an individual with PTSD may function very differently during an
evening session (when it is dark) versus during the day. Likewise, giving a speech
as part of an exposure for an individual with social anxiety disorder may be experienced very differently depending whether cues of anxious performance are present
(e.g., dry mouth and a pounding heart). It is the clinician’s central task to determine
the nature of the safety learning that needs to be achieved from the exposure. For
example in the treatment of panic disorder, the richness of the cues around driving
concerns can help reveal the top-of-the-hierarchy cues for exposure as well as relevant steps along the way in building the hierarchy of exposure successes. Rather
than simply focusing on driving in traffic as the relevant exposure, the top-of-thehierarchy cues should be thought of as the additive influence of all the relevant
stimuli: in car + driving the expressway + rush hour + no exits available + alone
+ panic symptoms present + the thoughts “I can’t make it; I am going to crash
the car.”
If extinction represents the active reacquisition of safety in response to these cues,
then the clinician needs to arrange for the stepwise exposure to each of these elements either alone or in combination. The degree of combination rests on how high
the clinician wants to start in the fear hierarchy (see staging of exposure below) to
help ensure stepwise success. For panic disorder, current protocols start this process
with exposure to the feared panic sensations using interoceptive exposure techniques
(see “Avoiding Treatment Failures in Social Anxiety Disorder” by S. G. Hofmann
et al., this volume). The goal is to have the patient do nothing in response to these
sensations to learn that they are not dangerous or in need of management. Once
safety is learned to this element of the larger top-of-the-hierarchy fear, the clinician
can begin chaining together the fear cues. Exposure homework away from the therapist can help create safety for the stimulus panic sensations + alone. Following
success with this stimulus context, the clinician can assign interoceptive exposure
in the car to achieve safety learning for panic sensations + alone + car. When comfort is achieved with this cue, the next step may be to re-introduce the catastrophic
thoughts as part of the extinction stimulus (following cognitive restructuring to help
the patient gain perspective on the inaccuracy of these thoughts): panic sensations
+ alone + car + “I can’t make it; I am going to crash the car.” Interoceptive exposure followed by practice driving safely under conditions of feeling odd may be the
next step, and finally, when so many of the cues of the top-of-the-hierarchy concern
34
M.B. Powers et al.
have been exposed to safety learning, the clinician is in the position of assigning
driving the expressway as an exposure homework. This can be done both with and
without interoceptive exposure to help the patient create a true sense of safety in
this situation regardless of the presence of anxiety symptoms. With the completion
of this work driving the expressway should become incapable of eliciting a panic
attack (Hofmann, Richey, Asnaani, Sawyer, this volume).
The chaining together of feared cues can be crucial for helping the clinician target the most durable and relevant learning for the anxiety disorder. In the case of
social anxiety disorder, it is easy to focus on the acquisition of safety around a welldone social performance. Under these conditions the clinician should expect that
the patient has learned relative safety under conditions of a well-done social performance. Fuller acquisition of safety may require the acquisition of safety under
poor performance conditions. Indeed the focus on “social mishap” exposures in the
treatment of social anxiety disorder (see Hofmann & Otto, 2008; Hofmann, Richey,
Asnaani, & Sawyer, this volume) is focused on helping patients undo the true core
fear of the consequences of poor social performance (not just the lower level fear
of any social performance). Hence, programming in social difficult exposure (e.g.,
spilling a coffee; see Hofmann & Otto) should lead to fuller safety learning than a
focus on adequate performance exposures alone.
Finally, to help lock in this safety learning, patients need to have confidence in
that negative outcomes do not occur despite variations in the conditions in which
they confront their feared cues (for animal studies see Gunther, Denniston, &
Miller, 1998; Chelonis, Calton, Hart, & Schachtman, 1999, but see Bouton, GarciaGutierrez, Zilski, & Moody, 2006; for clinical studies see Rowe & Craske, 1998b;
Vansteenwegen et al., 2007). As clinicians know well, a patient’s phobic concern
may differ greatly depending on the context in which it is encountered, e.g., on a
good versus bad day.1 These contextual factors have a powerful influence not only
on the degree of anxiety elicited by a feared cue, but, as reviewed below, can serve
as a powerful factor in incomplete treatment and relapse. To provide a full accounting of the power of context in extinction, we turn toward both animal and applied
research.
Context Effects
The conceptualization of extinction as new learning rather than the erasure of
old learning is supported by findings from a range of animal, analogue, and clinical studies that illustrate the return of fear with a shift in contextual (recall)
cues for either extinction or original fear learning (for review see Bouton, 2002;
1 Although
clinicians may not be privy to the full learning history of their patients, and hence
may not know fully what cues are simply a setting condition (not directly feared by signaling
conditions under which the phobic cues are more concerning) or are a fear cue in their own
right, this conceptual confusion rarely translates to clinical confusion when it comes to arranging
exposure.
Helping Exposure Succeed
35
Craske, Hermans, & Vansteenwegen, 2006). In terms of clinical application, fear
renewal refers to the return of the fear response when there is a context shift
after treatment. Contexts can include both internal (i.e., drug state) and external
(i.e., darkness) factors. The most widely accepted evidence for the role of contexts in animal and human fear acquisition, extinction, and relapse is provided
by the contextual renewal paradigm. The contextual renewal paradigm includes
an acquisition (fear learning) phase in one context (A), an extinction phase in a
second context (B), and finally an evaluation of which memory (fear or safety
learning) is dominant in a test context (the fear context, A; the extinction/safety
context, B; or a novel context C). For example, a patient may develop claustrophobia in one context A (i.e., a closet as a child), then receive treatment in a
second context B (i.e., claustrophobic treatment chamber), and the “test” then is
after treatment in a third context C (an elevator). Unfortunately for clinical treatment, there is ample evidence that extinction learning, as compared to the original
fear learning, is much more sensitive to context effects. This conclusion, and the
return of a fear after a shift in context (fear renewal), is supported by (a) animal studies with an ABA design (e.g., Bouton & King, 1983), an ABC design
(e.g., Bouton & Brooks, 1993) and an AAB design (e.g., Bouton & Ricker, 1994),
(b) human conditioning with an ABA design (Vansteenwegen et al., 2005; Milad,
Orr, Pitman, & Rauch, 2005) and an ABC design (Effting & Kindt, 2007), and
(c) human treatment studies (Mineka, Mystkowski, Hladek, & Rodriguez, 1999;
Mystkowski, Craske, & Echiverri, 2002; Mystkowski, Mineka, Vernon, & Zinbarg,
2003; Rodriguez, Craske, Mineka, & Hladek, 1999). In these studies, context can
be such stimuli as the external environment (e.g., cage design; Bouton, 1993;
Harris, Jones, Bailey, & Westbrook, 2000), internal stimuli (e.g., level of drug
modulated arousal; Bouton, Kenney, & Rosengard, 1990), or recent events (e.g.,
Bouton, Rosengard, Achenbach, Peck, & Brooks, 1993). For example, animal
research indicates that internal state (e.g., anxiety/arousal modulation from benzodiazepine administration) is a sufficiently context cue such that extinction (safety)
learning may be achieved solely in that context (Bouton, Kenney, & Rosengard,
1990). In an experimental demonstration of a similar effect in humans, Mystkowski
et al. observed a significant return of fear among phobic patients who underwent
exposure therapy after they had ingested either caffeine (arousal induction) or
placebo (no arousal reduction) and then were tested at a follow-up period in the
context of either the same or different arousal condition. Regardless of the direction of the change in internal context (caffeine to placebo or placebo to caffeine)
those who were tested under a different internal state had more return of fear
than those tested under the same arousal condition as during extinction. Indeed,
this context (internal state) dependency has been used to explain the apparent
loss of CBT efficacy when it is delivered in the context of medication treatment that is later discontinued (Otto, Smits, & Reese, 2005; see Hofmann et al.,
this volume).
To date, three mechanisms have been proposed for the renewal of fear responses
including the following: (a) the Modulatory Mechanism – new extinction information only applies in the extinction context (Bouton, 1988, 2000), (b) the Inhibitory
36
M.B. Powers et al.
Mechanism (Lovibond, Davis, & O′ Flaherty, 2000) – the extinction context predicts
no US and thus protects the CS from extinction (“I not at risk under these conditions”); and (c) Generalization Decrement (Lovibond, Preston, & Mackintosh,
1984) – the extinction stimulus is “wrong” and thus protects the acquisition stimulus
from extinction (“I was never afraid of this”). All accounts stress the match between
extinction and the contexts that signal that the fear cue is really to be feared. Future
research may determine which theory best fits the data.
Return of fear can also occur with the mere passage of time following extinction
training (spontaneous recovery: Brooks & Bouton, 1993; Brooks & Bowker, 2001;
Brooks, Karamanlian, & Foster, 2001; for a demonstration in humans, see Marescau,
Vansteenwegen, Vervliet, & Eelen, unpublished manuscript). Bouton (2002) has
argued that “time” can also function as a context (as internal and external contexts
change over time). In that sense, testing the extinguished CS at a later moment
in time is conceptually equivalent to contextual renewal. Accordingly, a fading of
treatment sessions or the use of a booster session months after the last weekly session may have a valuable influence on helping patients know that they can still
respond well to phobic cues despite passage of time. These procedures help ensure
that the passage of time since extinction training is linked in memory to continued
extinction success not to the old fear memories. This procedure also serves as a nice
introduction to one of the core feature of our heuristic for the application of exposure (Fig. 1) – exposure should be programmed across relevant contexts to ensure
that memories of success will be available at the time of need. Given the extraordinary cognitive abilities of humans, this programming can occur in these realms
in addition to the active practice of exposure across contexts. Even these cognitive
procedures are consistent with the notion from animal research that contextual cues
set up “expectancies” for extinction or fear memories. In the case of time cues, in
addition to the use of booster sessions and booster homework assignments (e.g.,
the programming of exposure homework for intervals after formal therapy ends),
the therapist may help the patient understand the nature of the treatment changes to
help the patient be prepared on how to approach phobic situations in the future (e.g.,
“I am different now that I have had treatment, I know how to approach my phobic
situations/events differently now.”).
In addition to the external and internal environment, contextual cues also include
what the patient does in the situation (e.g., superstitious behaviors that create a
context for the patient that signals relative safety). As explicated by all three of
the theoretical accounts of context effects, these behaviors could signal trouble
for extinction. According to the Modulatory Mechanism, the use of these superstitious behaviors would help insulate extinction learning from true safety should
those superstitious behaviors not be used or available. According to the Inhibitory
Mechanism no aversive outcome would be expected anyway under these conditions (“I knew I would be OK because I. . .”); and, similarly, according to the
Generalization Decrement “I was never afraid of the exposure stimulus as long as I
could. . ..” To broaden this discussion, we will broaden and re-label the concept of
superstitious behavior as “safety behaviors.”
Helping Exposure Succeed
37
Constructing a Program of Exposure
1. Construct a model of the top-of-the-hierarchy fear for the patient using an additive model.
In constructing the model, consider the range of additive cues that are part of the core fear
including external as well as internal environments (including feeling states, thoughts, and
actions taken by the patient). Select the most relevant exposure exercises (e.g.,
interoceptive exposure for panic disorder or social exposures for social anxiety disorder),
but then create a hierarchy of exposures by varying the additive cues present in the
exposures.
2. Conduct the exposures while evaluating the safety learned by the patient. Elicitation of
anxiety at exposure onset is a useful measure of a good match between the cues and the
fear (indicating a relevant exposure), but good anxiety reduction across the exposure and
evidence that feared outcomes did not occur (or were not as aversive as assumed) is the
goal of the exposure practice.
3. Continue conducting the exposures with an eye toward varying the contexts of the
exposure to ensure that the learning of safety is not conditional on a specific context.
Make sure to vary the pre-comfort of the patient when going into exposures (idiosyncratic
definitions of good vs. bad days such as the presence of fatigue or anticipatory anxiety),
and the presence of the therapist or significant others, the presence of other safety cues
and behaviors. Use the Assessment Worksheet (Figure 2) to aid in the assessment of
these cues.
Fig. 1 A heuristic for exposure planning
Safety Behaviors
Safety behaviors are subtle avoidance behaviors people use to reduce anxiety or
prevent a perceived threat that can undermine the efficacy of exposure (Wells et al.,
1995). Some examples include carrying a cell phone for fear of needing help, carrying rescue medication (benzodiazepines) to take in the event of a panic attack,
using air conditioning to reduce sweating, drinking alcohol to reduce anxiety, gripping the wheel tightly while driving to prevent an accident, or asking questions
38
M.B. Powers et al.
excessively to prevent ambiguity. As we see from the list the defining characteristic
of a safety behavior is not the form of the behavior but rather the function that
is important. If the perceived threat is a potential “true alarm” (i.e., car accident)
then the safety behavior may be adaptive (i.e., wearing a seatbelt). However, if the
threat is “false alarm” (i.e., panic attack) then using safety behaviors may prevent
the learning of unambiguous safety – I’m safe as long as I have my medication
in my pocket. Indeed, Powers, Smits, and Telch (2004) showed that participants
who had safety behaviors available during exposure treatment reported significantly
less improvement compared to participants who did not rely on safety behaviors
(i.e., response rates were 45% versus 95%). Interestingly, the deleterious effects
of safety behaviors were evident whether patients used them or not – suggesting
the mere availability of safety behaviors can interfere with fear reduction. These
data are consistent with clinical observations that patients who carry rescue medications (i.e., benzodiazepines) are at greater risk of relapse even if they never
take them.
When it comes to medication treatment, one direct measure of the context
specificity of exposure learning is the attribution of treatment gains. For example,
Basoglu et al. (1994) reported a 60% relapse rate at medication-free follow-up if
patients in their combination treatment trial attributed their gains to medication.
This is compared to no relapses in the group that attributed their gains to their
own efforts. However, this correlational design prevents causal inferences. Powers,
Smits, Whitley, Bystritsky, and Telch (2008) conducted a randomized trial with
claustrophobic participants who underwent exposure-based treatment in the context of a pill placebo that they were led to believe was a medication that made
the exposures easier (sedating side-effect profile) or more difficult (activating sideeffect profile). Consistent with prediction, an attribution for pill facilitation led to
higher relapse. The return of fear rate at follow-up was nearly 40% in the medication attribution group compared to 0% in the other conditions. These data highlight
the importance of monitoring patient attributions for improvement.
Taken together, a central implication of these context studies is that clinicians
must plan for the generalization of safety learning from the treatment environment
(at the clinic, with the therapist, etc.) to non-treatment contexts and across the presence and absence of safety behaviors. Repeated exposure sessions on different days
(when the patient is entering the session in different mood states, after different life
events) and when exposure is conducted in different ways (standing, sitting, after
induction of dizziness), as well as the use of homework (exposure without the presence of the therapist or clinic context) should help achieve this variability in training.
Clinicians should also carefully consider the role of relaxation training in their anxiety treatment. Teaching the patient to relax in the presence of the phobic stimulus
may create a unique context for safety learning, a context that may be lost should
the patient be unable to relax adequately at a later point in time. In the treatment
of research, there is evidence that relaxation training or breathing retraining does
not lead to superior outcome (e.g., Schmidt et al., 2000), and accordingly protocols
that encourage the experience of anxiety as part of the stimulus context (Eifert &
Forsyth, 2005) may lead to more durable extinction.
Helping Exposure Succeed
39
Exposure Planning Checklist
Attending to the Correct Core Fear:
What is/are the core fear or fears that should be targeted by treatment? Ask the patient: “what is so bad
about….” to elucidate the central feared features.
_____________________________________________________________
_____________________________________________________________
_____________________________________________________________
Attending to the Contexts Surrounding the Fear:
Aggravating Contexts
What are the contexts in which this fear is worse? Consider the following:
o
Time of day/year (including light dark, certain weather condi ons (e.g., hot weather in the case of
panic disorder): ___________________________
o
Presence of others (known or unknown people: ___________________________
o
Presence of symptoms (e.g., muscle tension, certain worries, etc.): ________________________
o
Mental or physical fa gue (also including menstrual cycle): ___________________________
o
Interpersonal conflict: ___________________________
o
Other ___________________________
o
Other ___________________________
Safety Behaviors/Events
What are the behaviors or events that lead the patient to assume relative safety from the feared
outcomes?
o
Contact with others (e.g., cell phone, presence of safe other, knowledge of availability of safe other):
___________________________
o
Food or drink (bo le of water, mints, antacids, crackers, fruit): ___________________________
o
Something to hold (glass)/ posi on near a wall or door: ___________________________
o
Medica on (o en benzodiazepine or beta-blocker use): ___________________________
o
Cogni ve rituals (e.g., affirma ons, lucky sayings): ___________________________
o
Body posi ons/eye contact (aver ng one’s eyes while speaking, clasping the hands, leaning against a
wall, bracing against a chair): ___________________________
o
Talking with others: ___________________________
o
Other: ___________________________
o
Other: ___________________________
o
Other: ___________________________
Fig. 2 Understanding exposure cues and contexts
Figure 2 is designed to help clinicians develop a plan for the application of exposure to core fears across contexts. It is used to help elucidate the range of contexts
40
M.B. Powers et al.
that need to be targeted in treatment. Treatment planning thus involves progression
along two types of hierarchies – movement toward the core fears that define the top
of a hierarchy of concerns and movement along a continuum of contexts, removing safety behaviors and ensuring that fear at the top of the hierarchy are rehearsed
across a range of contexts. An especially relevant context is medication use, and
as detailed in Powers et al. (this volume), reinstatement of CBT across medication
taper may be crucial for helping patients maintain their treatment gains when CBT
was learned originally in the context of medication use
Considering Exposure Parameters
By considering the core learning that needs to be achieved by the patient from exposure, and evaluating this learning in relation to the contexts under which it is to be
learned and applied, a surprising amount of research on exposure parameters can be
understood. In the following sections, individual exposure parameters are reviewed
and then discussed relative to safety learning and context considerations.
Exposure Duration and Spacing
Both animal and human studies indicate that continuous extinction trials yield better outcomes compared to distributed and interrupted extinction trials (Chaplin &
Levine, 1981; Girodo & Henry, 1976; Baum, Andrus, & Jacobs, 1990; Davis,
1970; Mackintosh, 1974; McCutcheon & Adams, 1975; Miller & Levis, 1971).
For example, Chaplin and Levine compared a single 50-min exposure with two
25-min exposures among participants with public speaking fear. The continuous
50-min condition outperformed the two 24-min exposures that were separated by a
10-min inter-trial interval. Clinical studies also demonstrate an advantage for continuous exposure (Foa, Jameson, Turner, & Payne, 1980; Grayson, Foa, & Steketee,
1986; Rabavilas, Boulougouris, & Stefanis, 1976; Stern & Marks, 1973). Stern
and Marks compared 2-h sessions with 41/2-h sessions of in vivo exposure for
panic disorder with agoraphobia and found that the longer sessions yielded higher
response rates. Foa et al. (1980) conducted a crossover study with agoraphobics and
found that massed exposure (10 daily sessions) was superior to spaced exposure
(10 weekly sessions), particularly in reducing avoidance. Foa and Kozak (1986)
also suggested that a long (90 min) exposure outperformed nine brief exposures
(30 s) with long inter-trial intervals (10 min) among participants with OCD. Another
consideration is when to terminate an exposure trial. Subjective fear and physiological response during exposure typically follows a curvilinear trajectory (Foa &
Chambless, 1978; Stern & Marks). As illustrated in Fig. 1, we can see that if a
patient were to terminate treatment during Session 1 after 40 min of exposure they
may be more “sensitized” than when they started treatment (Emmelkamp, 1982).
Helping Exposure Succeed
41
Ending exposure here may result in sensi za on
80
70
60
SUDS
50
Session 1
40
Session 2
30
20
10
0
0
20
40
Time (mins)
60
80
Fig. 3 Mean subjective anxiety ratings during exposure sessions
From the perspective of what is learned from therapy, longer exposures give a
greater opportunity for unambiguous learning that the exposure cues can be tolerated and do not lead to negative outcomes. Ending an exposure when anxiety is
low allows for the retention of a “comfortable” exposure experience and appears to
aid ultimate outcome (Hayes, Hope, & Heimberg, 2008).
Distribution of Sessions
Although massed sessions result in quicker extinction learning, spaced sessions
result in more resilient extinction learning at follow-up (see Cain, Blouin, & Barad,
2003). This is consistent with the notion that intensive (massed) practice provides
less ambiguous learning of safety, but that greater spaces between sessions allows
for the integration of this learning relative to the contextual cue of passage of time,
and hence reduces the likelihood of spontaneous recovery due to the passage of time
as a context cue for the original fear learning. Craske and colleagues suggest capitalizing on the acute advantage of each of these strengths by massing sessions early
in treatment and then gradually expanding intersession intervals to protect against
relapse (Lang & Craske, 2000; Rowe & Craske, 1998a; Tsao & Craske, 2000). An
example schedule of 12 treatment sessions for panic disorder may include twiceweekly sessions for 3 weeks then once-weekly sessions for 4 weeks and finally
once every other week for 4 weeks.
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M.B. Powers et al.
Stimulus Properties (Imaginal, In Vivo, Virtual Reality)
Learning theory posits that the salience of the feared stimulus is an important factor
influencing the speed of learning, both for the acquisition and extinction of conditioned fear (Rescorla & Wagner, 1972). Hence, it is anticipated that response
changes occur faster to high versus low salient stimuli. Indeed, direct comparisons show the superiority of in vivo over imaginal exposure (Barlow, Leitenberg,
Agras, & Wincze, 1969; Dyckman & Cowan, 1978; Emmelkamp & Wessels, 1975;
Litvak, 1969; Sherman, 1972; Stern & Marks, 1973; Watson, Mullett, & Pillay,
1973). Emmelkamp and Wessels (1975) compared: (a) 90 min of flooding in vivo,
(b) 90 min of imaginal flooding, (c) 45 min of imaginal flooding followed by 45 min
of flooding in vivo. The results clearly showed an advantage for flooding in vivo.
However, imaginal exposure can be effective when in vivo methods are not possible (Rentz, Powers, Smits, Cougle, & Telch, 2003; Rothbaum, Astin, & Marsteller,
2005). For example, flying phobics may find it difficult financially to regularly
conduct in vivo exposures. Likewise, virtual reality exposure treatment (VRET)
can be an option when in vivo exposure is difficult. A recent meta-analysis suggested that virtual reality treatment was more effective than waitlist and placebo
treatments and equipotent to exposure in vivo (Powers & Emmelkamp, 2008). The
meta-analysis of nine studies where virtual reality exposure therapy was compared
to an adequate control group yielded a large combined effect size of g = 1.05
(95% CI: 0.71–1.40). Emerging technology may further improve VR treatment. The
new technology known as CAVE (CAVE Automatic Virtual Environment) increases
the realism (immersion) resulting in more potent exposure (Cruz-Neira, Sandin, &
DeFanti, 1993). Taken together, perceptual proximity (salience) seems an important
factor for the efficacy of extinction treatments.
Gradation of Exposure
After constructing a fear hierarchy the patient and therapist must decide which exposure item should be the first target. Studies show that if patients stay in the exposure
session long enough there is little difference in outcome between starting on an easier or more difficult item on the fear hierarchy (Gelder et al., 1973). However, there
is some evidence that massed flooding outperforms spaced graded exposure at a
5-year follow-up (Feigenbaum, 1988). Even though flooding may be a viable option
more patients may either reject or drop out of this type of therapy (Emmelkamp
& Ultee, 1974; Emmelkamp & Wessels, 1975). A method that capitalizes on both
options is to choose a moderately difficult item in the context of an expandingspaced schedule (Foa & Wilson, 2001; Rowe & Craske, 1998a). For example, a
therapist may suggest beginning exposure to an item with a SUD of 60 or 70 from
the patient-generated fear hierarchy.
Helping Exposure Succeed
43
Fear Activation
Foa and Kozak (1986) proposed that successful exposure must include (a) activating the fear structure and (b) disconfirmatory evidence that must be available and
processed by the patient (Foa & Kozak). The first assertion led some to hypothesize
that with greater fear activation comes greater fear reduction. However, studies have
not supported the theory that higher fear during exposure leads to better outcome
(Hafner & Marks, 1976; Kirsch, Wolpin, & Knutson, 1975; Marks, Boulougouris,
& Marset, 1971; Telch et al., 2004). Possibly, the crucial factor is not the level of
fear, but the level of expectancy of negative outcomes. Indeed, associative learning
models (e.g., Rescorla & Wagner, 1972) anticipate stronger extinction learning with
a larger discrepancy between the expected presence of the aversive outcomes and its
actual absence.
Focus of Attention and Behavior During Extinction
It is widely accepted that attention is a necessary precondition for learning to occur
(Rescorla & Wagner, 1972; Mackintosh, 1975). However, although some clinical
studies suggest that distraction during exposure leads to poorer outcome (Kamphuis
& Telch, 2000; Telch et al., 2004), others do not (Johnstone & Page, 2004). In fact,
Johnstone and Page found an advantage when patients engaged in threat-irrelevant
conversation during exposure. Upon closer examination, it appears that the type of
distraction is most important. If the distraction prevents the patient from functional
exposure to the stimuli (i.e., cognitive load) then it will interfere with fear reduction
(Kamphuis & Telch, 2000). Borkovec and Grayson (1980) stated that, “objective
presentation of the stimuli does not guarantee functional exposure to those stimuli”
(Borkovec & Grayson, p. 118). However, if the patient is able to “act normal” by
having a conversation while still maintaining awareness of the stimuli then outcome
may be enhanced (Johnstone & Page). Telch and colleagues propose that acting in a
way that is inconsistent with fear sends safety information (Wolitzky & Telch, under
review). For example, a patient may be instructed to smile during exposure even
though inconsistent with their fear. Although such actions may enhance exposurebased treatment it is not yet certain why. However, research shows that producing a
smile (even when unobtrusively) or a fearful expression elicits a consistent emotion
(Flack, 2006; Larsen, Kasimatis, & Frey, 1992; Strack, Martin, & Stepper, 1988;
Zajonc, Murphy, & Inglehart, 1989). One obvious possibility is that these interfering emotions during exposure are conceptually similar to a counterconditioning
procedure. This procedure involves the pairing of the CS with a new US that has
contrasting affective value (e.g., an appetitive versus an aversive stimulus), and is
known to produce robust extinction of fear responses (e.g., Peck & Bouton, 1990)
and even changes the affective value of the feared stimulus (Baeyens, Eelen, Van
den Bergh, & Crombez, 1989). This counterconditioning hypothesis is fully consistent with the “new learning” account of extinction, and instead of pairing the CS
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M.B. Powers et al.
with “no aversive outcome” it pairs it with a positive stimulus. Further investigation
of this process in human fear conditioning is pending.
Concluding Comments
Research on the nature of fear extinction and relapse offers a number of valuable
heuristics to guide interventions to minimize treatment resistance and relapse. This
chapter highlighted a number of factors that may contribute to treatment resistance:
(1) Both conditioning and clinical research has demonstrated weakened extinction
effects with short and interrupted exposures to the feared stimulus, rather than long
and continuous ones. (2) Expanding-spaced sessions seem to capitalize both on a
Treatment Resistance Perspectives:
•
Long exposure > short exposure
•
Continuous > Interrupted
•
Expanding spaced sessions
•
In-vivo > imaginal
•
Flooding = Graduated (efficacy) but graduated can reduce drop-outs
•
Attention > Distraction
Treatment Relapse Perspectives:
•
Safety learning is an active process of new learning
•
New learning has to compete with old learning
•
New learning is particularly context dependent
•
Contexts can aid or impair recall of extinction depending on their meaning
(association with fear or safety)
Fig. 4 Summary of learning perspectives on treatment resistance and relapse
Helping Exposure Succeed
45
fast reduction of anxiety (through initial massed extinction trials) and better retention on the long run (through later spaced extinction trials). (3) Exposure to high
salience stimuli seems to produce better results, that is, in vivo exposure is more
powerful than imaginal exposure. Virtual reality protocols are promising in this
regard. (4) There is no clear picture on the graduated exposure versus flooding,
but the former may lead to fewer drop-outs. (5) There appears to be no supporting evidence for the widespread idea that more fear activation during exposure
leads to better extinction effects. Possibly, the expectancy of the occurrence of the
threatening event (which is disconfirmed in extinction) is more important than the
overt fear response. (6) Out-of-clinic practice (self-exposure) clearly improves the
outcome of exposure treatment and (7) comorbidity does not seem to be a major
problem for successful treatment of anxiety (Fig. 4).
It is now commonly acknowledged that extinction and exposure treatments are
active learning processes, and result in the formation of an extinction memory that
co-exists and competes with the original fear memory. Attention to the context of
treatment and post-treatment application of therapy appears to be crucial for the
long-term maintenance of treatment gains. We described a variety of procedures to
aid clinicians in targeting the correct core fear and providing unambiguous training
in safety learning across relevant contexts.
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Therapeutic Alliance and Common Factors
in Treatment
Daniella M. Halperin, Meara L. Weitzman, and Michael W. Otto
Changes in therapy can result from variables unique to a particular treatment
package (i.e., specific factors), as a function of variables common to a variety of
treatments (i.e., nonspecific/common factors), or a combination of both specific and
nonspecific ingredients (Kazdin, 1979). Nonspecific (or common) treatment factors
include variables that are common across different treatment modalities, which are
thought to influence outcomes in therapy but are often not well linked to a mechanism of change. Due to differences in what is posited to be important to the change
process by any one treatment theory, specific factors that are deemed crucial for one
theoretical approach might be considered a common factor for another approach
(Kazdin, 1979; Wilkins, 1979).
A unified perspective on the role and significance of common factors is made
more difficult by the degree to which similar nonspecific factors have been discussed as distinct concepts, with little guidance on the degree of overlap between
these concepts. For example, therapeutic alliance, empathy, goal consensus, and
therapist–patient collaboration have each been cited as important contributors to
therapeutic change (Norcross, 2002), despite the obvious overlap between these
concepts. For the organization of this chapter, we will use therapeutic alliance as
a central organizing concept for discussing a range of common factors. As such,
the focus of this chapter is on those factors distinct from the specific treatment
interventions that are most commonly the focus of randomized controlled treatment
trials. Particularly when a specific treatment is examined relative to a supportive
treatment comparison condition, nonspecific treatment factors, such as entry into a
supportive and caring professional relationship that has, as an explicit goal, the healing of a patient in need, are balanced across the two treatment conditions. Specific
treatment effects represent the benefits demonstrated beyond these common factors
(see Chambless & Hollon, 1998; Chambless & Ollendick, 2001). Specific treatment
effects are also the focus of the second section of this volume (Otto & Hofmann,
2009), and hence this chapter provides a complement to the direct attention on
empirically supported treatment strategies found in those chapters.
D.M. Halperin (B)
Department of Psychology, Boston University, Boston, MA, USA
e-mail: danih@bu.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_4,
C Springer Science+Business Media, LLC 2010
51
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The Concept of Therapeutic Alliance
Traditionally associated with psychoanalytic theory, the therapeutic alliance was
once conceptualized as a positive form of transference (Freud 1913/1958).
Humanistic theorists expanded upon this idea by emphasizing the role of therapist empathy and unconditional positive regard in treatment success (Rogers, 1957).
In recent years, the therapeutic alliance has gained recognition across treatment
modalities as a common factor correlated with treatment outcome (Constantino,
Castonguay, & Schut, 2002; Wolfe & Goldfried, 1988). Due to the early focus on
the therapeutic relationship as a primary mechanism of change in psychodynamic
therapy, there is sometimes an unfortunate tendency to use this theoretical frame of
reference when discussing issues in the therapeutic relationship. Cautioning against
this tendency, one of the founders of behavior therapy, Lazarus (2003), aptly stated:
Would any well-schooled CBT practitioner find it farfetched to point out to a client that
she appears to react to her therapist in the same way that she views her abusive husband,
and then use in-session cues to deal with the problem? Be that as it may, to refer to this as
“transference” takes us very wide of the observation that clients may have distorted perceptions of the therapist that seem to rest on reenactments with significant others.. . .To borrow
and use the murky term “transference” (on which many vague and complex psychoanalytic
tomes have been written) leads to obfuscation. Perhaps it behooves us to find a different
term that describes peoples’ penchant to generalize and project onto one another accurate
as well as distorted attributes and feelings that stem from past experiences. (p. 380)
Accordingly, common factors in general, and therapeutic alliance and its determinants in particular, need to be discussed in general terms that are free from the
theory-specific meanings reflected in their historical roots. Doing so frees clinicians and researchers to consider the range of understandings and interventions that
may be relevant to addressing therapy relationship issues and maximizing therapy
outcomes.
As the most frequently cited common factor, the alliance is now commonly
defined as the emotional and collaborative bond between the therapist and patient
(Martin, Garske, & Davis, 2000). According to Bordin (1979), the alliance is composed of three important factors: goals, tasks, and bonds. Goals refer to the desired
outcomes that must be endorsed by both parties. Tasks vary based on a therapist’s
theoretical orientation and should be tailored to facilitate progress toward a patient’s
individual goals. Both therapist and patient should believe that the tasks are necessary for treatment and accept the responsibility to execute them. Lastly, the bond
describes the therapist-patient attachment that depends largely upon high levels
of trust.
Empirical Support for the Therapeutic Alliance
Meta-analytic reviews across the years have shown a high degree of reliability in
providing estimates of the strength of alliance effects in predicting outcome. For
example, in a relatively recent large-scale meta-analysis of 79 studies, alliance was
Common Factors in Treatment
53
found to be moderately correlated to outcome (r = 0.22; Martin et al., 2000). This
analysis replicated a meta-analysis from almost a decade earlier (r = 0.21; Horvath
& Symonds, 1991), suggesting stability in these effect size estimates over time.
Likewise, in a meta-analysis of 23 studies examining treatment of children and adolescents, Shirk and Karver (2003) obtained almost identical results. All of these
estimates are in the small range according to Cohen’s (1988) standards.
By way of comparison, a meta-analysis of controlled trials of the treatment
of anxiety disorders indicates a medium to large effect size (Hedges’ g = 0.73)
according to Cohen’s (1988) standards for the advantage of cognitive behavioral
therapy (CBT) over psychological or pill-placebo comparison conditions for individuals completing treatment (Hofmann & Smits, 2008). There are a number of
interpretations of this larger effect size. First, because alliance with caregivers is
likely to be a factor in both the active and comparison conditions reviewed by
Hofmann and Smits – the vast majority of control conditions were supportive
counseling, followed by select use of pill placebo or other interventions such as
relaxation or problem-solving training – these data may suggest that specific treatments offer substantial benefits beyond alliance and other common factor effects
alone. Alternatively, alliance effects may differ depending on the treatment being
offered, such that stronger alliance effects would be found in the CBT group relative
to the comparison conditions, and hence alliance may be a confounded component
in the larger effect sizes found for specific treatments.
There is evidence for such confounding between specific treatment and alliance
effects. For example, significantly greater alliance effects were found for CBT as
compared to interpersonal therapy in a study of the treatment of depression (Raue,
Goldfried, & Barkham, 1997). Empirical evidence supports that alliance increases
following treatment gains. For example, Tang and DeRubeis (1999) showed that
individuals who experience sudden gains in treatment have a subsequent enhancement in therapeutic alliance. Hence, treatments that differ in efficacy may also
differ in alliance, leading to a confounding in alliance assessments and variance
attributable to what may be the specific effects of treatment. Moreover, there may
be a mutually reinforcing cycle between alliance and treatment outcome, where
early gains may enhance alliance and alliance may make the patient more receptive to ongoing treatment efforts. In one study, after controlling for prior symptom
improvement in a sample of depressed patients, higher alliance scores on the
Working Alliance Inventory (WAI; Horvath & Greenberg, 1989) after Week 2 of
treatment predicted symptom change between Weeks 3 and 12 (Klein et al., 2003).
One role alliance may play, especially in relation to a confounding between specific treatment and alliance effects, is in enhancing engagement in treatment. In a
treatment like CBT, this may simply translate to greater application of in-session
or home assignments. An extended example may serve well to illustrate this point.
Cloitre, Koenen, Cohen, and Han (2002) examined the pattern of symptom change
in a treatment study where skills training in affective and interpersonal regulation
were used as a prelude to exposure-based treatment for post-traumatic stress disorder (PTSD) in 58 women who had experienced childhood abuse. This study is
of interest for understanding alliance effects in part because the participants – all
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who had PTSD due to abuse at the hands of caregivers – were those who would be
hypothesized to have alliance issues. First, PTSD-related anger symptoms have been
linked to ruptures in the therapeutic relationship, poorer treatment outcome, and
dropout (Chemtob, Novaco, Hamada, & Gross, 1997). Second, physical or sexual
abuse at the hands of caregivers is associated with feelings of distrust and disconnection in adulthood (Briere, 1988; Cole & Putnam, 1992). Cloitre et al. (2002)
assessed therapeutic alliance during sessions 3, 4, and 5 of the first (skill building)
stage of treatment and found a link to a reduction in PTSD symptoms, at a level
(r = .46) that was approximately double the mean in meta-analyses (as reviewed
earlier).
Indeed, in a subsequent analysis Cloitre, Stovall-McClough, Miranda, and
Chemtob (2004) showed that the degree of improvement in emotional regulation
skills mediated the prediction offered by alliance scores, such that the alliance scores
offered no prediction when improvements in emotional regulation were considered.
Interestingly, it was the change in emotional regulation across exposure that was
submitted for analysis; that is, it is not clear whether training in emotional regulation was important for intensifying the alliance or leading to clinical change, as the
relevant changes in emotional regulation were assessed across the exposure phase
(Phase 2 of treatment) rather than the emotional regulation skill building phase
(Phase 1 of treatment). Moreover, alliance ratings did not predict the 29% of patients
who failed to complete treatment. What, then, is the meaning of alliance scores during Phase 1 of treatment? It is possible that, as the authors suggest, the degree of
alliance during the first phase of treatment determined how well the patients were
able to make use of the exposure phase of treatment. It may simply be that patients
who agree with the goals and tasks of emotional regulation training are likely to give
higher alliance ratings during Phase 1 of treatment and are likely to fully engage in
and benefit from subsequent exposure treatment.
In summary, as noted in a review by Loeb et al. (2005), despite the consistency
of findings that the therapeutic alliance is moderately correlated with treatment outcome across different types of treatment, the role of the alliance has not been reliably
established as a causal mechanism of change. Alliance may result from, as much
as cause, successful treatment effects. Nonetheless, there is some evidence for a
mutually reinforcing cycle, where alliance may help patients engage in treatment,
and likewise successful engagement may lead to desired outcomes and an enhanced
alliance. One issue for the field, however, is that the research on alliance provides
little guidance on what may be the most operative characteristic for enhancing outcomes. It may be tempting to assume that the more interpersonally focused the
therapy, the more alliance issues will be addressed. However, this expectation is
not confirmed by research. For example, in comparative treatment trials, CBT has
been shown to have higher alliance scores than interpersonal psychotherapy (Raue
et al., 1997) or transference-focused psychotherapy (Spinhoven, Giesen-Bloo, van
Dyck, & Arntz, 2007). Moreover, if alliance is conceptualized as a concurrence
between therapist and patient on the goals, tasks, and bonds in therapy, then efforts
to improve alliance may presumably focus on any of these elements. In the following sections we thus consider strategies for enhancing the patient’s alliance with the
Common Factors in Treatment
55
therapist and the tasks of treatment. Concerning goals of treatment, therapists from a
variety of therapeutic orientations assert the importance of actively working to align
goals, intervening with the perceptions and hopes of the patient, so that they are in
accordance with treatment methods (Conoley, Padula, Payton, & Daniels, 1994). In
our discussion of these factors, we will consider the alignment of treatment goals
both in terms of (1) motivation for treatment and (2) specific treatment expectancies.
Motivation for Treatment
Patients enter treatment at varying stages of readiness for change (Maltby & Tolin,
2005), and may differ in their conceptualization of the mechanism of that change.
For example, individuals with generalized anxiety disorder (GAD) identify their
worry as problematic but may simultaneously view it as distracting and protective
(e.g., avoidant worry; Borkovec & Roemer, 1995). In obsessive-compulsive samples, anticipatory fear toward exposure-based therapies is not uncommon. Franklin
and Foa (1998) report that about 25% of patients with obsessive-compulsive disorder (OCD) refuse exposure plus response prevention (ERP) therapy. Moreover,
the initiation of psychological treatment is often accompanied by ambivalence or
opposition to the prospect of change (Miller & Rollnick, 2002).
Motivational interviewing (MI) is an intervention specifically designed to target
and resolve feelings of ambivalence that lead to patient resistance (Miller, 1983).
Client-centered theory is evident in MI, as the therapist must convey empathy and
minimize patient–therapist conflict (Slagle & Gray, 2007). Where MI differs from
client-centered approaches, however, is in the directive role of the therapist. The
goal of a therapist using MI is to persuade rather than coerce the patient to choose
goals that are consistent with his or her own values and motivations and are therefore more meaningful (Rubak, Sandboek, Lauritzen, & Christensen, 2005; Slagle
& Gray, 2007).
As a brief intervention for a wide variety of alcohol and drug use problems, MI is
a well-validated and useful intervention (Burke, Arkowtiz, & Menchola, 2003). In
its application to the treatment of anxiety disorders, MI has shown initial promise.
Specifically in a pilot study, participants meeting diagnostic criteria for at least one
anxiety disorder were randomly assigned to receive either group CBT for anxiety
management with MI as a pre-treatment or CBT without pre-treatment (NPT) spanning across a 4-week time period (Westra & Dozois, 2006). Treatment compliance
was measured by rates of attrition and homework completion as assessed by both
patient and therapist. Administered at baseline and subsequent to the pre-treatment
(or post NPT), the Anxiety Change Expectancy Scales (ACES; Dozois & Westra,
2005) was used to gauge an individual’s expectancy for change in treatment and,
more globally, MI efficacy. According to Miller and Rollnick (2002), proper MI
strengthens positive expectancies for change by increasing optimism. High scores
on the ACES were significantly correlated with improved symptoms across both
groups. Results showed that participants in the MI pre-treatment condition exhibited greater homework compliance, greater numbers of sudden gains, and greater
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positive expectancy relative to participants treated only with CBT. At 6-month
follow-up, the gains made in managing symptoms of anxiety were maintained in
both pre-treatment conditions.
Another study randomly assigned treatment-refusing OCD patients to a foursession readiness intervention (RI; a prelude treatment following the same principles
as MI) or waitlist (WL) condition before being given the option to enter into 15 sessions of ERP (Maltby & Tolin, 2005). Subsequent to completing the pre-treatment,
a greater proportion of patients in the RI condition accepted ERP compared to WL
(86% vs. 20%). However, before beginning the exposure treatment, the two groups
did not show any difference in symptom severity, indicating a differential effect
of readiness training on treatment cooperation rather than efficacy for those who
received the RI.
In addition to motivation for treatment, expectancies about the nature of treatment can have an impact on treatment acceptability and outcome. Some argue that
expectancies in therapy are related to the general concept of hope (Frank & Frank,
1991; Snyder, Michael, & Cheavens, 1999). Hope is commonly defined as wishes or
desires that are tied to an expectation of achieving desired results (Dew & Bickman,
2005). Snyder and colleagues argue that hope involves both conceptualizing specific
goals based on one’s own ability to work towards reaching the goals (pathway thinking), and also being able to continue to strive towards the goals (agency thinking).
The model of hope put forth by Snyder, Ilardi, Michael, and Cheavens (2000) posits
that an individual’s perceived ability to begin and sustain movement toward a goal,
combined with a belief in the pathways available to reach the goal, leads to positive
outcomes in psychotherapy.
As compared to the more global concept of hope, expectancy effects have
received more specific attention, with three types of expectancy effects commonly
described in the literature: role expectancies, outcome expectancies, and control
expectancies.
Role Expectancies
In general, role expectancies refer to the patterns of behavior viewed as appropriate for a person in a specific role (Delsignore & Schnyder, 2007; Dew & Bickman,
2005). In a therapeutic context, this involves the expected roles of the patient and
the therapist. Patients may have expectations regarding their role (e.g., expecting
that there will be a collaboration in therapy) and the therapist’s role (e.g., expecting
to be given advice from the therapist) in the therapeutic process (Arnkoff, Glass, &
Shapiro, 2002). Helping patients form expectations of an active treatment role for
themselves may be particularly important, given the general association between
homework adherence and treatment outcome for the anxiety disorders (Westra,
Dozois, & Marcus, 2007), although not all studies have supported the association
between greater homework compliance and more positive outcomes in individuals
being treated with CBT (Woods, Chambless, & Steketee, 2002).
Common Factors in Treatment
57
Outcome Expectancies
Outcome expectancies (also referred to as treatment expectancies or prognostic
expectations in the literature) describe how strongly a patient presumes that a given
therapy will work (Arnkoff et al., 2002; Delsignore & Schnyder, 2007; Greenberg,
Constantino, & Bruce, 2006). Outcome expectancies directly relate to the progress
that a patient believes will be made in therapy (Dew & Bickman, 2005; Delsignore
& Schnyder, 2007). This form of patient expectation has received the most empirical
attention in the literature (Arnkoff et al., 2002; Greenberg et al., 2006).
Outcome expectancies may appear to be similar to other patient variables, such as
motivation for treatment and therapy preferences, but these are distinct constructs,
as it is possible for a patient to be highly motivated for therapy and still have low
prognostic expectations that they will benefit from therapy (Arnkoff et al., 2002;
Greenberg et al., 2006). Greenberg et al. differentiate between the types of outcome
expectancies found in the literature (e.g., pre-treatment, during-treatment). Pretreatment outcome expectancies refer to prognostic beliefs that a patient has prior
to any contact with the therapist or initiation of treatment. During-treatment outcome expectancies are examined after a patient has already met with the therapist.
Treatment credibility, a conceptually similar during-treatment construct, describes
how logical, believable, and convincing a particular treatment is (Greenberg et al.,
2006; Kazdin, 1979). Treatment credibility and treatment outcome expectancy are
related, yet distinct constructs that have predicted therapeutic change across a wide
range of studies (Borkovec & Costello, 1993; Chambless, Tran, & Glass, 1997;
Devilly & Borkovec, 2000; Dew & Bickman, 2005; Goossens, Vlaeyen, Hidding,
Kole-Snijders, & Evers, 2005). It is still unclear exactly how these constructs
are related to change; however, burgeoning research strongly suggests a link to
psychotherapy outcome.
Empirical Support for Patient Expectancies
A recent review of 35 studies investigated the relationship between specific patient
expectancies (e.g., role expectancies, outcome expectancies, and control expectancies) and outcomes in therapy (Delsignore & Schnyder, 2007). Overall, the authors
concluded that there was a modest direct relationship between specific expectancies and improvement in therapy, but there were inconsistent results relating to
global expectancies and therapy outcome. Findings varied widely among the studies specifically examining outcome expectancies, but generally reflected modest
effects, indicating that patients with higher positive outcome expectancies seemed
to benefit more from psychotherapy than patients who lacked confidence in the
therapy. Studies investigating role expectancies in therapy produced inconsistent
results, with four out of six studies reporting a positive association between a
patient’s expectancy about their role and therapy outcome across diverse treatment
approaches (Delsignore & Schnyder, 2007; see also Arnkoff et al., 2002).
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In another review examining both adult and child studies in the expectancy
literature, Dew and Bickman (2005) found a positive relationship between outcome
expectancies and patient improvement (with 10 out of 13 studies reporting a significant relationship), but the authors did not find a relationship between expectancies
and attrition. A complex association between expectancies and attrition was also
reported in a study by Nock and Kazdin (2001) who investigated parents’ pretreatment expectancies for their child’s psychotherapy in a large sample of children
with oppositional, aggressive, and antisocial behavior. Treatment included parent
management training as well as cognitive problem-solving skills training directed to
the child. Although, as might be expected, lower parental expectancies for treatment
predicted higher barriers to treatment, it was the parents with very high or very low
expectancies for treatment who attended the most therapy sessions and were least
likely to discontinue treatment. The authors explain that individuals with very high
expectancies for therapy might be more likely to attribute changes in therapy to the
treatment itself. Alternatively, individuals with very low expectancies may be less
likely to expect any positive changes resulting from the therapy, and are therefore
more likely to increase expectancies when observing any therapeutic gains, leading
to continued treatment attendance.
Linehan, Cochran, Mar, Levensky, and Comtios (2000) provide at least one
caution to the role of high expectancies. Individuals with borderline personality
disorder, a disorder characterized by marked interpersonal challenges, have been
shown to be more prone to burnout when therapeutic expectations are high.
However, it is important to note that pre-treatment expectancies may give only
part of the picture of the relationship between treatment expectancies, treatment
engagement, and improvement. Once therapy has begun, individuals may be more
likely to continue in therapy and achieve greater gains if their treatment expectancies match the capabilities of therapy, and they believe that the given treatment is
worthwhile (Frank & Frank, 1991; Garfield, 1994). In support of these hypotheses,
Westra et al. (2007) tested the assertion that positive expectancy can lead to greater
compliance in CBT, and influence subsequent outcomes. Their study examined the
relationship between pre-treatment expectancies for anxiety change and early homework compliance, and cognitive symptom change (initial change and total change)
throughout treatment. Westra and colleagues found that early homework compliance
mediated the relationship between expectancy for anxiety change assessed at baseline and initial change in CBT. Results also indicated that homework compliance
was positively correlated to overall treatment change, an effect that was mediated
by initial symptom change. In other words, initial cognitive symptom improvement mediated the relationship between homework compliance and post-treatment
outcome. The authors suggest that expectancy for change is an important cognitive variable that may serve to bolster the momentum for involvement in therapy,
thus contributing to subsequent gains. They also propose that the dynamics among
expectancy for change, homework compliance, initial symptom change, and overall treatment outcome might reflect a reciprocal relationship. Although not directly
tested in the present study, Westra et al. posit that this (reciprocal) pathway may
go through multiple iterations. For example, if expectancy influences homework
Common Factors in Treatment
59
compliance, homework compliance contributes to initial symptom change, and early
symptom change reinforces expectancies, the process could go on and on.
Changing Expectancies
Expectancies can be altered by adding pre-treatment interventions that provide
information about the therapy. In several studies, pre-treatment preparation has been
shown to affect both role and outcome expectancies. For example, Bonner and
Everett (1982) found that children who listened to an audiotape designed to prepare
them for treatment had more positive outcome expectancies and more appropriate role expectations than did the group that was denied pre-treatment information.
These findings were later replicated with both children and their parents (Bonner &
Everett, 1986). Preparatory videos and instructional brochures have also been shown
to affect expectancies (Day & Reznikoff, 1980; Shuman & Shapiro, 2002).
Post-treatment Expectancies: Attributions About
Treatment Gains
Treatment expectancies and attributions are also relevant to the post-treatment
period. Research indicates that how patients view the outcome of psychotherapy
impacts rates of relapse. There is evidence of a higher risk for relapse when a patient
makes external attributions (i.e., external locus of control) for success in therapy
because they believe that the therapy worked as a result of therapist skills or powerful treatment techniques (for review see Brewin & Antaki, 1982). Likewise, Brewin
and Antaki argue that patients who attribute gains to their own efforts are more
likely to maintain treatment gains than patients who attribute their improvement to
external factors (e.g., a drug’s action or a therapist’s abilities).
This argument is well supported in the anxiety disorders. For example, in a recent
study, Powers, Smits, Whitley, Bystritsky, and Telch (2008) actively manipulated
attributional processes concerning medication compliance on return to fear following an exposure-based intervention for individuals with claustrophobia. Participants
were randomized to a waitlist control condition, a psychological placebo condition,
a single session exposure-based treatment, or a single session exposure-based treatment in conjunction with an inactive pill. Participants in the exposure plus inactive
pill group were either led to believe that the pill they were given was a sedating
herbal supplement with anxiety-dampening effects, a stimulating herbal supplement
with anxiogenic effects, or a placebo pill that did not effect exposure treatment. By
manipulating patients’ perceptions of the pill’s effects, the researchers were able
to achieve differential attributions to treatment improvement and return of fear.
Results indicated that participants who were led to believe that they took a sedating
herb rated the pill as being more helpful than those who were told that they had
taken the stimulating herb or a placebo. Additionally, participants who believed that
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they had taken an herbal stimulant (that made the exposure more difficult) rated
the pill as hindering their treatment more than the other groups did. As predicted,
participants who were told after treatment that they had taken a sedating herb that
dampened their anxiety had a significantly higher return of fear at a 1-week followup. Moreover, at follow-up, participants in the exposure plus sedating herb condition
no longer outperformed the waitlist or psychological placebo condition, while the
other three exposure conditions (e.g., exposure alone, exposure plus a pill described
as a stimulating herb, and exposure plus a pill described as a placebo) maintained
improvement over the waitlist and psychological placebo conditions. These findings are consistent with previous correlational studies that found that individuals
who attributed their improvement to a medication were at risk of poorer maintenance of treatment gains (Basoglu, Marks, Kilic, Brewin, & Swinson, 1994; Biondi
& Picardi, 2003).
In one of these correlational studies, Basoglu et al. (1994) found that attribution of improvement to medication (alprazolam or placebo) predicted relapse in
patients with panic disorder with agoraphobia who were also being treated with a
psychological intervention (exposure or relaxation). Patients who attributed gains
to their own efforts maintained those gains at a 10-month follow-up better than
those who attributed their improvements to external factors (medication or the therapist). Patients had more severe withdrawal symptoms during tapering if they had
strongly believed that it was the medication that helped them. Patients who were
given alprazolam made more external (drug) attributions than those who were given
the placebo medication. Moreover, patients who made self-attributions were able to
make more outings into phobic situations during tapering than those who attributed
improvement to the medication.
In a subsequent study, Biondi and Picardi (2003) supported the relationship
between attribution of improvement to medication and risk of relapse in individuals with panic disorder with agoraphobia. Patients from a prior study who were
able to achieve remission after medication treatment, in conjunction with or without
CBT, became participants in this follow-up study. After patients had reached a satisfactory level of improvement, medication was gradually tapered over 1–2 months,
and the follow-up period ranged from 2 to 86 months. Results indicated that patients
who attributed their improvement to the medication were at a greater risk of relapse.
In a randomized controlled trial, Livanou et al. (2002) examined post-treatment
beliefs, sense of control, and treatment outcome in PTSD. The interventions
included exposure (five sessions of imaginal exposure and five sessions of graded
live exposure), cognitive restructuring (CR; ten sessions), both in combination (five
sessions of CR plus imaginal exposure and five sessions of CR plus live exposure),
or a placebo condition (ten sessions of deep muscle relaxation). In line with previous studies that found external attribution of improvement to generalize less at
post-treatment (for data on other disorders see Davison, Tsujimoto, & Glaros, 1973;
Jeffrey, 1974; Sonne & Janoff, 1979), Livanou and colleagues found that maintenance of PTSD treatment gains at follow-up were predicted by post-treatment sense
of control over symptoms and internal attribution of gains. However, baseline beliefs
and improvement of beliefs were not predictive of outcome, an unexpected finding
Common Factors in Treatment
61
that differed from previous studies on PTSD (Ehlers, Mayou, & Bryant, 1998),
agoraphobia (Chambless & Gracely, 1989), and OCD (Basoglu, Lax, Kasvikis, &
Marks, 1988), leading the authors to conclude that the divergent results may be due
to methodological differences between studies.
The dramatic attribution effects found by Powers et al. (2008), Basoglu et al.
(1994), and Biondi and Picardi (2003) have important implications for combined
drug-psychosocial treatments. Working with treatment attributions and the role of
(drug) context effects in therapy is discussed in more detail in “Combined Cognitive
Behavioral and Pharmacologic Treatment Strategies: Current Status and Future
Directions” by Smits et al. (this volume).
Treatment Adherence
Treatment adherence, or integrity, is described as the extent to which a set of
prescribed intervention principles and techniques are followed by the therapist
(Waltz, Addis, Koerner, & Jacobson, 1993). A recent study by Hogue et al. (2008)
examined adolescents with behavioral problems receiving CBT, focusing on treatment adherence as a main effect. Results indicated that intermediate levels of
adherence were associated with the greatest improvements, above and beyond
the effects of rigid and low adherence levels. In another study, participants low
in motivation receiving manualized CBT had poorer treatment outcome, while
outcome was unrelated to high protocol adherence in participants low in motivation (Huppert, Barlow, Gorman, Shear, & Woods, 2006). One interpretation of
these findings is that with high motivation, stricter adherence may better match
the level of motivation and expectancies of patients, providing additional circumstantial support for the importance of managing expectancies throughout the
therapy.
Efforts to strengthen alliance also appear to offer therapeutic benefit should
therapeutic relationship issues arise. Ruptures in therapeutic alliance, marked by
difficulty sustaining the relationship and an overall negative shift in quality, have
received considerable attention in alliance research (Strauss et al., 2006). Such a
problem may occur when a therapist does not attend to signs of relationship strain
(Safran, 1990). There is some evidence that alliance ruptures should be perceived
as opportunities to facilitate therapeutic change, whereby maladaptive patterns are
brought to attention and acknowledged. For example, Strauss and colleagues measured rupture-repair episodes in a sample of avoidant and obsessive-compulsive
individuals receiving cognitive therapy. Episodes were quantified by a decrease
of 7 or more points on the California Psychotherapy Alliance Scale (CALPAS;
Marmar, Weiss, & Gaston, 1989) followed by an increase of at least 7 points.
Of the patients that experienced a rupture-repair episode, a large portion evidenced greater symptom reduction across treatment measured by both self-report
(Wisconsin Personality Disorder Inventory; Klein et al., 2003) and clinician-rated
assessments (Structured Clinical Interview for DSM-III-R – Personality Disorders;
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Spitzer, Williams, Gibbons, & First, 1990). In effect, ruptures in alliance may have
a therapeutic effect if adequately managed and repaired.
Summary and Conclusions
The available evidence suggests that common factors in therapy – variables defined
as therapeutic alliance, motivation, and expectancies – have fairly reliable albeit limited effects on treatment outcome. As reviewed above, these effects have been shown
to be important for enhancing CBT outcome in many cases, but do not account
for CBT outcome effects. In this chapter, the degree of alliance, motivation, and
expectancies in therapy have been treated as both relevant and modifiable attributes.
The available evidence suggests that part of the task of the CBT therapist treating anxiety disorders should be: (1) helping patients clarify goals and values before
treatment, (2) establishing a link between these general goals and values and the specific goals and methods of treatment, and (3) monitoring and working to enhance
the ongoing congruence of these factors in the therapeutic relationship. Working
to enhance these common treatment factors, while offering empirically supported
CBT strategies, might provide an especially powerful approach to helping patients
in need.
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Combined Cognitive Behavioral
and Pharmacologic Treatment Strategies:
Current Status and Future Directions
Jasper A.J. Smits, Hannah E. Reese, Mark B. Powers, and Michael W. Otto
This chapter provides a review of the current status of traditional combined
treatment strategies: co-application of cognitive-behavioral therapy (CBT) and pharmacotherapy, most typically, with antidepressant or benzodiazepine medications.
The success of these strategies, as judged from the perspective of randomized clinical trials and naturalistic case series, will be reviewed and followed by an account
of some of the issues and complexities underlying the limited treatment efficacy
of this approach. Guidance is provided to clinicians on some of the contextual
factors that may hinder CBT efficacy in the context of co-occurring medication
treatment. Furthermore, we discuss the theory and potential for new combination
treatment strategies that avoid some of the issues associated with current approaches
and which rely much more on maximizing the core therapeutic learning offered by
exposure-based CBT approaches.
The Efficacy of Cognitive-Behavioral and Pharmacological
Treatments
A large body of work indicates that cognitive-behavioral and pharmacological treatments are both effective interventions for the acute-phase treatment of anxiety
disorders. Cognitive-behavioral therapy (CBT) is a learning-based approach aimed
at helping patients reacquire a sense of safety around cues associated with anxiety
and panic. To achieve this type of learning, CBT protocols, usually 12–15 weeks
in length, emphasize education about anxiety psychopathology as well as repeated
exposure to fear-eliciting cues, often in combination with restructuring of false
threat appraisals. For example, a patient suffering from panic disorder who fears
that panic attacks will cause her to faint (i.e., false threat appraisal) may be provided
with education about the physiology of panic to help her understand that dizziness (i.e., fear-eliciting cue) is a natural and harmless response to overbreathing.
J.A.J. Smits (B)
Department of Psychology, Southern Methodist University, Dallas, TX, USA
e-mail: jsmits@smu.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_5,
C Springer Science+Business Media, LLC 2010
67
68
J.A.J. Smits et al.
A review of previous personal experiences or experiences of others with dizziness
may provide further disconfirmatory evidence (e.g., “the chances of fainting when
feeling dizzy are slim;” “I have fainted before, but never did it cause any significant
harm”). Finally, repeated interoceptive exposure to activities such as chair spinning
or hyperventilation (activities which induced the feared sensations) offers the opportunity for the fear of dizziness to be confuted and ultimately extinguished. From a
neurobiological perspective, Gorman, Kent, Sullivan, and Coplan (2000) proposed
that CBT deconditions contextual fear at the level of the hippocampus and enhances
the ability of the prefrontal cortex to inhibit the amygdala.
A recent meta-analysis of randomized placebo-controlled trials indicated that
CBT protocols of this nature are associated with clinically meaningful improvements at the conclusion of acute-phase treatment across the anxiety disorders
(Hofmann & Smits, 2008). Although long-term follow-up studies are sparse, the
available data suggest that the gains achieved with CBT can be durable over time
(Gould, Buckminster, Pollack, Otto, & Yap, 1997; Gould, Otto, & Pollack, 1995;
Gould, Otto, Pollack, & Yap, 1997; Otto, Penava, Pollack, & Smoller, 1996).
However, many patients do seek further treatment, either because they remain
symptomatic or relapse over follow-up periods (e.g., Brown & Barlow, 1995).
In contrast to CBT, pharmacological interventions aim to directly target biochemical pathways underlying the anxiety elicited by disorder-specific cues (e.g.,
interoceptive cues for panic disorder patients or social scrutiny for social anxiety disorder) by decreasing activity in the amygdala (Gorman et al., 2000).
Pharmacological agents that have demonstrated efficacy for at least one anxiety disorder include selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase
inhibitors (MAOIs), tricyclic antidepressants, and benzodiazepines (Abramowitz,
1997; Lydiard, Brawman-Mintzer, & Ballenger, 1996; Mitte, Noack, & Hautzinger,
2005; Pollack, 2005; van Etten & Taylor, 1998). Treatment-free follow-up data suggest that pharmacotherapy is a long-term commitment; relapse is common following
medication discontinuation (e.g., Mavissakalian & Perel, 1992; Noyes, Garvey,
Cook, & Suelzer, 1991; Stein, Versiani, Hair, & Kumar, 2002; Walker et al., 2000).
In response to the desire for stronger acute and longer-term outcomes for anxiety treatments, one natural inclination is to combine the outcomes offered by
pharmacological and CBT interventions.
The Efficacy of Acute-Phase Combined Treatments
The efficacy of combined CBT and pharmacotherapy relative to either treatment
delivered alone has been studied most extensively in the treatment of panic disorder (PD), and to some extent in obsessive-compulsive disorder (OCD) and
social anxiety disorder (SAD). Limited data are available for generalized anxiety
disorder (GAD), and at the time of this writing, there was only one published
report evaluating sequential combined treatments for post-traumatic stress disorder (PTSD) or acute stress disorder (ASD). Overall, the results of the available
studies are mixed and seem to vary somewhat as a function of the target disorder,
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the prescribed pharmacological agent, as well as the time of assessment (i.e., acute
vs. follow-up outcomes; see for review Foa, Franklin, & Moser, 2002; Otto, Smits,
& Reese, 2005).
With respect to acute outcomes (i.e., assessment conducted immediately following acute-phase therapy), studies involving PD samples converge to suggest that
combining CBT with medications may offer an advantage over either modality
alone. A recent meta-analysis of 21 trials examining the efficacy of combined treatment for panic disorder yielded a slight advantage of combined treatments over
CBT (relative risk of response (RR) = 1.16) and pharmacotherapy (RR = 1.24;
Furukawa, Watanabe, & Churchill, 2006).
Several studies indicate that combination approaches may also offer advantages
in the acute phase over single-modality interventions for the treatment of OCD.
Early studies conducted by Marks, Stern, Mawson, Cobb, and McDonald (1980) and
Marks et al. (1988) indicated that the combination of exposure and response prevention (ERP) with clomipramine, a tricyclic agent, resulted in greater improvements
compared to ERP plus placebo or clomipramine plus relaxation or clomipramine
plus anti-exposure instructions. Short-term advantages of combination treatments
for OCD were also observed in two studies comparing the single and combined
effects of fluvoxamine, an SSRI, and ERP (Cottraux et al., 1990; Hohagen et al.,
1998). Of note, these two studies also provided evidence to suggest that the advantage of combined treatment was particularly evident among patients who presented
with comorbid depression. Hohagen et al. (1998) suggested that the antidepressant properties of the medication may successfully reduce the depressive symptoms
which enable individuals to more effectively engage in and benefit from ERP.
Findings of a recent randomized placebo-controlled trial (Foa et al., 2005) suggest that combining clomipramine with exposure and ritual prevention (EX/RP)
in the acute phase may not be cost-effective when the EX/RP treatment is delivered more intensely (i.e., 15 2-h sessions over 3 weeks). Although the combination
treatment yielded greater response rates than clomipramine alone (i.e., acutephase response rates 70% vs. 48%), the response rates for EX/RP alone were
not significantly different than for the combination treatment (i.e., 62% vs. 70%).
Unfortunately, patients with comorbid depression were excluded from this trial,
which, in addition to the EX/RP delivery schedule, perhaps limits the generalizability of the study results to all patients. Nonetheless, the Foa et al., (2005) findings in
relation to those from Hohagen et al. (1998) support the notion that combined treatment strategies for OCD, relative to CBT alone, may have limited efficacy outside
patients’ samples with comorbid depression and/or clinical settings where intensive
CBT can be offered.
Limited positive effects of combination treatments have been observed for the
treatment of SAD. In a randomized placebo-controlled study, Blomhoff et al. (2001)
examined the single and combined effects of sertraline, an SSRI, and physicianguided exposure therapy for SAD. Response rates at the end of acute-phase
treatment were 45.5%, 40.2%, 33%, and 24% for the sertraline plus exposure, sertraline, exposure plus placebo, and placebo conditions, respectively. These findings
suggest that sertraline can augment the effects of exposure treatment, particularly
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when exposure treatment is delivered with minimal therapist contact (i.e., eight
20-min sessions involving instructions for homework exposures). However, these
benefits of combined treatment, relative to CBT alone, were no longer evident at a
1-year follow-up evaluation (Haug et al., 2003). Moreover, consistent with findings from Foa et al. (2005) for OCD, antidepressant medication treatment does
not appear to augment the acute effects of more comprehensive programs of CBT
for SAD. Davidson et al. (2004) compared the outcome of five treatment conditions: group CBT, fluoxetine (an SSRI), pill placebo, group CBT plus fluoxetine,
and group CBT plus placebo among individuals with generalized SAD. Fluoxetine
alone was associated with the strongest initial response at week 4, but the active
treatments were all significantly better than placebo and not significantly different
from each other at week 14, with response rates of approximately 50% in each of
the conditions.
Based on the available data as well as cost/benefit considerations (see Otto,
Pollack, & Maki, 2000; McHugh et al., 2007), it appears that there is no strong
justification for recommending that combined treatment be adopted as a standard,
first-line treatment for optimizing acute outcomes for the anxiety disorders. Whether
combination treatments are indicated for certain subgroups of patients with anxiety
disorders (e.g., those with comorbid depressive disorders) or in settings where CBT
cannot be delivered in its most optimized form (e.g., primary care) are questions
that deserve further inquiry.
Outcomes After Treatment Discontinuation
Certainly, a case can be made for approaching the treatment of anxiety disorders
as a chronic illness (see Bruce et al., 2005), requiring long-term interventions
(i.e., continuation-phase treatment) following acute-phase therapy (Mavissakalian
& Prien, 1996). Today’s practice of pharmacological and CBT interventions for the
anxiety disorders, however, appears to reflect an approach that is more in line with
treating anxiety psychopathology much like acute infectious illness. Indeed, CBT
is a short-term approach focusing mostly on the acute management of anxiety and
related avoidance. Likewise, although a long-term proposition, patients often fail
to adhere to pharmacological prescriptions over the long run (Cowley, Ha, & Roy
Byrne 1997; Sirey et al., 1999; Weilburg, O’Leary, Meigs, Hennen, & Stafford,
2003). Given this reality, it is important to examine outcomes of combination
treatments following treatment discontinuation.
Studies examining long-term outcomes following the discontinuation of acutephase combination treatments are limited in number. The available evidence
suggests that, if at all evident during the acute phase, advantages of combined treatments are lost during treatment-free follow-up among patients with OCD (Cottraux,
Mollard, Bouvard, & Marks, 1993; Marks et al., 1988) or SAD (Haug et al., 2003).
Findings from two large multi-center trials suggest that combining medication and
CBT in the acute-phase treatment of panic disorder may actually be associated with
poorer long-term outcomes compared to those conferred by CBT alone. Marks et al.
(1993) randomly assigned patients to receive alprazolam plus exposure, alprazolam
Combined Treatment Strategies
71
plus relaxation, placebo plus exposure, or placebo plus relaxation (double placebo).
The authors found that although combined treatment was associated with a modest advantage over monotherapy in the acute phase, it resulted in less improvement
relative to exposure alone at treatment-free follow-up. Similarly, Barlow, Gorman,
Shear, and Woods (2000) found that a combination of imipramine plus CBT was
slightly more efficacious than monotherapy at post-treatment, but after medication
discontinuation, the combined treatment was associated with the highest relapse
rates. These studies are of particular concern because they suggest that medication
treatment may actually weaken the effect of CBT over time after patients discontinue treatment. In the next section, we discuss some possible mechanisms that
may account for the deleterious effects of medication on the long-term effects of
acute-phase CBT.
Possible Mechanisms of Relapse Following Discontinuation
of Combined Treatments
There are several possible reasons for the increased risk of relapse following termination of combined exposure-based and pharmacological treatment (see for review,
Powers, Smits, Leyro, & Otto, 2007). Animal work on extinction has offered one
explanation (see Bouton, 2002). Specifically, animal studies have shown that extinction learning, which involves procedures similar to exposure-based treatments, is
context-specific (Bouton, 2002). That is, extinction of fear that occurs in one context
(e.g., room A) may not generalize to a second context (e.g., room B). Accordingly,
context shifts such as medication discontinuation (i.e., the drug-state is withdrawn)
may account for the loss of gains apparent during acute-phase treatment (i.e., the
extinction memory is specific to the state of being on medication). Mystkowski,
Mineka, and Vernon (2003) tested this hypothesis using a sample of spider-fearful
participants. They randomly allocated these participants to ingest either caffeine or a
pill placebo before receiving treatment involving exposure to live spiders. Outcome
was assessed by means of a behavioral approach task immediately following treatment completion. To test the hypothesis that extinction learning during CBT is
context-specific, and thus would be lost as a result of changing the drug state, the
investigators retested participants 1 week following treatment under conditions of
either the same or opposite drug context. Consistent with predictions, participants
who were randomly allocated to be tested under the incongruent condition (e.g.,
treated while taking caffeine and later tested while taking placebo) displayed greater
return of fear compared to those tested under the congruent condition (e.g., treated
while taking caffeine and later tested while taking caffeine).
Self-efficacy theory (Bandura, 1977) offers a possible alternative or complementary mechanism underlying the negative effects of medication on long-term effects
of CBT. Self-efficacy theory posits that phobic behavior is a function of one’s
perceived inability to execute effective coping behavior in response to potential phobic threats (Bandura, 1977). It seems plausible that medication-taking may cause
patients to attribute their gains to the medication instead of their own efforts and
accomplishments, thereby undermining self-efficacy enhancement. Indeed, patients
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with anxiety disorders tend to attribute treatment gains to external factors (Adler &
Price, 1985; Anderson & Arnoult, 1985; Broadbeck & Michelson, 1987; Cloitre,
Heimberg, Liebowitz, & Gitow, 1992; Emmelkamp & Cohen-Kettenis, 1975;
Hoffart & Martinsen, 1990). The influence of patients’ attributions of treatment
gains to medication on the outcome of combined treatments has been examined in a
few studies. Basoglu, Marks, Kilic, Brewin, and Swinson (1994) reported that attributions of improvement to the medication (i.e., alprazolam or placebo) significantly
predicted relapse in panic disorder patients treated with exposure in combination
with medication (Basoglu et al.). Interestingly, Biondi and Picardi (2003) reported
that making external/medication attributions was associated with a 60% relapse rate,
whereas making internal attributions was associated with a 0% relapse rate.
Perhaps the strongest evidence for the causal role of external attributions
in relapse following the discontinuation of combined treatments comes from a
recent analogue study by Powers, Smits, Whitley, Bystritsky, & Telch (2008).
Using an experimental design, the investigators first randomly assigned participants displaying marked claustrophobic fear to one of four conditions: (1) waitlist;
(2) psychological placebo; (3) exposure-based treatment, (4) exposure-based treatment plus an inactive pill. Following post-treatment assessment that revealed an
advantage of exposure over control conditions and no effects of pill taking, they
manipulated attributions concerning medication taking by randomly assigning participants in the exposure-based treatment plus pill placebo condition to one of three
instructional sets: (1) the pill was described as a sedating herb that likely made
exposure treatment easier; (2) the pill was described as a stimulating herb that likely
made exposure treatment more difficult; or (3) the pill was described as a placebo
that had no effect on exposure treatment. Assessments at follow-up showed a relapse
rate of 39% among participants who believed that the pill had a sedating effect,
whereas a relapse rate of 0% was observed among participants in the other two conditions involving medication taking. Moreover, reduced self-efficacy accounted for
the elevated relapse rates associated with the sedating instructional set.
Collectively, these findings suggest that the practice of acute-phase combined
treatments may warrant the utilization of specific relapse prevention strategies,
including the assessment and possible modification of patient attributions regarding the improvements achieved with treatment as well the continuance of exposure
practice following the termination of medication treatment. In the next section,
we discuss the evidence for this approach of offering sequential as opposed to
concurrent combined interventions.
Starting CBT as a Strategy for Discontinuation
of Pharmacotherapy
There is evidence that when CBT is continued or reinstated during medication discontinuation, it may help patients maintain their treatment gains. For patients who
have received CBT concurrently with medication, continuing CBT treatment during and after the taper period may help the individual extend their learning to a
Combined Treatment Strategies
73
medication-free context. Additionally, CBT has been found effective in helping
patients tolerate the discontinuation symptoms of benzodiazepine taper in PD
(Hegel, Ravaris, & Ahles, 1994; Otto et al., 1993; Spiegel, Bruce, Gregg, &
Nuzzarello, 1994) and GAD (Gosselin, Ladouceur, Morin, Dugas, & Baillaregon,
2006). For example, Gosselin et al. (2006) found that patients who received CBT
during benzodiazepine taper were more successful at stopping the medication and
also had lower relapse rates relative to those individuals who received a control treatment emphasizing active listening. Similarly promising findings have been reported
for the addition of CBT during SSRI discontinuations in panic disorder (Whittal,
Otto, & Hong, 2001; Schmidt, Wollaway-Bickel, Trakowsky, Santiago, & Vasey,
2002).
Starting CBT when Pharmacotherapy Fails
CBT has been shown to be an effective treatment for individuals who have failed
to respond to medication treatment for PTSD (Otto et al., 2003), OCD (Kampman,
Keijsers, Hoogdiun, & Verbraak, 2004), and PD (Otto, Pollack, Penava, & Zucker,
1999; Pollack, Otto, Kaspi, Hammerness, & Rosenbaum, 1994; Heldt et al., 2006).
For example, Heldt et al. (2006) offered 12 weekly sessions of group CBT to individuals with panic disorder who had remained symptomatic despite an average of 3
years of pharmacotherapy. At 1-year follow-up, nearly two-thirds of the participants
met remission criteria. Given that psychiatrists and primary-care physicians greatly
outnumber psychologists trained in CBT, the most readily available treatment for the
anxiety disorders is often medication. Thus, the use of CBT as a treatment strategy
for individuals who have not benefited from medication may be a practical solution
when treatment resources are limited.
Starting Pharmacotherapy when CBT Fails
There is also some evidence that pharmacotherapy may be effective when CBT
fails. For example, Kampman, Keijsers, Hoogduin, and Hendriks (2002) randomly
assigned individuals with panic disorder who remained symptomatic after 15 sessions of CBT to continued CBT plus paroxetine, or CBT plus placebo. Those
subjects who received the paroxetine experienced significant additional improvement on measures of avoidance and anxiety whereas those who received the placebo
did not.
Clinical Considerations
Our review of studies examining combined treatment strategies for the anxiety disorders suggests that it is too early to draw firm conclusions and to set specific clinical
guidelines. Although the evidence to date provides no justification for recommending combined treatments as a first-line intervention for the anxiety disorders, it does
not rule out that the combined approach holds great value for many patients suffering
74
J.A.J. Smits et al.
from anxiety disorders. It appears that the utility of combined treatments may vary
depending on the combination of a number of factors, including, but not limited
to, patient preferences with respect to pharmacotherapeutic approaches, availability
of state-of-the-art CBT, and the presence of comorbid conditions at presentation.
In this section, we discuss some considerations with respect to the prescription of
combined intervention approaches for anxiety disorders (see Fig. 1).
Many patients seeking psychotherapy for anxiety are already taking medication
when they arrive for treatment (Roy-Byrne et al., 2002; Taylor et al., 1989). As
such, the question of whether or not to provide CBT along with pharmacotherapy is one that is often presented to clinicians working with patients suffering
from anxiety disorders. During the initial evaluation, the clinician should obtain
Is the patient taking already
medications?
Yes
Is the medication
providing some
benefit?
Yes
Is the patient
willing to make a
long-term
commitment to
medication
treatment?
Yes
Begin CBT.
Maintain
medication
treatment.
No
Consider
medication taper
(following
physicianapproved
schedule)
followed by
CBT.
No
Begin CBT. Upon
medication
discontinuation,
continue or
reinstate CBT into
medication-free
context.
No
Is a comorbid
mood disorder
present?
Yes
Combined
treatment with
appropriate
antidepressant
and CBT may
provide most
benefit. This is
particularly
recommended
for those patients
whose
depression
would prevent
them from
engaging in
CBT.
No
Begin CBT.
Fig. 1 Considerations with respect to the prescription of combined interventions for the acute
treatment of anxiety disorders
Combined Treatment Strategies
75
information about the prescribed medications the patient is taking. In addition to the
type and dosing of the medication, the clinician should assess the degree to which
the patient has received benefits from taking the medication. In this context, it is
important to consider the effects of the medication on problems often comorbid with
anxiety disorders. Indeed, suboptimal outcomes after CBT (e.g., response, attrition)
may be particularly common among adults who present with anxiety disorders and
are also diagnosed with unipolar depression (e.g., MDD, dysthymia; Lincoln, Rief,
Hahlweg, et al., 2005; Rief, Trenkamp, Auer, & Fichter, 2000; Steketee , Chambless,
Tran, 2001). Accordingly, the extent to which ongoing pharmacotherapy effectively
manages depression in addition to anxiety is an important factor to consider in
deciding to either continue or discontinue medications during acute-phase CBT.
Equally important in this decision is the preference of the patient with respect
to continued pharmacological treatment. Irrespective of the benefits of pharmacotherapy, many patients may wish to stop taking medications during the course
of CBT. Some patients may indicate that stopping medications is necessary (e.g.,
women who wish to become pregnant, patients who experience severe side effects);
others may indicate that taking medications over longer periods of time is not consistent with personal values (e.g., patients who do not like being “dependent” on
medications). When the patient wishes to discontinue pharmacotherapy, the clinician should consult with the patient’s physician and determine a tapering schedule
appropriate for the prescribed medication. An important aspect of medication discontinuation is preparing the patient for the potential consequences of stopping
pharmacotherapy. In addition to the possible relapse of mood and anxiety episodes
that can occur with medication discontinuation, the tapering of medications, particularly with benzodiazepines, is associated with the emergence of a host of physical
sensations. These withdrawal symptoms present an additional challenge to patients
with elevated levels of anxiety sensitivity (i.e., fear of anxiety and related sensations; Reiss & McNally, 1985), as they are more likely to respond with anxiety or
panic when exposed to physical sensations.
In order to assist patients in medication discontinuation, the clinician can offer
a combination of informational (e.g., education, cognitive restructuring) and behavioral (e.g., behavioral experiments, (interoceptive) exposure) interventions designed
to correct false threat appraisals as well as to enhance tolerance of physical sensations and negative affect (see Fig. 2). Manual-based guidance for both clinicians
and patients is available for this task (Otto & Pollack, 2009 a,b). Because extinction learning may be context-specific, it is important to continue these interventions
following the completion of the taper. This approach may also be beneficial for the
patient who attributes the success of treatment to medication taking. Indeed, patients
may be less likely to hold on to external attributions of therapy gains, and are therefore less likely to relapse, if they experience continued improvement with treatment
following medication discontinuation.
What if the patient wishes to stay on medication? The appropriate proposed
plan of action offered by the clinician depends on the extent to which the patient
has received benefits from medication treatment. Clearly, the lack of substantial
improvement following an adequate course of pharmacotherapy provides a rationale
76
J.A.J. Smits et al.
•
Prepare patient for discontinuation through providing information
(e.g., education, cognitive restructuring)
•
Discuss physical withdrawal symptoms as interoceptive exposure
•
Taper off medications slowly
•
Apply/Reapply CBT during the taper
•
Assess and modify external/medication attributions for improvement
Fig. 2 Strategies for patients wishing to discontinue medication
for discontinuation and subsequent application of CBT. However, clinicians must
approach this process with appropriate caution, with sensitivity to the therapeutic relationship established between the patient and their prescribing physician.
Education of both the patient and their previous provider about the options available
for the next phase of treatment and the potential for CBT to aid with medication
discontinuation may be important for successful intervention. The clinician could
use a cognitive framework (i.e., with gentle challenging the patient’s beliefs about
medications and its effects) to present this proposed intervention plan.
If the medication has exerted positive effects, supporting the patient’s preference to continue pharmacotherapy during acute-phase CBT is appropriate in many
circumstances. For example, for patients with panic disorder or comorbid mood
conditions, and in settings where conducting state-of-the-art CBT is not feasible,
ongoing pharmacotherapy may assist the psychologist in achieving optimal outcomes with acute-phase CBT. To help patients attribute additional gains to their
efforts in CBT, we recommend initiating CBT when a stable dose of medication
over weeks has been achieved and combining CBT with close monitoring of symptoms. Therapy can then include a review of the link between the patients efforts in
CBT and changes in symptom levels and the attainment of well being and enhanced
role functioning. Also, clinicians need to recognize that many patients fail to adhere
to long-term antidepressant treatments. Accordingly, the monitoring of medication
adherence is critical and the clinician should be prepared to prolong or re-initiate
therapy to allow the patient to extend their learning to a medication-free context.
Novel Combination Strategies
We end this chapter discussing a recent development in the strategy of combining
pharmacotherapy and CBT that may hold particular promise for the future. An accumulating body of work initiated by Davis and colleagues on D-cycloserine (DCS),
a partial agonist at the glutaminergic N-methyl-D-aspartate (NMDA) receptor,
suggests that DCS may be an effective augmentation strategy for exposure-based
Combined Treatment Strategies
77
CBT. Prompted by animal studies implicating a critical role for NMDA receptors in
extinction learning (Falls, Miserendino, & Davis, 1992), Davis and others investigated the effects of DCS on extinction learning in rats (cf. Davis, Ressler, Rothbaum,
& Richardson, 2006). The results of these studies converge to suggest that DCS
facilitates extinction consolidation in animals (Davis et al., 2006). Following this
work, initial studies with humans indicate that the administration of DCS prior to
exposure therapy sessions enhances treatment outcome among patients with height
phobia (Ressler et al., 2004, social phobia (Hofmann et al., 2006), and obsessivecompulsive disorder (Kushner, et al., 2007; Wilhelm, et al., 2008; for review of
effect sizes see Norberg, Krystal, & Tolin, 2008). These exciting findings await
replication and extension to other anxiety disorders, but they do suggest that a new
approach to combined treatment – where the pharmacotherapy element is targeted
to memory enhancement rather than affect management – may offer a new perspective on strategies for enhancing CBT efficacy. Research on other mechanisms for
enhancing therapeutic learning from exposure-based strategies are also underway
(Cain, Blouin, & Barad, 2003; Powers, Smits, Otto, Sanders, & Emmelkamp, 2009),
and together these approaches represent a particular achievement of translational
research, and a promising new approach for extending the efficiency or efficacy of
CBT for the anxiety disorders (Anderson & Insel, 2006).
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Cultural Considerations and Treatment
Complications
Stuart J. Spendlove, Carolyn T. Jackson, and Joaquin P. Borrego, Jr.
Introduction
As ethnic and racial minority groups continue to grow (United States Bureau of the
Census, 2005), the field of clinical psychology must meet mental health needs in a
culturally appropriate manner. Despite the acknowledgement of the need for culturally relevant responses, the Surgeon General reports that ethnic minority members:
(1) have less access and availability to mental health services, (2) are less likely to
receive needed mental health intervention, (3) often receive poorer quality of care,
(4) experience stigma associated with seeking treatment, and (5) are not always
able to be matched with a practitioner that shares their language (U.S. Department
of Health and Human Services [USDHHS], 2001). Unfortunately, data also suggest that ethnic and racial minority members experience higher poverty rates and
greater incidence of related social stressors that negatively impact psychological
functioning than their Caucasian counterparts (Mays & Albee, 1992; USDHHS). In
addition, explicit conflicts between the cultural values of ethnic and racial minority
clients and the mainstream values often exemplified in traditional psychotherapies
introduce several treatment complications. In short, we are not adequately meeting
the needs of our underrepresented populations.
Since psychotherapy is a cultural phenomenon, it follows that culture should play
a substantial role in treatment (Bernal & Saez-Santiago, 2006; Bernal & Scharrondel-Rio, 2001). Historically, clinical research with cognitive-behavioral therapy
(CBT) has largely focused on individuals of European-American descent (Bernal
& Scharron-del-Rio, 2001) with relatively little attention given to the application
of CBT techniques within various ethnic minority cultural groups (Bhugra & Bhui,
1998). As a result, there is a noticeable lack of concrete and organized intervention
strategies and techniques that cognitive-behavioral clinicians can utilize when aiming to reduce treatment complications for their clients. At the same time, the tenets
of CBT do implicitly accentuate the unique circumstances and experiences of the
S.J. Spendlove (B)
Texas Tech University, Lubbock, TX, USA
e-mail: stu.kat.spendlove@gmail.com
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_6,
C Springer Science+Business Media, LLC 2010
83
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individual client (Hays & Iwamasa, 2006). As such, the basic techniques of CBT
serve as an excellent foundation from which therapeutic approaches within clinical
psychology can continue to be made more culturally responsive.
The purpose of this chapter is to provide evidence for the need and importance
of considering culture in the conceptualization, diagnosis, and treatment of anxiety
disorders among ethnic and racial minority clients. These factors will be reviewed
through a discussion of some of the cultural issues specific to individuals of ethnic
and racial minority groups, and also through an examination of how these issues
might relate to culture-specific treatment complications and treatment resistance.
This review is approached from the perspective that learning more about how the
issues faced by this portion of our population might complicate clinical case conceptualization, diagnosis, and treatment and with a view that increasing our knowledge
about these potential complications will, in turn, increase our ability to meet the psychological needs of members of these groups. Accordingly, the empirical research
literature will be briefly reviewed to highlight the importance of these topics as they
relate to the psychological well-being of ethnic and racial minority members and
specific recommendations will be provided to assist clinicians working with clients
from diverse populations.
Prevalence of Psychological Disorders Among Ethnic
and Racial Minorities
Inequities in the availability and accessibility of psychological assessment and treatment services combined with other factors, such as a general paucity of research
relating to rates of psychological disorders among ethnic and racial minorities
(USDHHS, 1999, 2001), make the task of efficiently and accurately examining
prevalence rates of psychological disorders among various racial and ethnic groups
complex. Some of this complexity relates to diagnosis, as members of some ethnic and racial minority groups are more likely to be over-diagnosed with particular
types of psychological disorders. For instance, African-Americans tend to be overdiagnosed with schizophrenia (e.g., USDHHS, 1999). Similarly, among Latino/a
groups, depressive disorders with psychotic features are also often misdiagnosed
as schizophrenia (Lawson, 2003). On the other hand, members of some racial
and ethnic minority groups might be subject to underdiagnosis of certain disorders. Indeed, among African-Americans, depression may be underdiagnosed (Skaer,
Selar, Robison, & Galin, 2000).
In addition to problems related to misdiagnosis, members of some minority
groups also appear more likely to present with a greater incidence of certain
symptomology. For example, a significant proportion of ethnic and racial minority group members experience an elevated incidence of substance-related disorders
(Thomason, 2000). Indeed, alcoholism among Native-American populations occurs
at nearly twice the rate of that noted among any other population group (USDHHS,
1999). Incidence of suicide among this group is also staggering; with a rate that is
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85
consistently 50% higher than the national average (USDHHS, 2001). Moreover, use
and abuse of illicit substances is higher among African-American groups than rates
found within any other racial group (USDHHS, 2000). Specific examples related to
anxiety disorders are highlighted by Zhang and Snowden (1999), who found that
African-Americans were significantly more likely than Caucasians to have a phobic
disorder, and Glover, Pumariega, Holzer, Wise, and Rodriguez (1999), who found
that anxiety disorders were more prevalent in some Latino/a populations than among
other groups.
Another issue related to the prevalence of psychological disorders among many
ethnic and racial minority groups is socioeconomic status. In the U.S., ethnic and
racial minority members are three times as likely as Caucasians to live below the
federal poverty line (USDHHS, 2001). The most important implications of this fact
are that people who live in poverty experience poorer overall psychological health
(Miranda, Nakumura, & Bernal, 2003) and are up to three times as likely as those
in higher socioeconomic strata to experience significant psychological problems
(Muntaner, Eaton, Diala, Kessler, & Sorlie, 1998; USDHHS, 2001). What is more,
people who are poverty-stricken also often reside in destitute neighborhoods and
communities that present a multitude of risk factors for increased psychopathology
(Miranda et al.).
Although the process of understanding prevalence rates of psychological disorders across racial and ethnic groups is convoluted, what is clear is that ethnic and
racial minority group members experience psychological problems at a similar or
higher rate as Caucasians (e.g., DHHS, 2001). Yet, there still exist notable disparities
in utilization patterns among ethnic and racial groups. For instance, Latino/as underutilize all psychological services (O’Sullivan, Peterson, Cox, & Kirkeby, 1989;
Sue, 1991). African-Americans also underutilize outpatient psychiatric services, but
overutilize inpatient services (Snowden & Cheung, 1990). Furthermore, ethnic and
racial minority populations are more likely than Caucasians to seek treatment in
primary care settings than from agencies specializing in psychological health services and frequently access psychological treatment through hospital emergency
rooms (USDHHS, 2001). African-Americans are also more likely than other racial
groups to prematurely terminate treatment (Diala et al., 2000; Sue, Ivey, & Pederson,
1996), with up to 50% of African-American clientele dropping out after just one
session (Council of National Psychological Associations for the Advancement of
Ethnic Minority Interests, 2003). Finally, Asian-Americans and Native-Americans
appear to underutilize services even more than African-Americans and Latinos/as
(USDHHS, 1999).
In brief, it is evident that quality social and psychological services are as necessary for ethnic minority members, but are also less available and accessible to
these groups than they are to Caucasians. Thus, for the purposes of this chapter,
it is important for clinicians to note that the source of some anxiety-related symptomology among many ethnic and racial minority clients could be a direct effect
of their environment and life circumstances, rather than only being attributable to
intra-individual characteristics.
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Culture and Treatment Complications
Culture and Treatment Resistance
An important issue related to work with ethnic and racial minority members is what
many clinicians might view as treatment resistance. One of the most significant correlates of apparent resistance to engaging psychological treatment is social stigma
(USDHHS, 2001), which could impede treatment. Although stigmatization is ubiquitous in psychological services and exacerbates the difficulties of anxiety disorders
in general, certain ethnic minority populations might hold beliefs that compound the
perception of stigma related to those services. Stigmatization related to treatment
seeking may be attributable to social situations (i.e., overt discrimination), cognitive
appraisals (i.e., perception and fear of discrimination), and/or schema (i.e., internalization of socially introduced stigma; Green, Hayes, Dickinson, Whittaker, &
Gilheany, 2003). Social stigma related to psychological problems might be so prevalent among some ethnic minority groups that members fail to seek and engage in any
sort of psychological treatment. For instance, in a sample of both African-American
and Caucasian clients, Copper-Patrick et al. (1997) found that African-Americans
were more likely than their Caucasian counterparts to say that they were concerned with the social stigma that might be associated with receiving psychological
treatment. Likewise, Thompson, Bazile, and Akbar (2004) found that common perceptions of psychological services among African-American populations involved
high levels of perceived stigma and embarrassment associated with engaging services that were specifically related to psychological health. In other words, while
many Americans likely perceive the need for and choice to seek psychological
intervention as an embarrassing and stigmatizing prospect, this might be especially
relevant for members of ethnic and racial minority groups.
Another important factor associated with perceived treatment resistance relates
to the apparent mistrust that some ethnic and racial minority group members feel
toward potential psychological service providers. Indeed, the USDHHS (1999)
reported that members of some ethnic and racial groups cite fear of the treatment and/or treatment provider as the foremost reason for failing to seek and
engage needed psychological intervention. Obviously, interpersonal trust or mistrust will have some impact on whether any individual will present for treatment,
but again this association appears especially relevant among ethnic and racial
minority populations. In addition, people with psychological problems are often
the victims of degradation, rejection, and prejudice because they are considered
sick, dangerous, worthless, and insincere (Biernat & Dovidio, 2000). This prejudice has been described as being similar to what many ethnic minority groups in
the United States have endured for years thus compounding the problem of psychological problems in underserved populations (Biernat & Dovidio). For instance,
in a study of African-American students, Nickerson, Helms, and Terrell (1994)
found that those who endorsed high rates of cultural mistrust of Caucasians were
significantly less likely to seek psychological services than those who endorsed
lower rates of cultural mistrust. Likewise, Boyd-Franklin (2003) reported that some
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87
African-Americans appear to cope with the realities of racism and oppression by
refusing to extend interpersonal trust to individuals who differ from them in color
or economic class. Thompson et al. (2004) also reported that a significant proportion of African-Americans who were engaged in discussion of whether they can
trust psychological treatment providers asserted their belief that most clinicians are
elitist and biased against African-American concerns. This brief sampling of empirical findings highlights the fact that even in areas where psychological services and
treatment facilities are available, misunderstanding or fear about services and service providers probably impede their usage among some ethnic and racial minority
groups (USDHHS, 1999).
It is also clear that family ties are especially strong among many ethnic and racial
minority communities and that the family system is often one of the primary or sole
sources of support (e.g., USDHHS, 1999; Wilson & Stith, 1991). These ties and
notions of inter-familial reliance might be so strong, in fact, that some ethnic minorities are likely to strive to overcome psychological problems with family support
and guidance in lieu of seeking formalized psychological intervention (Snowden,
1996). Related to both stigma and family ties, African-Americans might be more
likely to experience the stigma of treatment because relying on non-familiar third
parties to solve personal problems goes directly against a common cultural belief of
inter-familial and self-reliance (Snowden, 1996).
Moreover, while many of our traditional psychotherapy models emphasize the
treatment of the individual, many ethnic and racial minority group members live
with extended family (e.g., grandparents, cousins) and might place greater emphasis
on the family than on the individual and expect the family to be involved in the
treatment process (USDHHS, 1999) and, thus, be less likely engage in treatment if
these family members are not included. In short, ethnic and racial minority clients’
expectations about the format in which psychological treatments are provided might
account for a portion of perceived treatment resistance among some members of
these groups.
Much like the importance of the family system, religion and spirituality also
serve important intrapersonal and interpersonal roles among many ethnic and
racial minority populations (e.g., Bernal & Saez-Santiago, 2006; Kelly, 2006).
Accordingly, some ethnic and racial minority group members appear more likely
to seek guidance from religious figures, rather than psychological health professionals, when faced with personal difficulties (USDHHS, 1999). Concisely, some
ethnic and racial minority clients have been found to endorse more traditional methods of intervention (e.g., use of folk healers) as a means of treating psychological
problems and might be less likely to seek treatment if they believe that traditional
methods will not be integrated into the treatment process (Thomason, 2000).
As discussed above, it is evident that ethnic minority members are also uniquely
subject to significant inequalities in psychological service availability and accessibility (USDHHS, 2001). In a word, access to psychological services is almost
always lower for poorer communities than more affluent ones (Gresenz, Stockdale,
& Wells, 2000; Zane, Hall, Sue, Young, & Nunez, 2004). Also, ethnic and racial
minority members are also less likely than Caucasians to have private health
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S.J. Spendlove et al.
insurance resources to pay for necessary psychological treatment (USDHHS, 1999).
Thus, cost of services has also been noted as one of the primary barriers to treatment
for many ethnic and racial minorities (Thompson et al., 2004; USDHHS, 2001).
Therefore, the cost associated with psychological treatment probably also necessitates and explains some ethnic and racial minority members’ increased tendency to
engage in alternative means of treatment. For instance, data from a series of focus
group discussions with a large group of African-American participants revealed
that excessive fees and preference for using low-cost, self-help methods such as
prayer and consultation with religious leaders were the most commonly cited reasons why many clients did not engage in needed psychological services (Thompson
et al., 2004) Thus, another significant cultural issue which complicates psychological treatment for many ethnic and racial minority group members has to do with
cost and affordability of necessary treatment, as opposed to characteristics of the
specific treatment or treatment provider. Meaning, some members of these groups
might want to engage our services, but are precluded from doing so due to the price
associated with a given treatment.
Culture and Language
Language is one of the primary means by which cultural information is conveyed;
so it follows that to be most effective, psychological services should be provided
in the language each client prefers. Yet the majority of psychological health professionals are monolingual, English-speakers (Zane et al., 2004). This means that the
majority of ethnic and racial minority members who do present for treatment will
see a clinician who only speaks English and to whom they might not be as able to
accurately convey their thoughts, feelings, and experiences. Obviously, this reality
means that the misinterpretation of verbal expression probably affects the manner in
which clinicians conceptualize a given problem and its appropriate method of treatment (Barona & Santos de Barona, 2003; Bernal & Saez-Santiago, 2006), posing
another significant treatment complication. More specifically, when working with
immigrant populations (e.g., Chinese or Mexican) language can present a major
complication for treatment. The effort expended in communication by bilingual
clients interviewed in a non-native language may produce greater vigilance and control over emotion than is desirable for proper assessment of distress (Malagady &
Zayas, 2001).
Language complications in treatment are not limited to English versus nonEnglish languages. Cultural values and language customs from any particular group
may impede progress in treatment because cultural idioms of distress may not be
understood. Indeed, many nuances of communication are contained in the cultural
expressions of thoughts, feelings, and emotions (Ayonrinde, 2003). For example,
an English-speaking Chinese-American may express the anxiety of living in a new
country in terms of how the honor of the family is affected rather than in terms of
personal worry or fear. Language and behavior used to express distress in ethnic
minority populations may lead to misdiagnosis in assessment and further treatment
Cultural Issues and Treatment Complications
89
complications due to misunderstanding of both verbal and non-verbal expression
(Malgady & Zayas, 2001). Throughout the relevant literature, these and other types
of variations in culture-specific ways of talking about and relating distress are often
termed cultural idioms of distress (e.g., Minhas & Nizami, 2006).
Culture and Idioms of Distress
One of the most prevalent idioms of distress among many ethnic minority groups is
somatic presentation of psychological symptoms, particularly in relation to anxiety
disorders (USDHHS, 1999). For instance, Ataque de Nervios, which is noted among
some Latino/a populations, is a cultural idiom that is so common that it has been
termed a culture-bound syndrome (APA, 2000). Ataque de Nervios is the manifestation of anxiety in which the individual might engage in uncontrollable shouting,
verbal or physical aggression, crying, and/or trembling (e.g., Liebowitz et al., 1994).
These symptoms might therefore lead to a misdiagnosis of a cluster B personality
disorder when, in reality, the individual is expressing culturally specific symptoms
of anxiety. Obviously, because these types of conditions might sometimes obscure
or explain psychopathology, clinicians and researchers must account for cultural
influences of behavior to realize the most accurate understanding, measurement,
and diagnosis of psychological problems (Vega & Rumbaut, 1991).
Linguistic misinterpretations of expressions of distress by ethnic minority
populations may also be attributable to the stress particular to acculturation.
Acculturation involves the sociocultural process by which an individual from
one culture comes into contact with and acquires a new culture (Berry, 2003).
Individuals experiencing this process will experience group (termed cultural) and
individual (termed psychological) levels of change. After contact with a host culture, individuals are likely to experience behavioral shifts first as they learn new
behaviors associated with their new roles at work or school (Sue, 2003). Contact
with a new culture may be accompanied by acculturative stress, or stress associated
with behavioral shifts in learning new customs, language, and cultural practices. In
many instances, acculturative stress is a direct result of prejudice and discrimination from the larger society (Berry, 1998). Although prejudice and discrimination
are not as overt as in the past, it continues to be a significant problem presented
in more subtle ways (Nelson, 2006). For example, when ethnic minority groups
attempt to access adequate housing, medical care, or political rights, they may be
denied these otherwise desirable features of a society because of implicit policies
designed to exclude acculturating groups from full participation in society (Berry,
1998). Consequently, acculturating groups may be marginalized by the larger society leading to increases in stress, anxiety, and general malaise that can complicate
treatment or prevent treatment seeking (Kanel, 2002).
Although conceptualized as necessary for an individual’s sociocultural adaptation (Berry, 2003), acculturative stress has been linked to various psychological
outcomes. For example, Latino/a adults have been found to experience more psychological problems (e.g., anxiety and substance use) as they increase in level of
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acculturation (Ortega, Rosenheck, Alegria, & Desai, 2000). In addition, acculturative stress in Mexican-American adolescents has been shown to be significantly
associated with increased depressive symptoms, lower self-esteem (Romero &
Roberts, 2003), increased suicidal ideation, lower family functioning, and increased
anxiety about the future (Hovey & King, 1996). Thus, acculturative stress can
further complicate treatment and must be addressed in a culturally appropriate
manner.
Even if these issues are addressed and ethnic and racial minority individuals
present for treatment, it is important for clinicians to be aware of the differences in
manifestation of symptoms linked to religious beliefs, values, and the understanding
of one’s place in society (Varela et al., 2004). Specific to anxiety disorders, anxiety sensitivity has been identified as a potentially culturally-relevant phenomenon
among underserved ethnic minority populations. Anxiety sensitivity is the degree
to which anxiety-related somatic/physiological symptoms are viewed as distressing
or aversive (Peterson & Heilbronner, 1987). This is distinct from trait anxiety (a
majority Anglo/Caucasian cultural construct) for ethnic minority youth (Silverman,
Fleisig, Rabian, & Peterson, 1991) and adults (Peterson & Heilbronner) such that
somatic signs of anxiety receive more attention and concern than cognitive and
behavioral indicators. However, at this point it is essential to remember that the
practice of drawing overarching conclusions about any individual based solely
on group membership must be avoided. This caution will help us to remember
that there is always a risk that cumulative suppositions about what are assumed
to be cultural norms will be overgeneralized, misleading, and possibly stereotypic in describing treatment-seeking behaviors among ethnic and racial minority
populations (Donohue et al., 2006; Zane et al., 2004).
As an example, when the first author worked with a 30-year-old MexicanAmerican woman diagnosed with generalized anxiety disorder, it was quickly
discovered in assessment that cognitions related to fears and worry were not as
distressing to her as her heart palpitations, shortness of breath, and dizziness.
Specifically, when describing a particularly anxious evening reviewing her finances,
she rated the severity of her distress related to feeling her heart “beat like it would
break [her] ribs” and her stomach “being rung out like a wet towel” at a 9 out of
10 while she rated her worrisome thoughts of being evicted over late rent at a 4 out
of 10 in severity of distress. In contrast, a 25-year-old Caucasian college student
presented to the same clinic with descriptions of anxiety focused on her distressing
thoughts that new acquaintances may think she is strange or “disturbed” by simple
small talk. In assessing her cognitive and physiological symptoms, she reported the
severity of detailed anxious thoughts such as “they’re expecting me to say something but I’ll sound stupid” and “I wish I hadn’t said anything” at 8 out of 10 in
distress. However, when asked, the Caucasian woman rated vague descriptions of
her physiological status, such as “butterflies in [her] stomach,” during such troublesome thoughts at 3 out of 10 in severity. Thus, when working with underserved
ethnic minority populations, it may be important to include sensitivity to physiological symptoms as part of the behavioral conceptualization of anxiety rather
than emphasizing cognitive aspects. This has the potential of assisting clinicians to
Cultural Issues and Treatment Complications
91
focus treatment techniques on that which can help reduce or manage the physiological aspects of anxiety (e.g., shortness of breath, racing heart, sweating, etc.) and
therefore reduce overall distress.
Resolving Treatment Complications
The above discussion of potential treatment complications related to work with
some ethnic and racial minority group members highlights the necessity to examine and appropriately modify our standards of practice to meet the needs of these
populations. As previously noted, the basic techniques of CBT serve as an excellent
foundation from which therapeutic approaches within clinical psychology can continue to be made more culturally responsive. However, this is best accomplished by
first accentuating the unique circumstances and experiences of the individual client
in assessment (Hays & Iwamasa, 2006). In that way, culturally sensitive treatment
adaptations will be based on individual cultural explanations of distress rather than
broad sweeping generalizations that generally lead to prescribed treatment models
that fail to recognize the within-group variability of various cultural groups.
Culturally Appropriate Psychological Assessment
In a review of cognitive-behavioral theory and techniques in assessment, Okazaki
and Tanaka-Matsumi (2006) highlighted seven culturally responsive assessment
paradigms that might have clinical utility in the cognitive-behavioral assessment
of anxiety disorders across diverse cultural groups. The seven paradigms reviewed
by Okazaki and Tanaka-Matsumi include (1) functional analysis, (2) the Culturally
Informed Functional Assessment Interview (CIFA), (3) the DSM-IV-TR Outline
for Cultural Formulation, (4) the Multicultural Assessment Procedure (MAP),
(5) the ADDRESSING Framework, (6) the Explanatory Model Interview Catalogue,
and (7) the Bicultural Evaluation. However, for the purposes of this chapter the
Bicultural Evaluation will be discussed in further detail. Interested readers are
referred to Okazaki and Tanaka-Matsumi for an excellent resource for a review
of assessment techniques currently available with utility in culturally responsive
assessment, case conceptualization, and treatment modifications.
As an extension of the functional analysis, the Bicultural Evaluation method
proposed by Evans and Paewai (1999) is an example of culturally responsive assessment. This cognitive-behavioral model of case conceptualization is intended to
build rapport, ensure cultural fairness, and use multiple sources of data similar to
the functional analysis approach. In extending the functional analysis, Evans and
Paewai created a checklist of 15 points of quality indicators of cultural responsive
assessment. The checklist includes assessment of the cultural identity of the client,
idioms of distress used in that client’s cultural group, and the culturally relevant
social support available to the client. In so doing, one may also assess the degree to
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S.J. Spendlove et al.
which conflicting demands in the social environment causes, maintains, or exacerbates distress that may be present due to acculturative stress (Berry, 1998; Evans &
Paewai, 1999). Although this checklist of culturally responsive functional analysis
was developed for the Maori people of New Zealand, it is easy to see how such a
cognitive-behavioral assessment could be applied to various cultural groups.
It has also been suggested that an important general first step in culturally sensitive psychological assessment is comprised of working toward the development of a
cultural schema (Hays & Iwamasa, 2006). In exercising this cultural schema in their
work with culturally different clients, clinicians should gather cultural information
about the population within which their interventions will be applied, obtain information from their clients regarding their specific personal experiences within their
culture, and consult with culturally diverse colleagues (Hays & Iwamasa, 2006).
Specific to anxiety disorders, another crucial aspect of moving toward more culturally relevant treatment involves the inclusion of broader aspects of the client’s
culture in case conceptualization and treatment delivery. This can be accomplished
by employing some previously mentioned assessment paradigms that have been
empirically supported to be sensitive to the idiographic nature of psychotherapy. For
instance, in the assessment of anxiety, demographic characteristics are accepted as
important considerations (e.g., Cooley & Boyce, 2004). However, failure to respond
to the treatment of anxiety disorders has been conceptualized as a problem in the
function of anxiety (Davies, Dubovsky, Gabbert, & Chapman, 2000).
Thus, proper assessment of the function of anxiety for a client can lead to more
appropriate treatment options. For example, a thorough assessment may reveal that
anxiety is a reaction to a comorbid psychological problem (e.g., schizophrenia)
rather than being the primary disorder of concern. Davies and associates (2000) provide a fairly extensive list of 11 possible functions of anxiety that may be assessed
from a medical/psychiatric standpoint. Some examples include questions such as
“is anxiety caused by a medication?” and “is the family exacerbating the patient’s
anxiety?” (pp. A25 and A26, respectively). Although this list of questions is not a
complete examination of the functions of anxiety, it may serve as the catalyst for
further exploration of the client’s particular situation which will invariably include
their cultural beliefs and practices.
Culturally Appropriate Treatment Adaptations
Appropriate culturally sensitive assessment will assist clinicians in arriving at a
specific case conceptualization and treatment planning similar to widely accepted
methods of assessment and case conceptualization (e.g., Funnel Approach of
Behavioral Assessment; Haynes & O’Brien, 2000). Marin (1993) suggested that
a culturally appropriate intervention is one wherein the treatment strategies are
expressly based on the cultural values of the group being served and are reflective of the subjective characteristics of the members of the group (e.g., attitudes,
expectancies about treatment). More generally, cultural adaptations are characterized as adjustments that are applied to established treatments to better accommodate
Cultural Issues and Treatment Complications
93
the specific beliefs, values, and practices of the person being treated (Whaley &
Davis, 2007). Although we do not have a well-studied and extensive understanding
of the factors that will aid in the development of appropriate cultural responses to
members of many ethnic and racial minority groups (e.g., Thompson et al., 2004),
there are some considerations that might help begin to resolve treatment complications and enhance the psychological services and interventions we provide. Since
we know that applied cultural adaptations appear to improve the therapeutic alliance
and increase professional credibility (Ancis, 2004; Wampold, 2001) and that clients
who were engaged in treatment programs that are specifically tailored for their specific ethnic minority group are significantly less likely to drop out of treatment than
ethnic minority clients participating in more mainstream treatment programs (e.g.,
Takeuchi, Sue, & Yeh, 1995) it is important for all clinicians who work with members of diverse ethnic and racial groups to give ongoing consideration to these and
other recommendations in the services they provide.
In terms of beginning to acknowledge and resolve some of the stigma that some
ethnic and racial minority groups members might associate with psychological
treatment, Hays (1996) offered that as part of her initial engagement of culturally
different clients she explains the process as counseling rather than therapy. This
recommendation could help to communicate the notion that clinician and client are
partners in the treatment process, rather than subordinates and insubordinates. Hays
also acknowledged that she seldom uses the terms cognitive-behavioral therapy in
an effort to avoid conveying a disregard for the social, emotional, and spiritual
aspects of the human experience. Concisely, one useful step in making CBT less
stigmatizing and more culturally relevant might be as simple as changing the manner
in which it is presented and discussed.
A recent meta-analytic review revealed that one of the most frequently acknowledged cultural adaptations involved explicitly acknowledging and discussing
varying cultural values and experiences (Griner & Smith, 2006). This group of recommendations can serve several purposes, including the diminishment of client fear
and mistrust toward the clinician. For instance, Gim, Atkinson, and Kim (1991)
found that clinicians who openly acknowledged the importance of understanding
facets of the client’s ethnicity and culture were rated as more credible than clinicians who did not acknowledge these factors. Similarly, Thompson, Worthington,
and Atkinson (1994) conducted a study in which clinicians discussed issues of being
African-American with some of their clients and not with others. Results revealed
that African-American clients in the group that was engaged in discussion of their
racial background were subsequently more willing to disclose personal information
to the clinician than those who were not engaged in such discussion. Moreover,
in a sample of Asian international students, Zhang and Dixon (2001) found that
clinicians’ interest and regard for other cultures, including that of the client, was
positively associated with student ratings of clinician trustworthiness and expertise. Thompson et al. (2004) also reported that African-American clients were more
likely to report feeling interpersonal comfort and rapport with clinicians who were
willing to openly acknowledge their interest in the client’s background and ethnic experiences. Data such as these support the point that an important cultural
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consideration that can be applied to any therapeutic paradigm is open and deliberate
discussion of the background and experiences of the individual client.
In terms of making CBT more accessible and appropriate for culturally different
clients, the above recommendation might be realized through working to validate
the client’s individual experiences with racism and discrimination and assessing
how these might influence the problem and means for resolving it (Kelly, 2006).
Inclusion of a candid dialog about the meanings of race and ethnicity to the individual client and discussion of his or her experiences as a member of a minority group
might help reiterate the clinician’s role as both an expert and a trustworthy confidant.
In addition, when clinicians strive to express a genuine curiosity about the diverse
experiences of their ethnic or culturally different clients, they might also facilitate
beneficial treatment impacts like reduction of interpersonal mistrust and compensatory increases in therapeutic rapport. Also, ensuring we engage these types of
discussion might also help us to remember that these experiences themselves place
our clients at greater risk for anxiety-related disorders (USDHHS, 2001). Lastly, it
is constructive to emphasize clients’ ethnic and racial differences as assets rather
than inadequacies (Quintana & Bernal, 1995). Therefore, clinicians should consider
talking with ethnically and racially diverse clients about the facets of their heritage
that bring them joy, satisfaction, and pride.
Given the above discussion of the importance of family ties among some ethnic and racial minority populations, some members of these groups might be
more likely to seek professional intervention if their extended family system is
also directly involved in the treatment process (USDHHS, 1999). Thus, clinicians should assess for these preferences and consider involving client’s families to
increase the likelihood that they will seek needed psychological services. Similarly,
clinicians should also consider that they might be better able to retain ethnic
or cultural minority clients in treatment if they contemplate ways in which they
might integrate alternative methods into their already established scientificallybased interventions (e.g., encouraging prayer as a form of counter cognitions for
anxiety).
Griner and Smith (2006) found that an often-mentioned cultural adaptation is
to strive for an ethnic-match between client and therapist. For instance, Russell,
Fujino, Sue, Cheung, and Snowden (1996) found that African-American adult
clients who were matched with an African-American therapist were judged to have
made more psychological improvements following treatment than those who were
not matched. Likewise, in a sample of African-American adolescents, Yeh, Eastman,
and Cheung (1994) found that clients who were matched with an African-American
therapist were significantly less likely to drop out of treatment than those who
were not matched with a therapist of the same race. Similarly, Sue, Fujino, Hu,
Takeuchi, and Zane (1991) found that client-therapist ethnic match was related to
lower treatment drop-out and increased use of psychological services for AsianAmerican and Latino/a clients. However, given the abovementioned percentage of
clinicians who are Caucasian and presumably Anglo in culture, it would be difficult
to realize this adaptation. Therefore, it is essential that the clinician acknowledges
ethnic, racial, or cultural similarities and differences, while also understanding how
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95
clients’ cultural values foster specific expectations of the therapeutic process and
the clinician’s role in it (Bernal & Saez-Santiago, 2006). This could mean that
the clinician engages the client in discussion of his or her ethical and professional limitations while attempting to clarify the client’s expectations about the
treatment.
Sue (2006) suggested that some culturally different clients might not even know
what therapy is, what it can do, and what to expect from the process. Thus, another
recommendation involves the engagement of the client in discussion of the purposes of the therapeutic process before treatment even begins. These types of
pre-therapy interventions or client-orientation programs typically familiarize clients
to psychotherapy by explaining the process, typical roles of clinicians and clients,
what can be expected from treatment, and issues of confidentiality (Sue, 2006).
In a study of the overall effectiveness of a pre-therapy intervention program with
a sample of African-American clients, Acosta, Yamamoto, Evans, and Stillbeck
(1983) found that engagement in a client-orientation program significantly increased
general client knowledge about and favorable attitudes toward engaging in psychotherapy. Likewise, in a sample of Asian-American clients, Lambert and Lambert
(1984) found that clients who were engaged in pre-therapy intervention reported
being more satisfied with treatment and dropped out of treatment less often than
those who did not receive pre-therapy intervention. In light of these data, it is important for clinicians to consider the potential benefits of taking extra time at the outset
of the therapy process to ensure that their clients are aware of what will take place
over the course of assessment and treatment.
Although we might not be able to impart significant change in the overarching
costs associated with our expertise and services, we can apply specific adaptations
to the treatment itself that might make the intervention more cost effective. The key,
it seems, is to think of creative ways that might make our treatment suggestions
more attainable for clients who do not have the financial resources that are more
often noted among the majority population. For instance, one treatment for anxietyrelated disorders is to include social activities as part of behavioral activation (Hays,
1996). A CBT therapist sensitive to the economic difficulties of the client might
emphasize social activity lists that include enjoyable endeavors which do not require
money.
Regarding culture and language, Sue (1998) found that clients matched to therapist with the same native-language were significantly less likely to prematurely
terminate treatment and more likely to report satisfaction with interventions provided, as compared to non-matched clients. Therefore, whenever possible, it is
essential that clients be matched with a clinician who is fluent in their preferred
language. This could not only help the client to feel more comfortable and able to
accurately reflect his or her experiences, but might also increase his or her willingness to remain in treatment. Of course, it will not always be possible for clients
to be matched with a clinician who speaks their preferred language. However,
we must still strive to make the language we do use more culturally syntonic.
Bernal and Saez-Santiago (2006) discussed how the language used in interventions should always be culturally appropriate for the person receiving the treatment.
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They suggested that this will require more than just broad translation of a given
intervention, but also the engagement of client with culturally syntonic language
that gives reference to existing differences in regional and subcultural group dialects
and preferences. Obviously, it would also prove beneficial to recruit and employ a
larger number of bilingual clinicians.
Conclusion
Although the topics discussed in this chapter are not exhaustive, those that are discussed here are considered most important by the authors to the understanding of
cultural treatment complications and resolutions. The general issues of culture as it
relates to treatment resistance, language, and idioms of distress have been examined.
However, it was the direct intention of the authors to provide broad recommendations for culturally appropriate assessment and treatment. It is hoped that clinicians
recognize that while some examples of possible assessment and treatment techniques that lend to culturally relevant assessment and treatment were discussed,
it remains the responsibility of mental health providers to utilize sensitive clinical
judgment that recognizes the importance of the individual and within-group variability. Thus, as the ethnic and racial minority populations of the United States continue
to grow rapidly (U.S. Bureau of the Census, 2005) the field of clinical psychology
will be more prepared to respond to the current and future mental health needs of
underserved populations.
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Part II
Avoiding Treatment Failures:
Disorder-Specific Perspectives
Avoiding Treatment Failures in Panic Disorder
Heather W. Murray, R. Kathryn McHugh, and Michael W. Otto
Panic disorder (PD) is characterized by recurrent panic attacks accompanied by
worry about future attacks, worry about the consequences of the attacks (e.g., having a heart attack), or substantial behavioral changes in response to the attacks
(American Psychiatric Association, 1994). Panic attacks themselves are distinct
periods of intense fear accompanied by four or more physical symptoms which
begin suddenly and reach a peak of intensity within 10 min. Panic attacks are
ubiquitous to a wide range of anxiety disorders, but in PD the focus of the phobic concern is on the anxiety symptoms themselves and the feared consequences of
these symptoms (Barlow, 2002).
Initial panic attacks are predicted by stress as well as the interaction between
stress and the vulnerability factor, anxiety sensitivity. Anxiety sensitivity is the
fear of anxiety-related somatic sensations based on the presumed catastrophic consequences of these sensations (McNally, 2002), and is an effective predictor of
individuals who panic in response to the biological provocation of these symptoms
(e.g., Rapee & Medoro, 1994; Schmidt & Mallott, 2006). Whereas stress may be a
prospective predictor of first panic attacks (Watanabe, Nakao, Tokuyama, & Takeda,
2005), those with higher anxiety sensitivity appear to be particularly at risk for panic
when confronted by stress (Schmidt, Lerew, & Jackson, 1997; Zvolensky, Kotov,
Antipova, Leen-Feldner, & Schmidt, 2005).
Although panic attacks can occur in nonclinical populations and across the spectrum of anxiety and mood disorders, few individuals proceed to develop PD. For
example, whereas approximately 10% of people experience a panic attack that meets
full criteria each year (Norton, Cox, & Malan, 1992), the estimated lifetime prevalence of PD in the U.S.is approximately 3.5–5% (Grant et al., 2006; Kessler et al.,
1994, 2006). The lifetime prevalence of PD with agoraphobia (PDA) is approximately 1%, and both PD and agoraphobia occur in isolation, with prevalence rates
of 3.5–4% and 0.2–0.8%, respectively (Grant et al.; Kessler et al.). Women are more
likely to develop PD than men, with higher numbers of women characterizing those
with more extreme agoraphobia (Yonkers et al., 1998).
H.W. Murray (B)
Department of Psychology, Boston University, Boston, MA, USA
e-mail: hwmurray@bu.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_7,
C Springer Science+Business Media, LLC 2010
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From a cognitive-behavioral perspective, PD is conceptualized as the learned fear
of autonomic arousal and its associated physical sensations. Panic attacks consist of
the sympathetic nervous system “fight-or-flight response” activated outside of the
context of an identifiable threat. The development and maintenance of PD following the presence of one or several unexpected panic attacks can be facilitated by
the aversive nature of the physical symptoms themselves and catastrophic interpretations of the symptoms. Frequently, panic attacks are misinterpreted as signs of
impending death (e.g., a heart attack or stroke), disability (e.g., fainting or going
crazy), or loss of control (e.g., inability to escape). Although fears of humiliation
may serve to intensify the catastrophic interpretation of some of these sensations
(“others will see I am losing control,” “they will think I am an anxious fool”), panic
is differentiated from social anxiety disorder by the fear of these sensations independent of social evaluation. Fears and catastrophic misinterpretations of symptoms
along with subsequent hypervigilance for somatic sensations help create a selfperpetuating pattern of anticipatory anxiety, vigilance for symptoms, memories of
past attacks, and fears of future attacks (Barlow, 2002; Clark, 1996). Future panic
attacks can be cued by minor psychological and physical changes, which become
associated with danger and the resultant panic cycle (Bouton, Mineka, & Barlow,
2001). Furthermore, anxiety and tension resulting from hypervigilance can mimic
the symptoms of panic and further contribute to this pattern. This cycle of panic
maintains and may exacerbate the core fear of panic-like physical sensations.
Similar cycles of fear and vigilance characterize a number of other disorders. For
example, hypochondriasis has been characterized as a feed-forward cycle of misinterpretation of bodily symptoms, anxious apprehension and increased vigilance
to these symptoms accompanied by checking behaviors and reassurance seeking
(Warwick & Salkovskis, 1990). Indeed, generalized anxiety, worries about somatic
symptoms, and tendencies toward avoidance appear to characterize the premorbid
state of many patients with PD. For example, 18 of a series of 20 patients with PDA
reported a history of generalized anxiety, hypochondriacal fears and beliefs, and/or
agoraphobic avoidance before the first panic attack (Fava, Grandi, & Canestrari,
1988; see also Fava, Grandi, Rafanelli, & Canestrari, 1992). For example, Fava,
Grandi, Saviotti, and Conti (1990, p.352) describe the following case:
Mrs E. was a 50-year-old blue-collar worker with a 35-year history of disease phobia (consistently focused on the heart) and hypochondriasis. Eight months prior to the assessment,
the patient’s sister, to whom she felt very close, had surgery for gastric carcinoma. Shortly
afterwards, Mrs. E. ’s preoccupations with having a heart attack increased, and panic attacks
ensued.
According to the cognitive-behavioral model of PD, once these panic attacks
occur, and are catastrophically misinterpreted, then a fear-of-fear cycle can ensue
with recurrent panic attacks accompanied by vigilance to symptoms and avoidance
of events and situations associated with panic attacks. This model is summarized
pictorially below (Fig. 1). The value of the model is in providing an overview
of the primary patterns in PD, and in identifying elements of the panic cycle for
intervention.
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105
Fig. 1 Cognitive-behavioral model of panic disorder. Adapted from Otto and Gould (1996)
Core Elements of Treatment
Core interventions for PD include psychoeducation, cognitive interventions, and,
particularly, interoceptive (internal) and in vivo exposure (Fig. 1). Psychoeducation
includes the nature and source of panic symptoms, the nature and style of catastrophic misinterpretations of these symptoms, associated anxious apprehension and
vigilance, and the role of avoidance behaviors. This education is complemented by
prospective monitoring of symptoms to help to build awareness of panic patterns
within the new framework provided by the model of the disorder.
Cognitive interventions are aimed at eliminating catastrophic misinterpretations of symptoms and establishing more adaptive thinking patterns. Of particular
importance to cognitive restructuring efforts for PD are the cognitive errors of:
(1) overestimating the probability of negative outcomes, and (2) assuming the consequences will be unmanageable (i.e., catastrophizing). Reviewing these maladaptive
cognitive patterns and teaching the patient to challenge these thoughts can reduce
their salience, and shift interpretation of these thoughts from “fact” to “guess.”
These strategies include evaluating evidence for the thought and evaluating the cost
of the feared outcome (e.g., could you cope with fainting in public?). Subsequent
exposure interventions provide patients with direct opportunities to examine negative predictions about the consequences of anxiety and panic symptoms and to learn
directly from experience.
In current treatment protocols, exposure is initially targeted to feared internal
sensations (Craske & Barlow, 2007; Otto & Pollack, in press). A range of physical
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exercises are used to induce these sensations. For example, head rolling can be used
to induce dizziness; hyperventilation can be used to induce dizziness, shortness or
breath, dry mouth, hot flushes, and numbness and tingling; stair running can be used
to induce a racing heart, shortness of breath, and sensations of heavy legs; breathing
through a straw can be used to induce shortness of breath; and spinning in a chair
can be used to induce dizziness and nausea.
During exposure patients are to attend to these sensations without engaging in
defensive behaviors (e.g., tensing, moving, escaping the situation). By learning to
do nothing in response to these sensations, patients have the opportunity to examine the degree to which the sensations are tolerable and manageable. As fears of
the sensations decline, these sensations lose the ability to provoke panic. Figure 2
summarizes the use of interoceptive exposure to help train an alternate response to
symptoms.
Fig. 2 Training Alternative Responses to Feared Somatic Sensations; From Smits and Otto (2009)
(Reprinted with permission from Oxford University Press)
The progression of exposure, like in other exposure treatments, should be
graded. Therapists work to provide more intense interoceptive exposure procedures
while also fading out safety cues (e.g., practicing independently of the therapist,
practicing away from home). Likewise, as therapists transition to treating the fear
of situations, a hierarchy of agoraphobic situations should be identified. For each
exposure, patients should expect initial anxiety, and apply skills learned during
interoceptive exposure (note the anxiety but do not try to control it) while waiting
for the anxiety to dissipate and completing goal-directed activities (e.g., shopping
during exposure to a mall).
A critical component to the success of exposures is the accurate identification
and fading of safety cues or behaviors. Individuals often have developed behaviors
to reduce the anxiety experienced and/or to feel an increased sense of safety while
remaining in the feared situation. These behaviors are referred to as “safety behaviors”, and contribute to the cycle of PD in that the individual “learns” that he/she
needs to engage in these behaviors to cope with the situation. Safety behaviors may
Avoiding Treatment Failures in Panic Disorder
107
be difficult for the patient to identify, as the patient may have been engaging in such
behaviors for years without fully recognizing the function of their behavior. Also,
individuals with PD engage in cognitive strategies to reduce anxiety. An example
of a cognitive safety strategy is praying before entering an elevator. These safety
behaviors are often very subtle; therefore, taking the time to identify such behaviors
or cognitive strategies is important before initiating the exposure to order for the
patient to experience the anxiety fully when completing the exposure task. These
can be important to the grading of exposures in allowing for the adjustment of difficulty level as exposures progress. For example, the patient may first go to the mall
with a friend (i.e., a “safe” person) and carry her cell phone and a bottle of water.
Subsequent exposures can begin to strip away these safety cues in order to increase
the difficulty of the exposure. It is of particular importance to identify and eventually
remove any signs of safety to ensure that learning has generalized and is not limited
by conditional thought (e.g., “I was only OK because I had my cell phone.”).
Table 1 Key elements of exposure
• Review rationale in the context of the cognitive-behavioral model of panic, including
emphasizing the importance of re-learning safety to innocuous sensations and situations.
• Evaluate feared physical sensations and situations.
• Emphasize the importance of remaining in the exposure despite anxiety and not utilizing
management strategies (observe for any subtle strategies).
• Instruct the patient how to induce sensations and what sensations to expect from each
induction. Model inductions for the patient to ensure proper use.
• Begin with exposures of moderate difficulty to provide a model for more difficult exposures
and to build patient efficacy in tolerating feared sensations.
• Instruct the patient to evaluate the nature, intensity, and similarity of sensations to panic.
• Use exposures as an opportunity to test beliefs about panic (e.g., “I will faint if I feel dizzy.”)
• Conduct interoceptive exposures first in-session, ensuring adequate duration of induction
and repeating each exposure at least twice.
• Change the context of interoceptive exposures to increase difficulty and facilitate
generalization of learning (i.e., conduct exposures outside of the session, alone, etc.).
• Introduce in vivo exposures in a graded fashion beginning again with moderate difficulty.
Combine in vivo and interoceptive exposures to increase difficulty.
• Evaluate and remove safety cues and behaviors with continued in vivo exposures.
• Consider additional context changes (e.g., time of day, with caffeine or after a meal, with
various people).
Non-essential Elements of Treatment
Research evidence suggests that some commonly used components are not necessary for achieving positive outcomes (see Schmidt et al., 2000). Some cognitivebehavioral treatments for PD include components of training in skills for reducing
anxiogenic responses to bodily sensations, such as diaphragmatic breathing and
progressive muscle relaxation. These techniques are introduced to reduce levels
of anxiety and to assist in the preparation for exposures. Although an excellent strategy for reducing tension and arousal, particularly for generalized anxiety
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(see Behar & Borkovec, this volume), the use of these strategies for PD may
be deleterious to treatment outcomes if they are adopted as avoidance or safety
behaviors (Schmidt et al., 2000).
Format of Treatment
Individual CBT for panic typically consists of 12–15 weekly, 1-hour sessions
(Craske & Barlow, 2007). Briefer versions have also demonstrated efficacy, including four-session (Craske, Maidenberg, & Bystritsky, 1995) and five-session treatments (Clark et al., 1999). Brief CBT has also been applied in a primary care setting.
Roy-Byrne et al. (2005) found that patients randomized to six sessions of CBT
in combination with a patient manual (“Mastery of your Anxiety and Panic”, 3rd
edition; Barlow & Craske, 2000) compared to TAU, sustained gradually increased
improvements relative to TAU on both PD symptoms, overall mental health functioning, and disability scales. Furthermore, the CBT was delivered by mid-level
behavioral health specialist with little or no CBT experience prior to training for
this study, exemplifying that CBT can be disseminated in this manner. CBT can
also be administered in a group format while maintaining efficacy (e.g., Telch et al.,
1993) and may offer a particularly cost-effective option.
Treatment Example – Interoceptive Exposure
David is a 35-year-old male presenting with PDA. Onset of panic symptoms
occurred approximately 8 years ago following the death of his grandmother. His
panic attacks were characterized by heart palpitations, shortness of breath, choking
sensations, dizziness, sweating and fear of having a heart attack or insanity. Since
his initial panic attack, he has had several panic attacks while driving in traffic and
subsequently avoided driving during rush hour or on main roads.
Initial sessions were focused on psychoeducation providing treatment rationale
and information on the nature and maintenance of panic. Several sessions were dedicated to cognitive restructuring. David was able to identify his catastrophic thinking
patterns and to replace his cognitive distortions with more adaptive alternatives.
The rationale for interoceptive exposures was explained and the following dialog
highlights sticking points in this intervention.
Therapist (T): The first exercise we will try is hyperventilation. This exercise
will lead to feelings of dizziness, lightheaded, and occasionally numbness and tingling in the arms or around the mouth or scalp. Also, because your eyes may dilate
from hyperventilation, you may notice that things look bright after we finish. I will
demonstrate the exercise to do and then I will have you perform the exercise. We
will hyperventilate for a minute, and then I will tell you to stop (therapist briefly
demonstrates hyperventilation).
Avoiding Treatment Failures in Panic Disorder
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Patient (P): (patient discontinues exercise before therapist does) I don’t know
if I can do this.
T: I understand this is hard for you. You do have concerns about the symptoms
we are inducing. Why is this telling you that you cannot do this exercise?
P: I don’t understand why this is important.
T: I can understand why you would not want to bring on these distressing sensations. You’ve been really good at avoiding these sensations, and you have
been doing so for years. In what way has this avoidance been a problem for
you?
P: Well, I have had to rearrange my life to avoid the panic. I can’t go on
vacations with my family, I leave for work early, I can’t take business trips.
T: Right, avoiding these sensations is not working in the long run. These exercises give you the opportunity to confront these feared sensations to learn
to tolerate them. Let’s try it again. And this time, while doing the exercise,
attend to the sensations that you are feeling, so that you can describe them
to me. And as you notice these feelings, I would like you to do nothing to
manage them. Just let the feelings happen, notice them, and do nothing to
control them. (patient completes exercise)
T: Great. What physical sensations did you notice during the exercise?
P: I felt dizzy. It felt like I wasn’t getting enough air.
T: What else did you notice?
P: I also felt numb around my face.
T: OK, we knew that might happen. How did you do at not managing the
sensations.
P: Well I really wanted them to stop.
T: Why did that seem important?
P: I did not know what was going to happen. I kept thinking, “what if they get
worse.”
T: OK, so you started focusing on the future, and what could happen. But how
were the sensations that you actually felt.
P: They were weird. I was dizzy.
T: Yes, they are weird, but how did you do with the weird sensations when you
just let yourself feel them – in the present.
P: I guess they were OK. I did not like them, but they were OK.
T: OK, I would like you to try the exposure again, and let yourself really focus
on the present. Even though you may have thoughts about the future (“what
may happen next”) I want you to really focus on the sensations you are experiencing right now and see how comfortable you can be in just letting the
sensations occur.
P: OK. (Patient completes a second exposure.)
T: How do you feel?
P: Dizzy but OK.
T: Are you staying in the moment, or are you focusing on the future.
P: A little of both.
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T: OK, let me get a sense of how strong the dizziness was, from 0 to 100, with
0 representing “not at all” and 100 representing “the most intense dizziness
you can imagine.”
P: It was probably a 40.
T: How similar was this dizziness to what you feel during a panic attack, again
from 0 to 100?
P: Not that similar. Maybe a 50.
T: And how anxious did those sensations make you feel?
P: I felt pretty anxious the first time, but the second time was around a 50.
T: OK, it looks like we have a nice procedure to help you get comfortable with
the sensations linked to your panic. With some practice feeling the sensations
and doing nothing in response to the sensations, I think we can help you feel
much more comfortable with dizziness.
Several sessions later, David has successfully continued his interoceptive exposures and developed a fear and avoidance hierarchy. At this point, the focus shifts
to situational exposures (or if needed, imaginal exposures). Graded exposures were
planned, starting low on David’s hierarchy. In an early exposure, in which David
stayed in an enclosed space with the therapist, he was not experiencing sufficient
anxiety.
T: How anxious do you feel now, from 0 to 100?
P: Not very, maybe a 20.
T: What sensations are you feeling? And how intense are they?
P: I’m not really experiencing any physical sensations.
T: Let’s make this more challenging. What would make this more difficult for
you?
P: I don’t know.
T: Do you think if you were to do the hyperventilation exercise while staying
in this situation, that would increase your anxiety?
P: Yeah, it would. (patient completes hyperventilation)
T: How anxious do you feel now?
P: A little higher, maybe a 40.
T: Remember we talked about safety behaviors. Do you think you might be
engaging in one of those behaviors?
P: I don’t know. I don’t think so.
T: We talked about cognitive safety behaviors, what thoughts were you having
during the exposure?
P: I told myself that I just have to get through it because it will be over soon.
T: That sounds like a safety behavior to me. Let’s try this again, this time,
without those thoughts; instead just let yourself feel the sensations and see
what it is like when you don’t manage them.
After removing safety behaviors, David was able to engage in the exposure and
to experience moderate levels of anxiety. Later in treatment, David experienced
Avoiding Treatment Failures in Panic Disorder
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difficulty as exposures became more difficult. An exposure higher on his hierarchy
involved riding in an elevator. Prior to the exposure, the therapist reviewed the rationale for exposure and the patient chose to participate in the in-session exposure.
After several minutes in the elevator with the therapist, David reported that his
anxiety remained high.
P: My anxiety isn’t going down. I want to get off now.
T: Ah, and tell me what makes your anxiety seem so dangerous. You have been
learning that you can have anxiety sensations and still be OK. Just ride it out
and it will decrease on its own. This is good practice to see that the anxiety
isn’t dangerous.
P: But if I can’t leave, I am not sure if I can stand my anxiety. What if I really
panic?
T: There is one of those “what if” thoughts. And you are focusing on a need to
escape and you seem to be actively trying to make your anxiety go down. I
am sure that isn’t helping. I want to give you a chance to experience anxiety
and notice what happens if you let yourself stay in the elevator, to know you
are in the elevator, and to not focus on the door or leaving. Will you try it?
(therapist is hesitant to engage in too much discussion as this may serve as a
cognition distraction)
P: I guess I can try it.
David continued in the exposure until his anxiety decreased. Following completion
of the exposure, the therapist reinforced his efforts and discussed his experience.
Homework assignments reflected in-session exposure and continued interoceptive
exposures.
Efficacy of CBT Treatment
Of the available treatments, CBT for PD has demonstrated excellent treatment
efficacy that equals or surpasses that for pharmacologic treatments (e.g., Barlow,
Gorman, Shear, & Woods, 2000; Furukawa, Watanabe, & Churchill, 2006; Gould,
Otto, & Pollack, 1995). Treatment for PD is well-tolerated by patients (Barlow et al.,
2000; Hofmann, et al., 1998), associated with quality of life improvement, including improvement in co-occurring disorders (Tsao, Mystkowski, Zucker, & Craske,
2002; Telch, Schmidt, Jaimez, Jacquin, & Harrington, 1995), and durability of gains
after treatment discontinuation (Margraf, Barlow, Clark, & Telch, 1993; Gould et al.,
1995; Barlow et al., 2000; Craske, Brown, & Barlow, 1991). CBT also improves
response to pharmacologic interventions (e.g., Marks et al., 1993; Mavissakalian,
1990; Schmidt, Wollaway-Bickel, Trakowski, Santiago, & Vasey, 2002) and is efficacious as a next-step strategy for patients who did not respond adequately to
pharmacotherapy (Heldt et al., 2003, 2006; Otto, Pollack, Penava, & Zucker, 1999;
Pollack, Otto, Kaspi, Hammerness, & Rosenbaum, 1994). Furthermore, CBT aids in
the discontinuation of anxiolytic (e.g., benzodiazepine, antidepressant) medications
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without loss of treatment efficacy (e.g., Otto, Hong, & Safren, 2002; Whittal, Otto,
& Hong, 2001).
The transportability of CBT outside of research settings is supported by its strong
cost-efficacy (McHugh et al., 2007; Otto, Pollack, & Maki, 2000), and effectiveness
in clinical practice (Addis et al., 2004; Stuart, Treat, & Wade, 2000; Wade, Treat,
& Stuart, 1998) and primary care settings (Roy-Byrne et al., 2005). For example, in a study of the clinical effectiveness of CBT relative to treatment as usual,
Addis and colleagues (2004) found that 49% of patients receiving CBT exhibited
significant symptom change over the course of treatment. Although decreases in
symptoms were also noted in the treatment as usual condition, less than 20% of
patients demonstrated significant change from pre- to post-treatment.
In summary, there is ample good news about the efficacy of CBT. In some trials, CBT has helped patients achieve panic-free rates in the range of 74–85% (e.g.,
Barlow et al., 2000). Moreover, maintenance of treatment gains during follow-up
periods of 1–2 years have shown equally promising panic-free rates ranging from
81% to 87% (DeRubeis & Crits-Christoph, 1998). However, it is also clear that
panic-free rates does not mean freedom from panic-related disability (Margraf et al.,
1993; Clark et al., 1994), nor are patients who are panic free at one assessment necessarily those who are panic free at the next assessment, and some patients also seek
additional treatment after the initial treatment episode (Brown & Barlow, 1995).
Also, in other investigations, lower response rates have been reported. For example, in a large, multi-site investigation of the relative efficacy of individual and
combined pharmacologic and cognitive-behavioral treatments for PD, cognitivebehavior therapy was associated with a 51% rate of non-responders at treatment
termination, which grew to approximately 67% at 6-months post-treatment (Barlow
et al., 2000). Consideration of predictors of non-response can provide a perspective
on these variables outcomes.
Depression Comorbidity and Treatment Resistance
The most common finding in the PD treatment literature is that CBT is often
resilient to the effects of comorbid depression (for review see Deveney & Otto, this
volume). This conclusion is based on studies where depression was evaluated by
symptom scores as well as diagnosis in individuals where the PD was the primary
target of treatment (e.g., Basoglu et al., 1994; Black, Wesner, Gabel, Bowers, &
Monahan, 1994; Barlow et al., 2000; Kampman, Keijsers, Hoogduin, & Hendriks,
2002; Laberge, Gauthier, Cote, Plamondon, & Cormier, 1993; McLean, Woody,
Taylor, & Koch, 1998; Wade et al., 1998). However, these findings are not without
inconsistencies, and there is evidence that at times depression does assert a negative
effect on CBT outcomes for PD (Basoglu et al., 1994; Maddock & Blacker, 1991;
Skeketee, Chambless, & Tran, 2001), as well as being associated with greater clinical impairment pretreatment (e.g., Joormann, Hertel, Brozovich, & Gotlib, 2005).
When it does have a negative impact, comorbid depression may assert its negative effects on any of a number of factors including motivation, the accuracy and
nature of cognition, problem solving, and the evaluation of treatment and progress.
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Interventions for these challenges are reviewed in Chapter 12 (Otto & Deveney, this
volume) and are not further reviewed here.
Comorbid Anxiety Disorders and Treatment Resistance
Patients with PD often have comorbid anxiety disorders; studies indicate 20–50% of
outpatients have comorbid social phobia (Stein, Shea, & Uhde, 1989), and between
3.5% and 5% of individuals have lifetime prevalence rates of both a PD and GAD
diagnosis (Kessler et al., 1994; Wittchen, Zhao, Kessler, & Eaton, 1994) and high
rates (27–32%) of panic symptoms with PTSD (Leskin & Sheikh, 2002). Comorbid
anxiety conditions may interfere with treatment and attenuate treatment response,
though the research supporting this is mixed (Tsao, Lewin, & Craske, 1998; Brown
et al., 1995; Tsao et al., 2002). CBT treatment strategies are specific to type of
anxiety disorder, though the skill of cognitive restructuring included in CBT for
PD can be helpful in intervening for a variety of cognitions. In addition, tolerance
to the physiological distress, in particular the distress related to panic attacks, can
generalize to similar distress associated with other anxiety disorders, particularly
those with similar physiological arousal such as social phobia and specific phobia. We recommend vigorous treatment of the primary presenting disorder, and
then subsequent evaluation of whether core fears underlying secondary disorders
have been adequately addressed. Therapists should consider re-designing exposures
to also take into account additional elements (e.g., fears of being embarrassed by
panic symptoms in individuals with comorbid social phobia) that may be inadequately addressed by standard disorder-specific exposure interventions. Likewise,
use of “worry-free zone” techniques (see Behar & Borkovec, this volume) to help
patients gain control over runaway worry processes may be necessary for individuals
with comorbid generalized anxiety disorder. A case example follows that illustrates
the shifting of exposure assignments to incorporate anxiogenic concerns that were
inadequately treated by core procedures for PD.
John is a 41-year-old African-American male presenting to the clinic with a primary diagnosis of PD and a secondary diagnosis of social anxiety disorder. John had
a long-standing history of panic attacks that made it difficult for him to take public
transportation and travel far from home. He reported fears of having a panic attack
when traveling which would either embarrass him in front of others or prevent him
from being able to escape. John avoided all travel for a period of time; however, this
became impractical given his job and he disliked the way that panic limited his ability to engage in activities farther away from his home. John began to research his
illness and successfully reduced his avoidance by forcing himself to go places and
“white knuckled” through the anxiety. Yet, John’s panic persisted and he presented
to treatment with the goals of reducing panic attacks and facilitating his ability to
travel farther from home.
After initial psychoeducation on the nature of PD, John fully embraced the fearof-fear model. He was able to accept the logic of his cognitive restructuring, but had
difficulty accepting his anxiogenic thoughts at an emotional level. For example, John
was able to develop rational responses to his panic fears (e.g., “I have never fainted;
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therefore, it is unlikely that I will faint this time”); yet, each time he experienced
panic-like physical sensations, the original catastrophic thoughts re-emerged. John
and his therapist utilized interoceptive exposure exercises as a way of retraining
his reactions to physical symptoms of panic. His therapist described the technique
of “doing nothing” in response to the sensations - simply observing the sensations
without reacting to them in a catastrophic manner. John participated in several interoceptive exposures, but had difficulty using this technique without safety behaviors
- he gripped the sides of his chair during hyperventilation and dizziness exercises
until the induction ceased. This “white knuckling” appears to be the same way he
has handled previous experiences with anxiety.
John began to understand how to react differently to his sensations when he was
able to link the physical sensations of panic with those that he experiences, and
tolerates, during physical exercise. It appeared as if the thought, “Huh, this is similar
to what I experience when working out”, allowed John to react differently to the
physical sensations which, in turn, resulted in a reduction of the sensations, without
him having to “white knuckle” through them.
Although this experience was a helpful breakthrough, John continued to report
significant anticipatory anxiety. He had difficulty using his interoceptive exposure
experience to challenge some of his panic thoughts, and he continued to fear that
the next bout of physical symptoms would result in marked embarrassment and
prolonged panic.
In light of these fears and John’s comorbid social anxiety disorder, his therapist
combined an exposure for PD (riding on public transportation) with a social anxiety exposure to address his inflated estimates of social cost (e.g., doing something
embarrassing while riding on public transportation). Once John’s anxiety around
riding public transportation had decreased somewhat, the therapist asked John to
identify the feared consequences of doing something embarrassing (e.g., sitting in
a strange way) while on the bus. John and his therapist then sat in an unusual way
on the bus and observed John’s anxiety as well as whether his feared consequences
came true. John’s anxiety peaked and then gradually declined, as he observed that
there was no social cost to this behavior. Hence, the inclusion of this social cost
exposure, more traditionally associated with social anxiety disorder, allowed John’s
fears of panic attacks to decline dramatically. During the following session, John
reported a marked reduction in anxiety and number of panic episodes. He also
reported more success discounting his catastrophic thoughts about panic, realizing
that not only was he unlikely to faint, but that others were unaware of his anxiety.
Marked progress followed this additional exposure.
Alcohol and Substance Use and Treatment Resistance
Alcohol dependence frequently co-occurs with PD (12-month prevalence rate of
11%) and PDA (12% prevalence rate) as indicated in a large study (Grant et al.,
2004). The 12-month prevalence rates for substance use disorders for individuals
Avoiding Treatment Failures in Panic Disorder
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with PD and PDA is 17% and 24%, respectively, and the rates of substance
dependence is 13% and 15%, respectively (Grant et al., 2004). Substance use and
withdrawal can mimic panic symptoms and impacts the quality of session retention
as well as overall treatment adherence rates. Interventions for these challenges with
comorbid alcohol and substance abuse and dependence are reviewed in Chapter 14
(Lejuez et al., this volume) and are not further reviewed here.
Personality Disorders and Treatment Resistance
Prevalence rates for comorbid personality disorders, most commonly avoidant,
dependent, histrionic, and borderline personality disorders, with PD is common
within the range of 40–70% of patients meeting criteria for both (Diaferia et al.,
1993, Mavissakalian & Hamann, 1988). A diagnosis of an Axis II disorder often
but does not necessarily predict poorer treatment outcome has been debated (Reich
& Vasile, 1993, Chambless, Renneberg, Goldstein, & Gracely, 1992; Mennin &
Heimberg, 2000; Reich & Green, 1991). Patients with comorbid anxiety disorders
and personality disorders often have higher severity of Axis I pathology at followup, though the severity is better accounted for by elevated severity at baseline (Van
Den Hout, Brouwers, & Oomen, 2006). For example, Van Den Hout et al. (2006)
large treatment outcome study found that 72% of the participants with an Axis II
disorder made significant clinical improvements with the CBT compared to 78% of
the participants without the Axis II disorder, though those patients with personality
disorders reported higher symptoms severity at baseline and follow-up.
Given that treatments targeting PD have shown reductions in personality pathology (Mavissakalian, 1990) as well as defensive style (Heldt et al., 2007), we
recommend initial targeting of the PD to see how many apparent personality symptoms change as part of the overall change in panic-related distress. Moreover, the
enhanced tolerance of emotion brought by interoceptive exposure procedures may
offer general benefits for symptoms well outside the domain of PD (Otto, in press).
However, when personality pathology appears to interfere with the completion of
treatment procedures, consideration of core concepts of dialectical behavior therapy (DBT; Linehan, 1993) may be of use. For example, a therapist may emphasize
communication styles that convey acceptance of their patient while focusing on
teaching their patient specific skills to change target (frequently avoidant) behaviors. In addition, highlighting behavioral action (exposure) as a choice and using
problem-solving techniques in deciding to complete the exposure exercises will
empower the patient and enhance the collaborative therapeutic relationship.
Incorporating DBT treatment strategies with panic interventions in the same session may be challenging with more severely impaired patients, particularly when
self-injurious behaviors and suicide ideation are endorsed. In these situations, a
patient’s distress of the week may overshadow the regular practice needed to help
patients progress with panic treatment. Under these conditions, it may be helpful
to schedule double weekly sessions, with clear demarcation of the focus of each,
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reserving one session for weekly distress and the other for skill building to undo
panic cycles.
Medical Factors
Certain medical illnesses and side effects from medication may present as PD and
may complicate assessment and treatment of panic. Hyperthyroidism, hyperparathyroidism, vestibular dysfunctions, seizure disorders, and cardiac conditions are a few
examples of medical conditions that should be evaluated and the impact of anxiety
determined before a diagnosis PD is assigned. Medications and medication discontinuation can also cause anxiety. In addition, prevalence rates of patients with
medical conditions developing panic attacks is high for patients with respiratory
disorders (such as asthma) and cardiac conditions (coronary artery disease), in part
because the sensations associated with the anxiety are believed to be related to the
medical condition. A comprehensive assessment will further identify medical conditions and medication that may be contributing to panic attacks, and addressing the
underlining factors may improve therapeutic interventions and increase efficacy of
treatment.
Life Stressors
The onset of life stressors, unrelated to PD, is not uncommon during the course of
treatment and may exacerbate symptoms of panic. Assessing life issues that are preventing attention to treatment goals and adjusting the treatment plan to address the
life issues may reduce overall anxieties and increase long-term adherence to treatment. Life stressors, including relationship conflicts, may arise due to a decrease
in panic symptoms and increased functioning. For example, a wife may become
resentful of her husband’s treatment since he, as a result of experiencing a reduction
in symptoms, is less willing to watch their children every evening when his wife
wants to go out and spend time with her friends. An informational couples session
is a strategy frequently employed to address changes in relationship roles as changes
in symptoms occur (e.g., Otto & Pollack, in press). Highlighting the short-term and
long-term benefits of treatment may help the patient continue to persist with the
treatment despite short-term consequences that may be challenging to relationship
roles. Also, more involved inclusion of couples in treatment has shown beneficial
effects (Barlow, O’Brien, & Last, 1984; Cerny, Barlow, Craske, & Himadi, 1987).
Addressing Inadequate Treatment Response
Given the overall success of CBT for PD, and evidence that the model of the disorder
is not only useful in treatment but also in predicting and preventing the onset of PD
(Gardenswartz & Craske, 2001), we believe that the first step in addressing treatment
Avoiding Treatment Failures in Panic Disorder
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resistance lies in a re-evaluation of core fears and better honed efforts at providing
the patient with the therapeutic learning most needed to address these fears. As such,
in the sections below, we consider the motivational and avoidance-based issues that
prevent patients from having a chance to learn from their own experiences, as well
as modifications that can be made in treatments to better provide patients with useful
learning once they do engage in exposure.
Considering avoidance of treatment interventions, a patient may be hesitant to
engage in the interoceptive and in vivo exposures when the rationale for the exposure is unclear or if the patient believes that engaging in the feared situation is not
helpful based on previous experiences. If this is the case, reviewing the principles
of exposure by utilizing metaphors and examples may facilitate a shift in sense of
control. In particular, a patient may begin to challenge himself or herself in facing his or her fears as opposed to feeling forced to engage in the activity based
on the therapist’s instructions. For patients that demonstrate rigid thinking patterns,
worksheets can also be helpful in making the connections. In addition, having your
patient explain why exposure reduces anxiety in the long run will help you determine the level of understanding your patient has for the concepts behind exposure.
When patients believe that their previous attempt to face their fears is evidence that
the exposure won’t work, help the patient to identify factors that contributed to their
experience. Often, patients will report engaging in safety behaviors, terminating
the exposure prematurely, and evaluating their experience based on their emotions
rather than their behaviors. Reviewing the rational of exposures and incorporating
the role of safety behaviors, duration of the exposure and setting up clear goals and
expectations, based on definable behaviors, will help ensure their future exposure
will be a success.
Motivation impacts treatment in many ways and can have many presentations.
Homework noncompliance, canceling sessions, refusing to complete in-session
assignments may be related to motivation, though a seasoned therapist will assess
the function of noncompliance to determine the role of avoidance in the noncompliance behavior. In addition, signs of noncompliance should lead to an evaluation
of barriers to treatment and is an opportunity to teach and practice problem-solving
strategies and time management skills as they apply to treatment. Restating expectations and verbalizing the framework of the treatment may also be appropriate.
Sometimes patients come to treatment believing that their therapist will “fix them”
rather than providing a model and training in the change process. Helping patients
play an active role in therapy, in part by discussing therapy as action based rather
than talk based, may help change these expectations.
Also, a lack of symptom reduction despite progressing through the treatment
phases may be linked to targeting the wrong core fears, prescribing exposure
exercises that are too specific, or compromising exposures with the use of safety
behaviors. Reconfirming the primary diagnosis and assessing comorbid conditions
is an excellent start to further examining the nature of current core fears affecting the patient. Also, we recommend attention to reassessing core fears through
Socratic questioning, and then re-examination between these fears and the exposures arranged to date. The goal is to assess whether the exposures are truly targeting
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the core concerns and fears and attempt to generalize the learning that occurs during
the exposures to other feared stimuli. In addition, treatment planning in the face of
non-response should include re-evaluating the role and use of safety behaviors and
planning to minimize safety behaviors during exposure practice. Table 2 provides a
summary of some of these targets for addressing treatment resistance. Also, review
Table 2 Troubleshooting non-response to CBT for panic disorder
If you believe that treatment
resistance is related to:
Then address the issue by trying:
1. Comorbid Axis I disorder
2. Comorbid Axis II
disorder
3. Medical Factors
4. Life Stressors Example:
relationship conflict due
to decreased panic
symptoms
5. Patient believes the
treatment approach will
not work
6. Barriers to treatment
7. Targeting the wrong
disorder
8. Targeting the wrong core
fears
9. Proscribing exposure
exercises that are too
specific
1. Often the CBT strategies generalize to symptoms other than
panic, though specific interventions addressing anxiety may
increase the response to the panic treatment.
Example: for depression, assign behavioral activation
for GAD, assign scheduled “worry time”.
2. Since CBT treatment for panic disorder decreases personality
pathology, targeting panic disorder is a good initial strategy
unless the personality pathology is interfering with the treatment
goals. Strategies to address personality pathology include:
a. Discussing general tolerance to uncomfortable physiological
responses (related to panic) and intense emotions.
b. Incorporate DBT techniques in treatment approach.
c. Scheduling split or double sessions to address both the panic
symptoms and personality pathology separately.
3. Refer out for medical treatment to address underlining medical
conditions contributing to the panic symptoms.
4. Assess stressors and the impact the stressors have on attaining
the treatment goals. Incorporate strategies to reduce life
stressors.
Example: Conduct an informative couple’s session describing
the short- and long-term benefits of symptom reduction.
5. Review the rationale for the treatment approach, utilizing
metaphors and examples. Assess contributing factors to your
patient’s beliefs.
Example: your patient believes that he has already completed
the exposures on his own and they didn’t work and concludes
that the treatment won’t work either.
Strategies to try: elicit specifics about the attempted exposures,
identify safety behaviors, duration of experience, and measure of
success of experience. Provide psychoeducation including
principles of exposures.
6. Assess and address barriers to treatment compliance utilizing
problem solving and time management skills.
7. Complete thorough diagnostic assessment and adjust the
treatment plan accordingly.
8. Assess the patient’s core fears and adjust cognitive restructuring
and exposure strategies to target fears.
9. To increase generalization, assign homework exposures in
various contexts.
Avoiding Treatment Failures in Panic Disorder
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of exposure parameters as summarized by Powers, Smits, and Otto (this volume)
can help ensure that the right context is being addressed by exposures of sufficient
duration to optimize change.
Other Psychosocial Treatments
Relative to the wealth of evidence for CBT for PD (e.g., Gould et al., 1995),
there is little evidence to guide the application of alternative psychosocial treatments. A multicenter trial of emotion-focused psychotherapy emphasizing empathic
listening and supportive strategies for managing painful emotions and stressors did not support its efficacy for PD (Shear, Houck, Greeno, & Masters,
2001). In contrast, a recent trial of a manualized psychoanalytical psychotherapy showed significantly greater benefit than applied relaxation alone, showing
a 73% response rate relative to the 39% found for the relaxation condition.
This response rate is promising, but was achieved across 24 sessions of treatment – roughly double that offered for many CBT protocols. Also, it is unclear
what elements of treatment were of importance to the manualized psychodynamic
therapy. It shares a number of elements with emotion-focused approaches, including exploration of feelings surrounding panic onset and the meanings of panic
symptoms. Additional elements of treatment were focused on investigating transference and working through recurrent conflicts. In addition, response in this
trial appeared to be moderated by the presence of Cluster C personality symptoms according to an exploratory analysis (Milrod, Leon, Barber, Markowitz, &
Graf, 2007), raising questions whether an additional focus on recurrent conflicts
(e.g., with problem-solving focused treatment) may be of value with this subgroup
of patients. Additional research is needed to clarify the reliability and strength
of these effects and the elements of treatment most associated with differential
responding.
Medication Treatments
Issues of combined treatment are covered in detail in “Combined Cognitive
Behavioral and Pharmacologic Treatment Strategies: Current Status and Future
Directions” Smits et al. (this volume), but it is also important to note here that
any assessment of treatment resistance should consider the nature and timing of
medication use. Medications taken on an as needed (PRN) basis almost surely function as a safety cue and can lead patients to attribute gains to factors other than
their own efforts. Also, if patients fail to respond to CBT, even after adequate
troubleshooting of factors that may be interfering with therapeutic learning, medication treatment is the dominant empirically supported alternative to CBT, and
should be considered in collaboration with the patient, as an option for addressing treatment non-response should continued CBT no longer appear to offer clear
benefit.
120
H.W. Murray et al.
Conclusions
CBT for PD is a powerful intervention that offers some of the best outcomes in
the empirical treatment literature. Nonetheless, partial and non-response to these
interventions continues to be a problem. In this chapter we introduce a number
of strategies for honing exposure interventions toward the core fears underlying
the patient’s disorder. In many ways, the art of therapy for the cognitive-behavior
therapist is successfully getting patients to use these interventions, providing the
therapeutic experiences that can undo the self-perpetuating cycles underlying PD.
With careful problem solving, and close collaboration with the patient, therapists
have a wide range of options for altering the timing, targets, context, and difficulty of
exposure interventions to provide the patient with this needed therapeutic learning.
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Avoiding Treatment Failures in Obsessive
Compulsive Disorder
Luana Marques, Anne Chosak, Dieu-My Phan, Jeanne Fama,
Shana Franklin, and Sabine Wilhelm
The Case of Maria: “Only a Horrible Mother Would
Have These Thoughts”
Maria is a 29-year-old, married, Caucasian female who was prompted by her husband Bob to seek treatment for Obsessive-Compulsive Disorder (OCD) following
the birth of their first child. At intake, Maria noted that she had a nursing degree
but had decided to stay home after her child was born. During the initial therapy
sessions, Maria was upset and reluctant to disclose her obsessions. She stated that
she has had some obsessive thoughts and behaviors since she was about 13 years
old, but in the past she had been able to work around them. She checked the locks
of her house excessively, cleaned the bathroom daily because of fear of germs, and
was very perfectionistic in her work as a nurse. Maria noted that when she became
more depressed, her OCD symptoms increased, which in turn made it more difficult
for her to manage at home and at work. In addition to being diagnosed with OCD
at intake, Maria was also given comorbid diagnoses of Major Depressive Disorder,
Recurrent (MDD) and Generalized Anxiety Disorder (GAD). She did not meet criteria for any personality disorders. Despite this level of interference and distress,
Maria never sought psychotherapy for OCD until she gave birth to her daughter
Sophia. Maria had seen a psychiatrist once for her OCD and MDD symptoms, at
which time the doctor had recommended that Maria consider taking a selective
serotonin reuptake inhibitor (SSRI), but she had refused it due to her desire to get
pregnant.
Since the delivery, Maria experienced horrifying, vivid, intrusive thoughts about
harming her daughter. Maria felt so guilty and ashamed of these obsessions that she
was initially afraid to disclose them to the therapist. Maria feared that if the therapist
became aware of the thoughts, she would judge Maria as a bad person who deserved
to be in prison.
L. Marques (B)
Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston,
MA, USA
e-mail: lmarques@partners.org
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_8,
C Springer Science+Business Media, LLC 2010
125
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L. Marques et al.
After psychoeducation and some normalization, Maria was able to discuss her
current obsessions in detail. She reported thoughts about accidentally dropping
Sophia or putting her in the microwave, which she interpreted as evidence that she
wanted to harm her daughter. In addition, Maria reported intrusive sexual obsessions when changing her daughter’s diaper. Again, Maria interpreted these thoughts
as evidence that she might want to molest her daughter, and in consequence was
terrified. To avoid the associated anxiety, Maria stopped changing Sophia’s diapers,
which created a great deal of stress in her marriage. When Sophia cried because
she had not been changed in hours, Maria would call her husband Bob at work and
demand he come home to change the baby. At first, Bob was sympathetic to her
fears and tried to reason with her, explaining that these were merely thoughts and
that she did not have a history of hurting children. Bob even came home a few times
because he was concerned for Maria’s well-being, as she sounded very upset on the
phone. However, as time passed, Maria got progressively worse, which led Bob to
become less understanding and more upset. Finally, Bob demanded that Maria seek
treatment.
Maria’s case provides an example of OCD symptoms that were significantly
exacerbated by the birth of a child. In Maria’s case, she had a long-standing history of OCD and some depressive symptoms, which she had previously found ways
to manage. When Maria sought therapy, her OCD symptoms were in the severe
range and she was on the verge of divorce.
Overview of Obsessive-Compulsive Disorder
Obsessions are defined as intrusive, recurrent, distressing thoughts, images, or
impulses that the person attempts to suppress or ignore (APA, 2000). Compulsions
are repetitive behaviors or mental rituals that the individual performs in an attempt
to minimize the anxiety generated by the obsessions (APA). Although individuals
suffering from OCD might be able to postpone their compulsive rituals, they often
cannot stop them. Performing compulsions can, in turn, trigger further obsessions or
doubts about whether the compulsions were done correctly, which leads to the need
to perform even more compulsions. As a result, untreated OCD symptoms often
maintain themselves or worsen over time.
According to the Diagnostic and Statistical Manual of Mental Disorders (DSMIV TR; APA, 2000), to be diagnosed with OCD, the individual must at some point
have insight that the disorder is unreasonable or excessive; the symptoms must
be time consuming (i.e., more than an hour a day); and the symptoms must lead
to interference and/or distress (APA). Patients with OCD vary in their level of
insight with regard to the senselessness of their symptoms (Foa & Kozak, 1993).
Low insight often occurs as a consequence of heightened discomfort/anxiety generated by intrusive thoughts (Kozak & Foa, 1994). Some obsessions may border
on delusions when the patient believes that the intrusive thoughts accurately reflect
reality.
Avoiding Treatment Failures in Obsessive Compulsive Disorder
127
OCD tends to be a chronic disorder. Symptoms may wax and wane over time, but
often do not remit without treatment. Lifetime prevalence for OCD has been estimated at approximately 2% (Weissman et al., 1994). Most often OCD begins during
early adolescence, with fewer cases being diagnosed after the age of 15, although
some cases do onset in early childhood (Rachman & Hodgson, 1980; Rasmussen
& Tsuang, 1986). On average, boys tend to develop symptoms younger than girls,
but the prevalence tends to be slightly higher for women than for men (Bellodi,
Scuito, Diaferia, Ronchi, & Smeraldi, 1992; Rasmussen & Eisen, 1990). Although
onset of OCD symptoms has been associated with stressful life events (Kolada,
Bland, & Newman, 1994; Rachman, 1997) and traumatic experiences (de Silva,
Marks, de Silva, & Marks, 1999; Rheaume, Freeston, Leger, & Ladouceur, 1998),
at least 40% of patients with OCD cannot pinpoint stressors or traumas that preceded
onset. As described in our case vignette, pregnancy and childbirth are stressors that
have been linked to onset of OCD for new mothers and fathers who are plagued
by obsessions regarding the harm of their newborn (Wisner, Peindl, Gigliotti, &
Hanusa, 1999).
In contrast to other anxiety disorders in which there is a great deal of symptom homogeneity, OCD symptoms can vary greatly in clinical presentation. For
example, patients might engage in ordering and arranging rituals, excessive washing
rituals, reassurance seeking, counting, praying to neutralize religious obscenities,
etc. Many researchers have attempted to create classification systems reflecting
OCD symptom sub-types (Abramowitz, Franklin, Schwartz, & Furr, 2003; Baer,
1994; Calamari, Wiegartz, & Janeck, 1999; Leckman et al., 1997; Mataix-Cols,
Rauch, Manzo, Jenike, & Baer, 1999; Summerfeldt, Richter, Antony, & Swinson,
1999). Research suggests that OCD symptoms tend to cluster into the following subtypes: (1) Harming, religious, and/or sexual obsessions with mental or checking
rituals; (2) contamination obsessions with cleaning or washing rituals; (3) obsessions about certainty/symmetry and ordering/arranging rituals; and (4) hoarding.
However, in clinical practice a patient’s symptoms may not fit neatly into these
categories. Most patients with OCD report several types of obsessions and compulsions, some of which may not fall within the proposed OCD sub-types. In addition,
even though most patients report obsessive thoughts, images, and impulses, some
patients cannot identify a clear obsessive thought that triggers their repetitive rituals.
Often these individuals report a feeling that they must engage in their compulsive
behaviors until it feels “just right.”
Comorbidities
The majority of patients with OCD will report symptoms of additional psychiatric disorders, most commonly another anxiety and/or mood disorder (Lucey,
Butcher, Clare, & Dinan, 1994; Rasmussen & Eisen, 1990; Yaryura-Tobias et al.,
2000). Patients with OCD are at a high risk for developing another anxiety disorder. For example, research suggests that 25–50% of patients with OCD experience
social anxiety disorder, GAD, and panic disorder (Eisen et al., 1999). In addition,
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some patients will report a comorbid diagnosis of post-traumatic stress disorder
(PTSD; Helzer, Robins, & McEvoy, 1987), which might pose an additional challenge for treatment of OCD. If a patient meets criteria for PTSD, this might
warrant treatment prior to addressing the OCD as some of the treatments for OCD
(i.e., exposure exercises to feared stimuli) can trigger trauma symptoms (e.g., if
the person is obsessed with cleanliness due to a past history of rape). Thus, it
is crucial for clinicians to perform comprehensive diagnostic assessments or a
behavioral analysis to ascertain which condition would require immediate treatment
and if there would be any reasons for addressing the PTSD prior to the OCD or
vice-versa.
Mood disorders are highly comorbid with OCD. Indeed, some research suggests that up to 75% of individuals with OCD report depressed mood (Rasmussen
& Eisen, 1992). Approximately 25–30% of patients with OCD will meet criteria for MDD and approximately 10% will meet criteria for dysthymia (Steketee,
Henninger, & Pollard, 2000). Research suggests that mood disorders are often secondary to OCD (Yaryura-Tobias et al., 2000; Rasmussen & Eisen, 1992; Welner,
Reich, Robins, Fishman, & VanDoren, 1976) and may contribute to the poor
functioning that is frequently associated with OCD.
Another common diagnostic challenge is distinguishing between OCD and
Obsessive-Compulsive Personality Disorder (OCPD), a personality disorder characterized by perfectionism, rigidity, and conformity to rules. OCPD is often associated
with OCD, yet their clinical relationship is still unclear. The majority of individuals
with OCD (75%) do not have OCPD and the majority of patients with OCPD (80%)
do not have OCD (Mancebo, Eisen, Grant, & Rasmussen, 2005). OCD patients were
more likely to meet diagnostic criteria for OCPD than healthy controls, but OCPD
was not more prevalent in OCD patients than those with Panic Disorder (Albert,
Maina, Forner, & Bogetto, 2004). However, there may be a genetic link between
the two disorders: first-degree relatives of OCD probands were twice as likely to
have OCPD than relatives of healthy controls (Samuels et al., 2000). OCD patients
with comorbid OCPD had significantly earlier onset of obsessive-compulsive symptoms and were significantly more likely to have symmetry and hoarding obsessions
as well as cleaning, repeating, and ordering compulsions than OCD patients
without comorbid OCPD (Coles, Pinto, Mancebo, Rasmussen, & Eisen, 2006).
This suggests that OCPD may influence OCD symptom presentation, onset, and
severity.
Diagnostic Challenges
It can be challenging for clinicians to accurately diagnose OCD, given that some
OCD symptoms appear similar to symptoms of other anxiety disorders (e.g., recurrent worries in individuals with GAD) and OC-spectrum disorders (e.g., checking
mirrors in individuals with Body Dysmorphic Disorder). A comprehensive clinical
evaluation that relies on empirically supported screening instruments for OCD such
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as the Yale-Brown Obsessive Compulsive Scale (YBOCS; Goodman et al., 1989)
can aid clinicians in making the appropriate diagnosis.
Patients who report sexual and harming obsessions (e.g., a man who reports
obsessions about molesting his newborn baby and related avoidance of young children) may be a source of uneasiness for clinicians trying to differentiate among
diagnoses of paraphilias, sexual cravings, and OCD. In these cases, the clinician
should inquire whether the thoughts provoke fear/anxiety (consistent with OCD) or
generate pleasure (consistent with paraphilias). In addition, clinicians should obtain
the patients’ sexual history and inquire about past history of sexual abuse/assault.
Patients with OCD will often report tremendous shame, anxiety, and avoidance
behavior associated with these thoughts, which is not as typical of patients with
paraphilias. Furthermore, patients with postpartum psychotic symptoms might also
note intrusive thoughts that could mimic OCD symptoms (e.g., harm to others),
which are inherently different from intrusive obsessive thoughts. Clinicians are
also advised to consider Antisocial Personality Disorder as a differential diagnosis
(Wilhelm & Steketee, 2006).
Another commonly discussed diagnostic challenge is differentiating between the
worries characteristic of GAD and obsessions indicative of OCD. Like obsessions,
worries tend to be intrusive, repetitive, and often uncontrollable. In addition, GADrelated worries might be associated with repetitive checking rituals (Brown, Moras,
Zinbarg, & Barlow, 1993; Schut, Castonguay, & Borkovec, 2001) that are related to
safety concerns, but might be mistaken for compulsive checking that is characteristic
of OCD. Although worries and obsessions are similar in that they increase the individuals’ anxiety and tend to have a repetitive, intrusive nature, worries differ from
obsessions in that worries usually involve realistic life concerns like health, finances,
or work performance and their content is not usually considered unacceptable. This
is in contrast to obsessions, which are more likely to be considered senseless, unacceptable, and ego-dystonic (Turner, Beidel, & Stanley, 1992). In addition, worries
often present as linguistic representations whereas obsessions present as images,
thoughts, and impulses (Turner et al., 1992).
PTSD also shares symptoms with OCD. Some researchers have postulated that
the association between OCD and PTSD might be weaker than previously thought
due to the symptom overlap between these disorders and major depression, which
has several symptoms that overlap with PTSD and OCD (Huppert et al., 2005). To
tease apart these disorders clinically, it is helpful to inquire about the focus/nature of
the repetitive thought. For patients with PTSD, intrusive thoughts tend to be recollections of actual traumatic events, and the ensuing anxiety is not typically followed
by repetitive or ritualized behaviors common in OCD.
OCD is often comorbid with several disorders that collectively have been referred
to as OC- or OCD-spectrum disorders. These are disorders that share a similar clinical presentation or tend to co-occur frequently with OCD. For example, research
suggests a symptom overlap between OCD and tic disorders such as Tourette’s
disorder (Mansueto, Keuler, Mansueto, & Keuler, 2005). One way to differentiate
between tics and compulsions is to keep in mind that the former are involuntary movements, the performance of which is unrelated to anxious thoughts or
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feared consequences. This is in contrast to compulsions, which are often purposely
performed to decrease anxiety generated by the obsession. As mentioned above,
sometimes patients with OCD do not report a specific obsession that triggers a compulsion, but rather they feel compelled to perform a behavior until it feels “just
right.” In such instances, it becomes challenging to differentiate between OCD and
tic disorders. Researchers have labeled this phenomenon “Tourettic OCD,” suggesting that the association between these disorders might be better accounted for by a
diagnosis encompassing both disorders (Mansueto et al., 2005).
Impulse control disorders such as hair pulling (Trichotillomania), skin picking,
and nail biting are also frequently comorbid with OCD. Often behaviors characteristic of these conditions can also be differentiated from compulsions, as the former,
like tics, are not performed to prevent feared consequences. However, there are
instances in which behaviors that are often characteristic of impulse control disorders may be best conceptualized as symptoms of OCD or other OC spectrum
disorders. For example, a patient presenting with repetitive hair pulling may be best
diagnosed with trichotillomania. However, if this patient reports she engages in hair
pulling in an attempt to make things symmetrical, e.g., to make sure that that her
hairline is perfectly even, then the behavior is likely a manifestation of OCD. If
the behavior is done to improve one’s appearance, a diagnosis of Body Dysmorphic
Disorder (a preoccupation with an imagined or slight defect in appearance) should
be considered. Indeed, patients suffering from Body Dysmorphic Disorder often
perform compulsive behaviors; however, they are usually triggered by thoughts of
being ugly or deformed, and are done to hide, improve, or check on their appearance concerns, which is distinctively different from a symmetry obsession in OCD
(Wilhelm, 2006).
Treatment for OCD
Overview of CBT Strategies
Empirically supported treatment strategies for OCD include behavior and cognitivebehavioral therapies (CBTs), such as exposure and response prevention (ERP), and
pharmacological treatments. However, it is important to note that serotonergic reuptake inhibitions (SRIs) such as clomipramine and SSRIs such as fluoxetine have
also been demonstrated to decrease OCD symptoms (e.g., Kobak, Greist, Jefferson,
Katzelnick, & Henk, 1998; O′ Connor et al., 2006; O′ Connor, Todorov, Robillard,
Borgeat, & Brault, 1999; van Blakom et al., 1994). Although these drugs are helpful, data suggest that they do not perform better than ERP (Kozak, Liebowitz, &
Foa, 2000), and that the combination of drugs and CBT is not more effective than
either treatment (Cottraux et al., 1990; Kozak et al.; van Balkom et al., 1998).
Although early psychotherapy outcome literature focused primarily on behavioral
treatments (e.g., ERP), recent data suggest that cognitive therapy, which focuses
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on understanding and correcting OCD-related beliefs (e.g., inflated responsibility,
need for certainty, perfectionism), is also effective in treating OCD (Wilhelm et al.,
2005). For the purposes of this chapter, we will focus primarily on a combination of
cognitive and behavioral strategies for treating OCD.
Research suggests that intrusive thoughts are a common occurrence in the general population, with approximately 80% of the population reporting such thoughts
(Rachman & de Silva, 1978; Salkovskis & Harrison, 1984). Cognitive models of
OCD postulate that OCD results not from the presence of intrusive thoughts per se,
but rather from the patients’ interpretations of intrusive thoughts as either harmful or
significant (e.g., as evidence that they might be responsible for something going horribly wrong, such as accidentally dropping a child; Salkovskis, Shafran, Rachman,
& Freeston, 1999; Salkovskis, 1985, 1989; Salkovskis, Campbell, Salkovskis, &
Campbell, 1994; Salkovskis & Harrison, 1984). Such interpretations, in turn, lead
patients to compulsively try to neutralize thoughts or avoid stimuli that might trigger the thoughts (e.g., Maria not changing her daughter’s diapers). Unfortunately,
such compulsions and avoidance behaviors reinforce OCD symptoms in the
long run.
Behavior therapy (BT) for OCD is based on research showing that compulsions
decrease the anxiety generated by obsessions (Rachman & Hodgson, 1980). In
the short term, patients are relieved after a successful compulsion. However, the
negative reinforcement (elimination of anxiety) increases the chance that the next
obsession will be followed by a compulsion, so in the long term doing compulsions
worsens the OCD. BT focuses primarily on prolonged exposures to feared stimuli
and response prevention of mental or behavioral rituals. Patients learn that in the
absence of ritualizing, anxiety will eventually decrease on its own. Through successive, repeated prolonged exposures, patients’ emotional discomfort to feared stimuli
decreases as habituation occurs.
In contrast, cognitive therapy (CT) from a Beckian tradition (Beck, 1976) uses
Socratic questioning to identify and challenge beliefs that are hypothesized to support OCD behaviors (Wilhelm & Steketee, 2006). Obsessive anxiety experienced
by OCD patients is thought to originate from dysfunctional core beliefs described
by the Obsessive Compulsive Cognitions Working Group (1997; see Table 1). In
addition to the beliefs, a recently published cognitive manual for CT for OCD adds
two additional cognitive domains that might be important for clinicians to address:
(1) Consequences of Anxiety and (2) Fear of Positive Experiences (see Table 1;
Wilhelm & Steketee, 2006). The goal of cognitive therapy is to assist in improving patients’ insight into the irrationality of their beliefs about intrusions and help
patients to learn cognitive strategies to decrease their anxiety. For further description
of CT for OCD, see Wilhelm & Steketee, 2006.
In summary, CBT for OCD relies on cognitive and behavioral principles that
suggest the importance of breaking the association between obsessions and compulsions and modifying maladaptive core beliefs that contribute to obsessional
fears and behaviors. For a complete guide to treating OCD patients, please refer
to Steketee (1996) and Wilhelm & Steketee (2006).
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Table 1 OCD-related beliefs
Type of belief
Definition and clinical examples
Overimportance
of thoughts1
• Belief that thoughts are important and require attention, including the
belief that thoughts can generate actions (i.e., thought–action fusion;
Rachman, 1993)
“If I have a thought about molesting my daughter, it means that I must
want to molest her”3
Control of
• Belief and desire to control one’s own intrusive thoughts, which result in
thoughts1
rebound effects. Often accompanied by mental rituals
“Only child molesters have this type of images; I must be out of control if I
cannot control these thoughts”
Overestimation
• Belief that things are dangerous unless proven otherwise. Patients often
of danger1
overestimate the likelihood of danger based on faulty data
“I am much more likely to be punished than others.” “There was one crime
in my area last year, so I should watch out to make sure my doors are
locked because there is a high chance I will be robbed”
Desire for
• Based on the hypothesis that patient’s desire for certainty is associated with
certainty1
their inability to cope with ambiguity (Sookman, Pinard, & Beck, 2001).
Often, desire for certainty motivated reassurance seeking and re-doing
ritual (i.e., checking, re-reading, etc.)
“If I am not 100% sure of all possible options, I am bound to make a
mistake”
Responsibility1
• Belief that the person has the power to prevent or cause unwanted
outcomes, often related to moral concerns
“If I don’t pick up the nail in the road, there will be a car accident because
of me”
Perfectionism1
• Based upon the belief that it is possible and desirable to find an exact
solution for every problem. There is some evidence suggesting that early
experiences with rigid teachings can create a vulnerability to perfectionist
standards and fear of failure (Frost & Steketee, 1997; McFall &
Wollersheim, 1979)
“If I don’t do my work perfectly, people will not respect me”
Consequences of • Irrational belief about one’s ability to tolerate anxiety or a fear that one
anxiety2
might “go crazy” if the anxiety feels too intense, despite a lack of evidence
“If I get too anxious, I will fall apart”
Fear of positive
• As patients progress in therapy, they might express concerns about being
expectations2
able to maintain their gains or that they are not worthy of getting better.
Sometimes these doubts might have a superstitious flavor or have a moral
tone, where people believe they do not deserve to get better
“Good events will be inevitably followed by bad ones”
1 Core
belief domains proposed by the Obsessive Compulsive Cognitions Working Group (1997).
belief domains proposed by Wilhelm and Steketee (2006).
3 Examples were designed for this chapter, based on several OCD patients seen by the authors.
2 Core
Treatment Response
Over the past several decades, many studies have documented the treatment efficacy
of behavioral, cognitive behavioral, and, most recently, cognitive treatments for individuals with OCD (Cottraux et al., 2001; Emmelkamp & Beens, 1991; Emmelkamp,
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Visser, & Hoekstra, 1988; Van Oppen, de Haan, Van Balkom, & Spinhoven, 1995;
Whittal, Thordarson, & McLean, 2005; Wilhelm et al., 2005). Many of these studies
focused on individual therapy, but a few have examined group therapy (Anderson &
Rees, 2007; Cordioli et al., 2003, 2002; Krone, Himle, & Nesse, 1991) or comparing the efficacy of individual versus group therapy (Fals-Stewart, Marks, & Schafer,
1993). This section will review what type of responses clinicians might expect when
treating patients with OCD, followed by a discussion of factors that might predict
treatment non-response.
Research has shown that ERP is highly effective. Meta-analytic reviews have
demonstrated the superiority of ERP to placebo ERP (van Blakom et al., 1994).
Approximately 75% who enroll in BT and do not drop out are likely to benefit from
treatment (Steketee & Frost, 1998). On average, patients treated with ERP tend to
drop from a severe range (YBOCS>25) prior to treatment to a mild/moderate range
(YBOCS between 10 and 17) over a course of approximately 15–20 sessions of
ERP (Steketee & Frost, 1998). A meta-analysis by Abramowitz (1997) suggested
that more hours of therapist-guided exposure exercises predicted better outcome
(Abramowitz, 1997). Although impressive, these results suggest there still is room
for improvement in current treatments. Future research should include the addition of relapse prevention strategies as patients who learned relapse prevention were
more likely to remain improved at follow-up compared to those that did not (Hiss,
Foa, & Kozak, 1994).
Researchers have also examined the benefits of cognitive therapy for OCD
(Emmelkamp et al., 1988). Results suggested that cognitive therapy was as effective
as exposure-based treatment, although it is arguably difficult to distinguish among
these therapeutic interventions. In a subsequent study, these researchers demonstrated that cognitive therapy in conjunction with ERP was not more effective than
either treatment alone (Emmelkamp & Beens, 1991).
More recently, researchers began examining the efficacy of Beckian cognitive
therapy (Beck, 1976) for OCD, with the first study suggesting that Beckian cognitive therapy was as effective as self-controlled ERP (Van Oppen et al., 1995).
Other investigators also conducted similar studies and have reported similar findings (Cottraux et al., 1990; Freeston et al., 1997; Whittal et al., 2005; Wilhelm et al.,
2005). Thus, cognitive therapy seems as effective as ERP in reducing symptoms
of OCD.
Predictors of Treatment Non-response
Despite the effectiveness of BT and CT, they are not effective for all patients.
Researchers have begun to examine predictors of non-response (e.g., Abramowitz,
1997; Castle et al., 1994; De Araujo, Ito, & Marks, 1996; Kohls, Bents, &
Pietrowsky, 2002; Mataix-Cols, Marks, Greist, Kobak, & Baer, 2002; Steketee,
Chambless, & Tran, 2001). However, one of the challenges of integrating this literature is the absence of a standardized definition of treatment response across
clinical trials.
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Treatment outcome is typically quantified as decreases in YBOCS scores from
pre- to post-treatment. However, there is no consensus as to the magnitude of
YBOCS drop required before a patient can be labeled a “responder.” For example, some studies have classified a patient as being treatment respondent if his/her
YBOCS score dropped by 20% (Pigott et al., 1990) versus other trials where
patients’ YBOCS would need to decrease by 50% in order for patients to be
classified as responders (Kozak et al., 2000). To shed light on this dilemma,
Tolin, Abramowitz, and Diefenbach (2005) conducted signal detection analyses of
YBOCS in an attempt to identify a percentage drop in YBOCS consistent with adequate sensitivity and specificity. These researchers suggest that patients should be
labeled “treatment responders” if their YBOCS scores decrease by 30% or more
after treatment (Tolin et al.). As highlighted by these researchers, this drop in
YBOCS is not equivalent to symptom remission, as most patients who met this criterion still had a post-treatment YBOCS score above 16, which is the conventional
cut-off score to warrant a diagnosis of OCD. Thus, it is likely that these patients
whose OC symptoms have decreased by at least 30% have responded to treatment but their symptoms severity might still remain within the mild-to-moderate
severity range.
Notwithstanding these discrepancies, researchers have identified some variables
that seem to bode poorly for CBT. Despite early speculation that overvalued ideation
might be associated with poor treatment outcome (Foa, 1979), more recent research
suggested that although poor insight might be associated with more severe symptoms (Eisen, Rasmussen, Eisen, & Rasmussen, 1993; Minichiello, Baer, & Jenike,
1987), it has not always been a predictor of poor treatment outcome (Basoglu, Lax,
Kasvikis, & Marks, 1988; Foa, 1979; Kozak & Foa, 1994). Still some maintain that
patients who hold strong beliefs about feared consequences might be more difficult
to treat (Foa, Abramowitz, Franklin, & Kozak, 1999), and that research examining poor insight has been limited by the lack of empirically validated measures of
insight. However, new measures of insight such as the Brown Assessment of Beliefs
Scale (BABS; Eisen et al., 1998) appear promising and might aid researchers in clarifying the association between lack of insight and treatment outcome. In fact, recent
data suggest that patients in India with low insight had poor outcome to drug treatment for OCD (Kishore, Samar, Reddy, Chandrasekhar, & Thennarasu, 2004). This
is an area of research that warrants further investigation.
There are some data to suggest that comorbid anxiety and/or mood symptoms
might be associated with treatment non-response. Specifically, some studies have
suggested that severe depressive symptoms negatively impact treatment outcome
(Foa et al., 1983) and some researchers have hypothesized that OCD patients with
many depressive symptoms might have slower habituation curves (Foa et al.).
However, other treatment outcome studies have failed to reveal differences between
OCD patients who were high versus low in depressive symptoms (Foa, Kozak,
Steketee, & McCarthy, 1992; Steketee & Shapiro, 1995). Although the data on
depressive symptoms are mixed, there is strong evidence suggesting that a comorbid diagnosis of MDD has a deleterious impact on treatment outcome (Eisen
et al., 1999; Steketee et al., 2001). When working with depressed OCD patients,
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it is advisable for clinicians to design case formulations that address depressive
symptoms in addition to OCD symptoms.
PTSD may also be associated with treatment non-response for patients with
OCD. Results of small studies and case reports to date suggest that patients who
have comorbid OCD and PTSD may respond poorly to CBT (Gershuny, Baer,
Jenike, Minichiello, & Wilhelm, 2002; Gershuny, Baer, Radomsky, Wilson, &
Jenike, 2003; Sasson et al., 2005).
Data also suggest that some personality disorders might predict poorer treatment
outcome for patients with OCD. Some studies have documented a negative effect of
borderline personality disorder (Hermesh, Shahar, & Munitz, 1987) and schizotypal
personality disorder (Minichiello et al., 1987). However, attempts to replicate these
findings have not been successful (Steketee et al., 2001). Similarly, it is unclear
if comorbid OCPD has a negative treatment outcome, given that data have been
contradictory (Mancebo et al., 2005).
Although more research is needed before definitive conclusions can be drawn
about the predictive utility of specific comorbid disorders, it seems reasonable at the
present time to suggest that clinicians consider the potential influence of comorbid
conditions when designing treatment plans.
Challenges in Treatment Delivery for OCD
It is not uncommon for OCD patients to exhibit treatment-interfering behavior that
substantially hinders treatment progress. OCD patients are often ambivalent about
treatment. They may wish to decrease the distress and interference of the disorder, but they may be quite reluctant or fearful to challenge long-standing beliefs
and refrain from compulsions. For example, patients who report that they are motivated to seek treatment might still frequently cancel sessions. Therapists should
address cancellations immediately. Setting clear goals for treatment or creating a
treatment contract that includes length and frequency of sessions may help prevent
these problems (Wilhelm & Steketee 2006). However, if cancellations are frequent,
therapists should address non-compliance by explaining the relationship between
treatment compliance and improvement. Therapists should consider using cognitive
strategies to help patients to explore dysfunctional beliefs that might be associated
with treatment-interfering behaviors. Cognitive strategies such as downward arrows
(Greenberger & Padesky, 1995) can help the patient to explore these beliefs, which
might lead to better treatment compliance.
If treatment compliance becomes an issue later in therapy, then the patient might
have irrational beliefs about getting better. As illustrated in Table 1, some patients
have a fear of positive expectations or believe that they do not deserve to get better.
They might therefore begin avoiding sessions when they start to improve. A therapist might want to consider using the downward arrow and Socratic questioning
together to help the patient explore his/her thoughts about treatment non-compliance
(for a description of these techniques, see Beck, 1995). For example, in the
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aforementioned case, Maria initially suggested that she was afraid that she would
never get better, which in turn would mean that she was doomed to be a bad mother.
After several sessions marked by improvement, Maria still had a difficult time
acknowledging that she was getting better. In fact, Maria began to fear that, even
if she were to continue improving, she would inevitably relapse.
Cognitive restructuring was initially used to help Maria identify cognitive distortions related to her thought that improvement in treatment had a direct relationship
to her role as a mother (e.g., overgeneralization, fortune-telling) and to collect evidence for and against these distortions. As therapy progressed, the downward arrow
strategy was used to help Maria identify her core belief related to fear of failure in
her role as a mother. Below is an example of this interchange.
T: Maria, I have been so impressed by your progress. You were able to hold
your baby near the microwave several times in the past week. Yet, you
mentioned that you are afraid that you will relapse.
P: Yes, I have been thinking that the progress has been too good to be true. In
fact, I am sure I will relapse in the next few weeks.
T: Okay, I can see how that thought would make you anxious. How about we
spend a few minutes exploring the meaning of this thought for you? What
would that mean to you if you relapsed?
P: It would mean that I failed treatment.
T: And if you have a thought such as “I failed treatment,” what would that
mean?
P: That I might never be able to get better.
T: And what would that mean for you if you would never get better?
P: It would mean that I will continue to be sick and not be able to take care of
the baby.
T: What would it mean for you if were not able to take care of your baby?
P: It would mean that I am a horrible mother that cannot even take care of her
baby.
T: What would it mean about you, if you were a bad mother?
P: It would mean that I am a failure.
T: Okay, Maria this is an important point. It looks like you are afraid to improve
in treatment because you are afraid that if you were to relapse, it would mean
that you failed, which in turn would mean that you are a bad mother. Is that
right?
P: Yes!
T: I can understand why this thought makes you so anxious. Why don’t we
spend a few minutes examining how this core belief of being a failure is
getting in the way of our work together?
The therapist continued this dialogue by using Socratic questioning to help
Maria examine the evidence for and against her core belief and to find alternative
ways to think about her progress in therapy. Furthermore, Maria and the therapist
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collaboratively designed a behavioral experiment that challenged Maria’s core belief
by helping her collect actual evidence against this belief.
Another treatment-interfering behavior is session tardiness. Patients often get
stuck ritualizing at home or in the bathroom at the therapist’s office and thus are
late for session. Patients might also cancel at the last minute because they feel
overwhelmed about coming to session or are stuck in a ritual. Therapists should
address this behavior right away. For example, therapists might discuss alternative
hypotheses for reasons why they are not coming to session on time. If the patient
suggests that they have a difficult time managing their time, then time management skills (such as breaking down the steps needed prior to coming to session) can
help the patient improve attendance. Alternatively, if the patient is stuck ritualizing before session, then the therapist might want to create contingencies that might
help the patient come in on time such as telling patients that the appointment is
scheduled for an hour earlier to increase the likelihood that they will be on time for
session.
Homework compliance is a key predictor of treatment outcome for patients with
OCD. However, given that exposure-based homework can be unpleasant, it is not
uncommon for patients to avoid it. One way to address homework non-compliance
is to engage the patient in problem solving by conducting a pros–cons analysis of
completing homework. It is also helpful to engage patients in a discussion about
their short-term versus long-term goals. If the patient has set specific goals for treatment, the therapist can also use these goals to encourage the patient to complete
homework. Metaphors can also be helpful. For example, the therapist could suggest to the patient that completing homework is like riding a bike, or learning to
swim or drive. At first, such new activities can be somewhat anxiety-provoking.
However, with practice, it is likely that they will become “second nature” and less
anxiety-provoking. Regardless of the approach, it is very important that therapists
validate patients’ attempts to complete any homework. It is fine to be empathetic
about the challenges involved with homework, but it is essential for homework
non-compliance to be addressed before moving on. Below is an example of ways a
therapist might address homework non-compliance with OCD patients
T: Maria, what do you think got in the way of you doing the homework this
week?
P: I had a hectic week, so I just didn’t have any time.
T: Do you think that this will happen regularly, that your life is so busy that it
will be difficult to fit in the homework necessary for this therapy?
P: It is difficult for me to find extra time. I am always tied up either at work
or with the kids, who always need my attention. By the evening, I just feel
exhausted.
T: I can understand how difficult it can be to find time. But I think it is important
for us to figure this out before moving on. Perhaps, Maria, this is not the time
for you to be working on the OCD problems.
P: Oh no, I have to work on the OCD! I am concerned about the time I spend
on my rituals and that my kids will learn some of them from me. It broke my
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T:
P:
T:
P:
T:
P:
T:
heart when my daughter told me that she didn’t want to play with her toys
because it took me so long to put them away “the right way.”
Okay, so it sounds important to you and your family as well. So, let’s try
to brainstorm ways that you might find some time. If you think back to this
past week, can you think of any way you might have found time to do this
assignment?
I guess I could have asked my husband to watch the kids for a while in the
evening.
Do you think he would be willing to do that?
Well, I guess he might not like it but he also hates the OCD. So, I think if
I tell him I need time to complete my assignment to get better, he might be
willing to help me out.
Great idea, Maria. How confident are you that you will be able to complete
the assignment for the next week?
90%.
Okay. I think these are great odds. I am also very confident that you will
be able to complete the assignment. Let’s write that down as the first item
in your homework this week: discuss child care with husband tonight, and
identify when he would be willing to watch the children so you can do your
OCD homework.
This kind of dialogue conveys several messages to patients. It teaches them that
homework is important and that it is their responsibility to complete it. In addition,
it suggests to patients that you understand their difficulties, while at the same time
conveying the notion that you take homework seriously. Finally, it models problemsolving skills.
At times, patients will change the topic to less anxiety-provoking subjects as a
way to avoid discussing the OCD. One way to make sure to stay on topic is to set a
collaborative agenda in the beginning of the session. The therapist can also ask the
patient for permission to interrupt and redirect to the agenda, especially for patients
who get distracted easily. If despite these efforts patients continue to derail, then the
therapist and patient must assess if the OCD is the primary concern for the patient.
If not, the patient might need other treatments prior to addressing the OCD.
A very common challenge in working with patients with OCD is perfectionistic standards held by the patient, which can interfere with their interpretations of
progress in treatment. Patients might say or believe, “I still have a long way to go;
a little progress means nothing; I will never be able to get better.” Such statements
might be representative of core beliefs about being a failure, or reflect past unsuccessful therapy experiences. One way to address such concerns in the beginning of
therapy is to demystify progress in treatment by directly discussing patients’ expectations for progress versus what progress might realistically be like. It is important
to highlight to patients that there will be ups and downs in treatment but that they
would end up overall doing much better than if they were not in treatment. The
therapist can suggest that a monitoring form will be used weekly to monitor change
over time. This can be very important for perfectionistic patients, as data might help
Avoiding Treatment Failures in Obsessive Compulsive Disorder
139
them acknowledge progress. In addition, the therapist should include a discussion
of lapses in treatment as normal and expected, and perhaps suggest that these are
times in therapy when fine-tuning can be productive. If the therapist believes that
the patient’s core belief of being a failure is getting in the way of treatment, then
cognitive strategies such as downward arrow or behavioral experiments might help
the patient identify dysfunctional thoughts and challenge the core beliefs.
T: Last session we discussed your difficulties at work. You mentioned that you
are getting behind at work because you keep checking and rechecking your
memos, letters, and e-mails because you want to make sure that they are
perfect. During our session, you came to the conclusion that this behavior
was excessive and that the consequences of keeping this up was worse than
perhaps making the mistake. So, I was thinking it might be helpful for you
to conduct an experiment to test this belief. Are you willing to try this?
P: Does that mean I will have to do something different? I am always so scared
to do something different.
T: It makes sense that you would fear doing something different. So, perhaps
we should start small and see what happens. For example, how would it feel
to send a memo to your close co-workers where you purposefully misspell
something?
P: I guess I could do that. I am always fixing prepositions, and making sure I
get them correct. I guess I could use an ‘in’ when I know I should use ‘on’.
T: Great idea! Let’s begin there. This would mean that you write the e-mail and
leave a wrong preposition. I want to remind you that this also means that you
would not reread it more than once, and you would leave the mistake there,
right?
P: That will be hard to do, but I am willing to try it.
In summary, regardless of patient’s initial motivation for treatment, CBT for
OCD will challenge the patient’s dysfunctional beliefs and ask him/her to behaviorally confront anxiety-provoking situations. Thus, treatment itself is likely to be
difficult for patients, which might generate several of the therapy-interfering behaviors described above. It is important for clinicians to be mindful of what they are
asking patients to do and to find ways to collaboratively engage OCD patients in the
challenge of designing and implementing the strategies that can help them improve,
at a level that is appropriate to the patients’ abilities at the time.
Future Developments
OCD is a chronic disabling psychiatric disorder that has received increased research
attention in the past few decades. Despite the plethora of data, there is still more
research that needs to be done. An active area of research is treatment response
as described above. There is still no widely accepted definition in the literature of
140
L. Marques et al.
what constitutes treatment non-response or partial response. As discussed by Tolin
et al. (2005), there is little consistency in the way different researchers categorize
treatment response, with some studies using stringent YBOCS cut-off scores and
others using looser values. This makes it difficult to compare findings across different research studies. Similarly, leading OCD experts have begun to investigate
how to best define treatment-resistant OCD (Sookman et al., 2005; Wilhelm et al.,
2006). When several experts were asked about this, there was a wide variability in
responses. Thus, the Obsessive Compulsive Cognitions Working Group is in the process of trying to create a uniform definition of treatment-resistant OCD to explore it
more consistently across sites
Finally, although the treatment efficacy for OCD has come a long way, there are
still many patients who do not benefit sufficiently from treatment. In an attempt
to improve treatment efficacy, researchers have begun to explore the role of Dcycloserine (DCS) in augmenting behavioral treatments (Hoffman et al., 2006;
Ressler et al., 2004). DSC is an antibiotic that has shown to be effective in enhancing learning in animal trials. Researchers have hypothesized that it might aid in
exposure-based treatment for OCD (Wilhelm et al., work in progress). Although
results are still preliminary, DCS augmentation of BT appears to be a promising
avenue for improving treatment outcome (Wilhelm et al., work in progress)
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Wilhelm, S., Steketee, G., Reilly-Harrington, N. A., Deckersbach, T., Buhlmann, U., & Baer, L.
(2005). Effectiveness of cognitive therapy for obsessive-compulsive disorder: An open trial.
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disorder. Journal of Anxiety Disorders, 14(1), 19–30.
Avoiding Treatment Failures in PTSD
Claudia Zayfert and Jason C. DeViva
Tom is a 27-year-old married but separated Caucasian male U.S. Army veteran who
presented for treatment because he is tired all the time and wants help with his sleep.
He feels sleepy during the day, often nodding during breaks at work, though it often
takes him several hours to fall asleep at night. He stated that when he does sleep he
has nightmares about his service in Iraq. He went overseas with the initial invasion
force and participated in combat and house-to-house raids. He also provided aid
to injured civilians on several occasions. He keeps to himself at work and in his
daily life and as a result has minimal social support. He thinks others will judge him
negatively because of his war experiences, and he also gets irritated by the questions
civilians tend to ask (e.g., “Did you kill anyone?”). He stated that he would never
use “drugs” but disclosed drinking heavily two or three nights per week in order to
get thoughts about Iraq out of his head. He smokes marijuana occasionally, usually
to stop unwanted thoughts or to calm himself when he is in social situations.
His wife separated from him 2 years after he returned from Iraq because “she
didn’t know who I was anymore.” Their 4-year-old son lives with her, and Tom is
sometimes glad for that because he is scared of the possibility that he might physically abuse his son the way he was abused as a child. However, Tom does think
the abuse was good for him in at least one way – it taught him to “be strong”
and not give in to his feelings. Most days he wakes up feeling exhausted and
would like to stay in bed, but he manages to summon energy to face the day. He
often has trouble focusing at work and has to put a lot of effort into suppressing
thoughts of his experiences in Iraq. On a few occasions this month, he left work
early because he was suddenly reminded of his best buddy from the army who died
during the first month of their deployment when his vehicle hit an improvised explosive device alongside a road. Tom still feels responsible because he believes he
should have known there would be a danger on that road. His early departures
from work lead to conflicts with his supervisor and he has been put on probation at
his job as a manager in an office-supply company because he has not accomplished
his duties.
C. Zayfert (B)
Department of Psychiatry, Dartmouth Medical School, Lebanon, NH, USA
e-mail: claudia.zayfert@dartmouth.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_9,
C Springer Science+Business Media, LLC 2010
147
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Tom presents as a well-dressed, athletically built male appearing about his stated
age. He is physically healthy except for minor lower back pain from a fall he sustained in Iraq where he landed awkwardly on the pack he wore on his back. He
feels guilty about feeling this pain because so many others were injured while fighting, and because his pain comes from a fall, he doesn’t “deserve” to feel it. He is
leery about any treatments more intensive than sleep medication because he’s not
“crazy” or “weak” and doesn’t need “any of that other stuff.”
Introduction
Posttraumatic stress disorder (PTSD) is a highly prevalent anxiety disorder
that often follows exposure to traumatic events. There is a pressing need to
make effective treatments available to individuals suffering from this disabling
condition and the various problems that frequently accompany it. Cognitivebehavioral therapy (CBT) is currently the treatment of choice for PTSD. Several
meta-analyses (Bisson et al., 2007; Bradley, Greene, Russ, Dutra, & Westen,
2005) have concluded that there is a solid empirical basis for the use of CBT
to treat PTSD, and clinical practice guidelines recommend use of cognitivebehavioral strategies such as prolonged exposure therapy or cognitive therapy (Foa,
Keane, Friedman, & Cohen, 2008; Management of post-traumatic stress working
group, 2004).
Despite the accumulating evidence of its efficacy, much work remains to achieve
the goal of widespread clinical use of CBT for PTSD. For example, Rosen et al.
(2004) surveyed VA health care providers and found that few PTSD specialists routinely provided exposure therapy or cognitive therapy, and the rates of
PTSD specialists providing these treatments actually declined after the publication of clinical practice guidelines advocating their use. Similarly, a survey of
practicing psychologists in the United States found that only a small proportion
of providers use exposure therapy in the treatment of PTSD, and this was true
even among providers with a cognitive-behavioral orientation (Becker, Zayfert, &
Anderson, 2004).
The various challenges that clinicians face when implementing CBT for PTSD
may contribute to reluctance to use CBT, particularly with complicated cases, which
may be more prone to treatment failure. Our aim in this chapter is to provide guidance to clinicians who wish to implement CBT with the range of PTSD patients they
encounter in clinical practice. Successful treatment often depends on the clinician’s
ability to integrate knowledge of empirical findings with analysis of the individual case to meet the unique challenges that patients present. We will (1) review the
core components of CBT, (2) consider challenges clinicians may face when implementing CBT, including available data on risk factors for poor outcome, (3) explain
how to use a case formulation approach to guide treatment with complicated cases
to optimize treatment results, and (4) discuss several key strategies and tools for
troubleshooting when treatment derails from the intended plan.
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Core Components of PTSD Treatment
Understanding of the cognitive-behavioral models that support CBT is essential for
the clinician to determine whether treatment is proceeding in a manner consistent
with a successful outcome and, if necessary, to make adjustments to avert dropout or
failure. We will focus on prolonged exposure and cognitive restructuring as first-line
treatments because these are the most widely studied elements of CBT for PTSD.
Some CBT treatment programs also include relaxation and/or stress management
components (Blanchard et al., 2003; Foa, Rothbaum, Riggs, & Murdock, 1991),
but research has not shown that adding these components enhances efficacy (Foa
et al., 1999).
Exposure therapy is based on cognitive-behavioral models of PTSD (Foa &
Hearst-Ikeda, 1996), which hypothesize that cognitive fear networks (programs for
escaping danger) develop following exposure to life-threatening events. These theories propose that PTSD develops due to inaccurate fear networks, whereby the
individual erroneously associates benign stimuli with danger. Maladaptive interpretations result when trauma survivors interrupt processing of trauma-related stimuli
before they are able to incorporate corrective information that would lead to more
accurate conclusions. Thus, the goal of exposure therapy is to activate the fear
network (i.e., experience fear elicited by trauma cues) and integrate corrective
information about safety to promote new learning.
Exposure therapy for PTSD typically includes both imaginal and in vivo components. Imaginal exposure entails recalling a memory of a traumatic event and
evoking the associated emotions for a sustained period of time. Typically, this is
accomplished by having the individual relate the memory (usually verbally, though
sometimes in writing) in as much detail as possible. The memory is repeated in
session for a sustained period, typically 30–60 min, and audio recordings or written accounts are used to guide repeated exposure practice between sessions. In vivo
exposure involves exposing individuals to external stimuli that trigger excessive or
inappropriate anxiety as a result of their association with the traumatic event. For
example, Tom avoids public places with crowds of people, because he associated
those places with danger while in Iraq. At first, he might enter grocery stores on
weeknights with a friend who he thinks is a safe person. Then he might enter the
store on weeknights on his own, then during crowded weekend hours with his friend,
and finally on the weekends on his own, until he is able to remain in the store without significant discomfort. Each time Tom practices in vivo exposure, he records
his initial, maximum, and ending anxiety levels. This information is used to guide
further steps in treatment.
Research has demonstrated the prominent role of maladaptive cognitions in the
development and maintenance of PTSD, and these cognitions are featured in most
cognitive-behavioral models of PTSD (Ehlers & Clark, 2000). An important goal
of CBT is to correct misinterpretations that are learned as a result of the traumatic event. Cognitive restructuring (Beck, Emery, & Greenberg, 1985; Resick
& Schnicke, 1993) is a method of learning to identify and modify misinterpretations about the meaning of traumatic events with regard to oneself and the world.
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This entails teaching the patient to identify habitual patterns of thinking related to
the traumatic experiences and to examine these thoughts to determine the extent
to which they are realistic and helpful. Patients are further taught to respond to
unhelpful thoughts with more accurate or adaptive self-talk. Some PTSD protocols
focus patients’ efforts on specific content areas, such as safety, trust, esteem, power,
control, and intimacy (Resick & Schnicke, 1993a).
Numerous studies have provided support for the use of prolonged imaginal and
in vivo exposure and cognitive therapy for treatment of PTSD (Bryant, Moulds,
Guthrie, Dang, & Nixon, 2003; Foa et al., 2005; Marks, Lovell, Noshirvani,
Livanou, & Thrasher, 1998; Resick, Nishith, Weaver, Astin, & Feuer, 2002; Schnurr
et al., 2007; Tarrier et al., 1999). Research has been less clear, however, regarding
the benefits of combining exposure and cognitive interventions. Several studies have
found that a combination of exposure with cognitive therapy produced comparable
outcomes to either treatment alone (Foa et al.; Marks et al., 1998; Paunovic & Ost,
2001). In contrast, however, Bryant et al. found that a combination of imaginal exposure and cognitive restructuring was more effective than imaginal exposure alone.
Subsequently, Bryant et al. (2008) compared a combination of imaginal and in vivo
exposure plus cognitive restructuring to imaginal and in vivo exposure combined
and to each delivered alone. They found that the combined treatment produced the
best outcome.
Exposure therapy and cognitive therapy for PTSD share common elements and
differ primarily in the degree of emphasis placed on exposure to trauma memories
versus directly challenging erroneous cognitions related to the trauma. Most forms
of trauma-focused CBT involve some element of cognitive restructuring, although
various approaches differ in the degree of emphasis given to systematic restructuring of thoughts. For example, protocols for imaginal exposure typically include
instructions for the therapist to follow the exposure exercise with discussion aimed
at processing thoughts and reactions to the trauma memory (Riggs, Cahill, & Foa,
2006). Likewise, cognitive therapy is rarely devoid of exposure; cognitive processing therapy (Resick & Schnicke, 1993) includes writing about the trauma memory
primarily to facilitate formal cognitive restructuring, deemphasizing extinction via
repeated and prolonged exposure to the trauma memory. There is some evidence that
an approach that favors cognitive restructuring may be more effective in ameliorating symptoms of guilt and depression (Bryant et al., 2008). Due to the simplicity
of the underlying model, exposure-based treatment may be the most easily disseminated treatment. For the individual therapist, however, there is reason to consider
implementing cognitive restructuring along with exposure therapy (Riggs et al.) for
many cases of PTSD, particularly when guilt, shame, and depression are prominent.
Challenges Clinicians May Encounter when Implementing
CBT for PTSD
CBT for PTSD, particularly exposure, is unusual in that clinicians tend to have
concerns about implementing it. Respondents to the Becker et al. (2004) survey endorsed multiple contraindications for the use of exposure therapy, such as
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comorbid psychotic or dissociative identity disorder, severe suicidality, dissociation,
current victimization or perpetration of violence, homicidality, low social support,
severe numbing, and history of treatment adherence problems or non-response.
Respondents perceived various complications as likely to occur with exposure,
including increased symptom severity, dissociation, substance abuse/dependence,
overwhelming anxiety, numbing, self-harm or suicidality, homicidality, increased
desire to drop out of treatment, relationship problems, aggression, and damage to
the therapeutic alliance. Cook, Schnurr, and Foa (2004) listed patient barriers and
clinician “concerns and misconceptions” (p. 381) that may interfere with the use of
exposure therapy specifically and research-based treatments more generally. Cook
et al. cited additional patient barriers discussed in the literature, including reluctance
to engage with trauma memories, poor ability to image, ongoing crises, excessive shame or guilt, belief that treatment will increase symptoms, extreme anger,
emotional numbing, over-engagement with trauma memories, and history of perpetration. They also cited additional clinician barriers, such as low affect tolerance,
past failure experiences with exposure, and beliefs that treatment will re-victimize,
lead to decompensation, not be effective with patients with multiple traumas, take
too long, move patients too quickly, or damage the therapeutic relationship.
Some concerns expressed by clinicians are not supported by research. For
example, 83% of the clinicians surveyed by Becker et al. (2004) believed that
participation in exposure therapy was “somewhat” or “very” likely to result in worsening of re-experiencing symptoms, 87% believed hyperarousal would worsen, and
nearly 60% believed it would increase the likelihood of dropping out of therapy.
The actual rates of worsening of PTSD symptoms and dropout observed among
participants in randomized trials are substantially lower than clinicians expect, and
worsening of PTSD symptoms during therapy has not been associated with dropout
(Foa, Zoellner, Feeny, Hembree, & Alvarez-Conrad, 2002; Hembree et al., 2003). In
contrast to clinician concerns, research has not identified clear contraindications of
CBT for PTSD. Among many variables studied, only higher level of PTSD symptoms (particularly avoidance) (Bryant et al., 2003; Marks et al., 1998), depression
(Bryant et al.; McDonagh et al., 2005), anxiety (McDonagh et al.; van Minnen,
Arntz, & Keijsers, 2002), male gender, and alcohol use (van Minnen et al.) have
predicted dropout. Likewise, only a few variables have been linked to poor treatment outcome: trauma in childhood or multiple previous traumas (Hembree, Street,
Riggs, & Foa, 2004), prescription sedative use (van Minnen et al.), male gender,
high suicidality, living alone, inconsistent therapy attendance, generalized anxiety
disorder, higher levels of PTSD symptoms (van Minnen et al.), greater anger (Foa,
Riggs, Massie, & Yarczower, 1995), and greater physical pain (Koch & Haring,
2008). Though some predictors of dropout or poor outcome, such as trauma history,
cannot be changed, many can be modified by treatment. Also, there are efficacious
therapies for major depressive disorder, generalized anxiety disorder, alcohol use,
and chronic pain that may enhance outcomes if delivered prior to or simultaneously
with CBT for PTSD.
Despite the demonstrated efficacy of CBT for PTSD, not all patients have a positive outcome, whether treatment is delivered as part of a randomized trial or in a
clinic. Dropout rates from cognitive restructuring and exposure therapies for PTSD
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tend to be comparable, but usually are significantly higher than for non-traumafocused, supportive therapies (Hembree et al., 2003). In addition, there is some
evidence that dropout rates reported in randomized controlled trials are lower than
dropout rates in real-world clinical settings (Zayfert et al., 2005). Even strong advocates of CBT for PTSD note that some patient variables may make either exposure
or cognitive restructuring less appropriate for the treatment of PTSD (Cook et al.,
2004) (Moore, Zoellner, & Bittinger, 2004). Clinicians who are well-trained and prepared to implement CBT will nonetheless face a variety of obstacles that can hinder
treatment success. The problem list may include factors that impede the initiation
of CBT, such as co-occurring life problems (work stressors, relationship discord,
illness of self or family members) or shame-related beliefs about having symptoms
or seeking treatment. Other obstacles may interfere with implementation of CBT or
with maintaining the treatment focus on PTSD. Individuals with PTSD may have
difficulty trusting their therapists, be reluctant to engage in trauma-focused treatment, or present with comorbid anxiety, mood, substance abuse, and eating disorders
that can contribute significantly to impairment in daily functioning and interact
with PTSD. Behavioral obstacles, such as urges for self-harm or binge-eating,
can emerge during treatment and distract the focus from trauma-focused interventions. In addition, some individuals engaged in trauma-focused interventions may
show over-engagement with traumatic emotions (as evidenced by “flashing back”
or exceedingly slow rates of extinction), activation of intense anger or shame during treatment, or, conversely, difficulty engaging with the emotions associated with
the events. Indeed, the patient may not identify PTSD symptoms as the main treatment priority, or even as needing treatment at all. Trauma survivors may perceive
greater interference in daily functioning due to problems with sleep, relationship
dysfunction, chronic pain, or panic attacks, whereas avoidance of trauma reminders
is viewed as helpful. Many trauma survivors view their ability to contain or compartmentalize trauma memories and suppress or “bottle up” emotions as signs that they
are coping well with the events in their lives. In short, therapists treating individuals
with PTSD will benefit by preparing to manage a wide variety of challenges.
Using the Case Formulation Approach to Guide Treatment
Quite often patients bring many problems to the table and the task of organizing and prioritizing them to formulate a plan of treatment can be daunting. The
case formulation approach (Persons & Tompkins, 2007) (Zayfert & Becker, 2007)
is a fundamental tool for managing complex clinical presentations by organizing
evidence-based formulations of specific client problems to guide treatment according to an overarching individual case formulation. Using this approach the clinician
considers both the relevant evidence-based problem formulations and the unique
needs of the individual seeking treatment. The therapist develops a road map for
treatment that incorporates hypotheses about the interactions among multiple presenting problems and relies on the evidence-based formulations available for the
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various problems. This approach produces a treatment plan that maximizes clinical
utility because it enables the therapist to respond flexibly through a systematic
hypothesis-testing approach. We can apply it to Tom, whose case we described at
the beginning of this chapter.
Case Formulation
The first step in developing Tom’s case formulation is to assemble his problem list.
Tom’s problems include poor sleep, nightmares, and daytime intrusions relating to
events from Iraq and childhood physical abuse, social anxiety and isolation, alcohol and marijuana abuse, depressed mood, daytime fatigue, guilt, panic attacks cued
by trauma reminders and social encounters, negative self-judgment because of pain
and treatment needs, and back pain and associated guilt. Tom’s diagnoses are PTSD,
major depressive disorder, social phobia, and alcohol abuse, with further information needed to rule out marijuana abuse and an Axis II diagnosis. Treatment planning
begins with the hypothesis that PTSD is the principal, or anchoring, diagnosis.
The next step in case formulation is to examine relevant evidence-based formulations of the presenting issues. In Tom’s case these include cognitive-behavioral
models of PTSD (Clark & Ehlers, 2004), depression (Beck, Rush, Shaw, &
Emery, 1979), social phobia (Hofmann, 2007)comorbid PTSD and substance abuse
(Najavits, 2002), and comorbid PTSD and pain (Sharp & Harvey, 2001). The template is individualized by including Tom’s specific biological and somatic factors
(pain from back injury), behavioral factors (avoiding social situations in order to
avoid social anxiety or triggering questions, avoiding internal experiences by using
substances), and cognitive factors (“It’s my fault my friend died”; “I don’t deserve
to complain about this pain”; “No one will understand me”; “People can look at me
and see I’ve done wrong”; “People are generally dangerous and not to be trusted”;
“I am weak for coming in for help”).
Lastly, Tom’s therapist generated specific hypotheses about the relationships
among the presenting problems in order to guide treatment planning. Given the
absence of reported psychiatric history prior to deployment, Tom’s therapist hypothesized that his traumatic experiences in Iraq interacted with existing avoidance
behaviors and beliefs about the world derived from his childhood physical abuse
and his social anxiety to produce his current set of symptoms. Beliefs first generated by the earlier abuse, such as “I have to be on guard all the time” and “People
want to hurt me,” were further confirmed by his experiences in Iraq. Tom’s social
anxiety was exacerbated by the perception that others could see that he had let
a friend die and the expectation that others would ask uncomfortable questions
about the war and would not understand his responses. Dealing with the abuse by
pushing his feelings aside and being “strong” as a child predisposed him to avoid
the emotions associated with his Iraq experiences, which served to maintain and
increase through negative reinforcement the anxiety, guilt, and shame related to
those experiences. Beliefs about his inability to cope with his own emotions, as
well as negative thoughts about people and the world, led to a general hopelessness.
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Hopelessness, grief over the loss of his buddy in Iraq, and withdrawal from positive
social connections and leisure activities also contributed to depression. The therapist
further hypothesized that the strong emotions associated with the trauma memories,
as well as the efforts to “not think about them,” kept their associated memory networks highly potentiated and made them salient in Tom’s mind. Tom used alcohol
and marijuana to achieve a sense of control over the memories and emotions and to
avoid thinking about them.
Tom’s therapist planned to begin with several sessions of psychoeducation with
the goals of normalizing Tom’s reactions to the war as an early way to decrease
shame, providing a conceptual framework that would allow him to see the connections among his symptoms, and maximizing the likelihood he would see treatment
as necessary and acceptable. The treatment would then shift to a brief course of
emotion-regulation skills based on dialectical behavior therapy (Linehan, 1993a).
Given the presence of shame and guilt about treatment as well as about the trauma,
Tom’s therapist planned to implement cognitive restructuring with the aim of attenuating distress related to shame and guilt and preparing Tom to focus on fear during
subsequent exposure. Treatment would then shift to prolonged exposure therapy,
which would begin with environmental cues Tom avoided, such as hot places,
bearded men, and sand. Next, exposure would target memories of war experiences
and nightmare content related to the war and childhood trauma. Finally, exposure
would focus on social situations that Tom avoids. Because substance abuse was
hypothesized to function as a means of managing PTSD, the therapist decided not
to target it directly but rather to have Tom keep a diary of his use throughout treatment, so that adjustments could be made if it increased. Similarly, depression was
hypothesized to be secondary to issues that would be targeted in the initial plan, and
therefore might be expected to improve in response to these interventions. Thus, the
therapist opted to monitor depression levels and suicidality weekly, and consider
additional interventions focused on mood if depression persisted beyond resolution
of PTSD. Self-reported PTSD symptom levels, nightmare frequency, sleep impairment (including daytime fatigue), alcohol use, and daily activity would be used to
assess outcome and, if necessary, inform adjustments to the initial plan.
Strategies and Tools for Troubleshooting
As indicated above, an array of challenges face clinicians in implementing CBT
for PTSD. We will discuss some of the common issues that emerge and strategies
for handling them and refer the reader elsewhere for further guidance (Zayfert &
Becker, 2007).
Handling Multiple Trauma Memories
Like Tom, the majority of trauma survivors report multiple traumatic events and/or
events that were prolonged or repeated over time. Such patients often experience
symptoms relating to more than one memory. For example, Tom reported weekly
Avoiding Treatment Failures in PTSD
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nightmares about his time in Iraq as well as distress triggered by seeing parents
disciplining their children. Though they may be significant, the therapist may not be
aware of events not reported by the patient. Some patients disclose only the least
painful events during the early stages of assessment, or may not consider other
events to be significant. Maintaining focus on less distressing events can serve to
divert attention from a more painful event. In addition, the treatment setting may
affect inquiry or disclosure of traumas. For example, because Tom served in a
war zone and sought treatment at a Veterans Affairs Medical Center, he assumed
it was only permissible to discuss military trauma. Had his therapist not specifically
inquired about childhood and non-combat military trauma, he might have failed to
identify clinically important events.
Thorough assessment of trauma exposure and re-experiencing symptoms from
the outset will help the clinician to identify the array of potentially traumatic experiences throughout a patient’s life that may be relevant to treatment. When all
identified traumas have been addressed in treatment and symptoms persist despite
successful extinction of distress related to them, other undisclosed traumatic events
may be the subject of re-experiencing and avoidance. The therapist also should
consider the possibility of undisclosed events when a patient’s symptoms do not
seem consistent with the reported traumatic events (as when a woman who presents
for treatment of motor-vehicle-accident-related PTSD reports that she avoids being
alone with men).
One of the most important tasks of treatment planning is to identify the specific
memories and stimuli to target to maximize the overall treatment effect. Patients
then rate the distress associated with these intrusive memories, distressing dreams,
and avoided stimuli, and these ratings are used to construct hierarchies that will
guide the progression of exposure. The therapist works together with the patient to
select the memories and stimuli that are most suitable for exposure and are candidates to produce generalizable treatment results. Although starting with the most
distressing memory on the hierarchy will enhance downward generalization to other
(particularly similar) memories or stimuli on a hierarchy, beginning with a moderately distressing memory has the advantage of providing a less aversive initial
experience, thereby enhancing enthusiasm for the exposure process.
The therapist should conduct periodic re-assessment of re-experiencing symptoms using a standardized self-report measure (administered at least monthly,
ideally weekly) and review the hierarchy after achieving anxiety reduction for a particular memory to determine the next memory to target with imaginal exposure. In
a scenario where the patient shows engagement and fear reduction during exposure
and completes assigned exposure homework but shows little improvement in PTSD
symptoms, it is possible that relevant traumas were not identified, or the hierarchy
shifted during treatment. Additional memories may emerge or increase in prominence during treatment. After intensive work on one memory, a patient may be more
“ready” to address other, perhaps even more distressing memories. For example,
Tom’s therapist understood from him that a day-long firefight with many casualties
in Iraq was the worst event that he had experienced. After several weeks of exposure
to memories from this day and extinction of anxiety related to this memory, Tom’s
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PTSD symptoms showed no change. Upon discussion, his therapist became aware
that Tom was increasingly bothered by a previously undisclosed memory of trying
to save a child who eventually died from sniper fire and that this had become a more
prominent source of distress.
The Influence of Other Emotions: Sadness, Guilt,
Shame, and Anger
Though PTSD is currently classified as an anxiety disorder, an array of other emotions, including sadness, guilt, shame, and anger, are frequently sources of distress
for trauma survivors (Holmes, Grey, & Young, 2005). Research on the interplay of
various trauma-related emotions is in its early stages. Emotions other than anxiety not only are frequent and prominent aspects of peri-traumatic responding, they
also are likely to play a significant, albeit as yet under-studied, role in maintaining
the disorder. For example, Andrews et al. found that shame and anger experienced
in the first month after a criminal assault were the strongest predictors of PTSD
6 months later (Andrews, Brewin, Rose, & Kirk, 2000). Therapists should, therefore,
assess these emotions and be prepared to grapple with them in addition to anxiety.
Identifying these emotions at the outset of treatment will be conducive to developing a treatment plan aimed for success. This can be done with specific assessment
instruments, such as the Trauma-Related Guilt Inventory (Kubany et al., 1996), the
guilt and anger items of the Clinician Administered PTSD Scale (CAPS) (Blake
et al., 1990), or unstructured clinical interview. Therapists should listen carefully
for trauma-related beliefs associated with anger, guilt, or shame (e.g., “It shouldn’t
have happened that way,” “It was all my fault”) that patients may express during the
assessment process or during imaginal exposure.
Non-anxiety emotions have the potential to interfere with the effectiveness of
exposure therapy (Foa et al., 1995; Grunert, Weis, Smucker, & Christianson, 2007)
or decrease the patient’s motivation to disclose or confront specific trauma-related
beliefs or memories. If the patient exhibits a pattern of initial activation of anxiety during exposure followed by little or no decrease in reported distress over
time (i.e., no within-session extinction), the therapist should consider the possibility
that reported distress predominantly reflects other emotions. The absence of facial
expressions of fear is a further clue and is predictive of poor outcome from exposure therapy (Foa et al.). Failure to show reductions in peak anxiety across sessions
is another indicator that other emotions may be activated during exposure, influencing ratings of distress and interfering with fear reduction. It is important to detect
these emotions when they emerge in order to facilitate processing them effectively.
Sadness
Intense sadness often is associated with depression, a comorbid problem for approximately 50% of patients seeking treatment for PTSD (Zayfert, Becker, Unger, &
Shearer, 2002). The dilemma for the clinician in treating comorbid depression with
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PTSD is whether the depression is so severe that it warrants targeted treatment prior
to trauma-focused CBT, or whether it will resolve when PTSD is successfully ameliorated (Foa et al., 2005). Examining the issues underlying the individual’s sadness
will help the clinician decide how to manage sadness and depression and avert treatment failure due to worsening depression during trauma-focused treatment. Sadness
can be associated with grief over a loss incurred during the trauma (such as Tom’s
grief over the death of his army buddy). Sadness that is connected to grief is likely
to habituate during exposure (Shear, Frank, Houck, & Reynolds, 2005) and need
not be an obstacle to proceeding with either exposure or cognitive therapy; indeed,
protocols for cognitive processing therapy often contain an optional session specifically addressing traumatic grief. If, however, the grief is about loss of a meaningful
life experience or role, such as the loss of one’s childhood or the loss of the soldier’s role, then the therapist may also consider strategies aimed at recreating life
meaning.
Sadness may also be related to loss of self-worth in connection with traumatic
events, and in this way is often connected to shame and/or guilt. For example, for
most of his life, Tom had a sense that he was “no good,” something he repeatedly
heard from his father. This sadness was related to shame. Since returning from Iraq,
he has struggled with feeling responsible for his buddy’s death, and this magnified
his low appraisal of his own worth (“I didn’t deserve to live when I let him die”),
an example of sadness related to guilt. Sadness related to guilt and shame about
aspects of the trauma can often be successfully reduced using cognitive restructuring
to target maladaptive beliefs about self-worth connected to the trauma.
Shame and Guilt
Guilt and shame are two distinct, though related, emotions that are often experienced in relation to traumatic events. Guilt involves feelings of remorse or regret
accompanied by the belief that one has done something “wrong” or “bad” and that
one should have thought, felt, or acted differently according to internal standards
(Kubany & Watson, 2003). Guilt is distinct from shame in that the focus is on
behavior, while the self-concept remains intact. In contrast, shame, typically associated with an urge to hide from others, is a more devastating and painful emotion
in which the entire self, not just the behavior, is negatively evaluated. Shame theoretically involves feelings of worthlessness and powerlessness, and shame (but not
guilt) is associated with depression (Tangney, Wagner, & Gramzow, 1992).
Individuals who feel intense guilt or shame about a traumatic event may be
highly motivated to avoid thinking about the event, thereby interrupting processing
of the memory. Guilt and shame interfere with engagement with anxiety, so when
they become the focus during imaginal exposure they can prevent new learning,
thereby impeding therapy progress (Riggs et al., 2006). In some instances, disengagement may take the form of dissociating completely from the memory and even
from the present reality, such that the patient is no longer mentally present in the
therapist’s office. It is important to note that guilt may be present but may not activate during exposure therapy, thus causing no interference with treatment. Indeed,
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outcome studies have demonstrated that exposure therapy reduces overall levels
of guilt (Taylor, 2004). There is some evidence, however, that cognitive processing therapy may be more efficacious than exposure for decreasing trauma-related
guilt related to hindsight bias or perceived lack of justification for one’s behavior
(Resick et al., 2002).
Anger
Clinical lore long held that angry patients were not good candidates for exposure
therapy (Jaycox & Foa, 1996). In support of this, Foa et al. (1995) found that when
anger is activated during exposure the patient disengages from anxiety and distress
ratings elevate but do not diminish, a process which impedes the effectiveness of
exposure therapy. As in the case of guilt, however, anger that does not activate during exposure may not impede treatment success. Evidence suggests that patients
with high levels of anger often benefit from exposure and are likely to experience
reduction in anger as a result (Cahill, Rauch, Hembree, & Foa, 2003). Thus, as with
guilt, it is important for therapists to be aware of the presence of anger and its potential for interfering with treatment and then to monitor possible effects anger may
have on treatment progress. Clues that a patient is experiencing anger during imaginal exposure include non-verbal behavior such as facial expressions, tone of voice,
or actions. Also, when anxiety ratings do not decline during exposure, the clinician
may inquire whether the ratings reflect anger. For example, during exposure to a
memory of being abused as a child, the therapist noted that Tom’s distress ratings
did not change over several sessions despite homework compliance. The therapist
asked about his thoughts and feelings during exposure, and Tom reported that he
was angry with his father for having ruined the family. As a result of his focus on
anger, he no longer felt anxious when recalling this memory.
Overcoming Guilt, Shame, and Anger
When guilt, shame, or anger is prominent, the therapist should consider whether to
include cognitive restructuring or imagery rescripting (Arntz, Tiesema, & Kindt,
2007; Grunert et al., 2007; Rusch, Grunert, Mendelsohn, & Smucker, 2000) in
the initial treatment plan, or pending response to exposure interventions. Although
imagery rescripting can take various forms, the concept entails altering disturbing images associated with the trauma in a manner that enhances the individual’s
sense of mastery or control of the experience. Recent data suggest that augmenting
exposure with imagery rescripting produces greater effects on anger, guilt, and possibly shame (Arntz et al., 2007). If exposure is implemented first and the patient’s
anxiety fails to extinguish across exposure sessions, the therapist should assess
whether other emotions have been activated. If guilt or shame has been activated,
the therapist should consider postponing exposure and using cognitive restructuring or adding imagery rescripting to decrease guilt and shame. If re-experiencing
symptoms persist, resume exposure.
Avoiding Treatment Failures in PTSD
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If anger has been activated, the therapist should start by encouraging the patient
to “refocus” away from the anger to the primary emotions associated with the memory (Riggs et al., 2006). It is often helpful to validate the empowering effects of
anger. For most people, anger feels better than feeling frightened or vulnerable. In
particular, men are socialized to view emotions such as sadness and fear as signs of
weakness; in contrast, anger is more socially acceptable for men to feel and express.
If the patient is unable to maintain focus away from the anger, the therapist should
next inquire as to its source. Often, patients are able to identify another emotion –
such as loss, shame, or powerlessness – that underlies the anger and that the anger
allows them to avoid. If the primary emotions associated with the memory can extinguish via exposure (e.g., fear, sadness), the therapist can encourage the patient to
focus on the underlying emotion instead of the anger. With his therapist’s help,
Tom was able to identify a strong sense of loss of his childhood and his family life
underlying the anger that emerged during exposure to a memory of abuse. After
acknowledging and validating this loss, Tom was able to focus on the fear he felt
during that episode and exposure resumed. If shame or guilt underlies anger, cognitive restructuring may facilitate processing of those emotions so that exposure may
resume. Validating anger should always be part of this process. In some cases, focusing on acceptance of past wrongs, injustices, or losses and examining consequences
of maintaining attention on anger can help the patient to “let go.”
Sadness, anger, shame, and guilt that emerge in response to PTSD symptoms or
the decision to seek help often are involved in perpetuating PTSD symptoms and
can interfere with treatment success (Ehlers & Clark, 2000). Many cultures (for
example, the military) have expectations that individuals should be able to tolerate
significant discomfort and seeking mental health care is a sign of individual weakness. Patients may feel ashamed of their perceived weakness, sad about the fact
that they need treatment, or guilty for not coping more effectively. Clinicians should
listen for statements or questions about the implications of seeking mental health
care (e.g., “I can’t believe I’m in a place like this;” “Does this mean I’m crazy?”) or
ask directly about such attributions. Often, validation coupled with psychoeducation
can alleviate anxiety about the help-seeking process. Cognitive restructuring may be
necessary to decrease distress and increase the likelihood of treatment completion.
Facilitating Affect Regulation
Several of the strategies for dealing with sadness, shame, anger, and guilt depend
on the patient being able to attend to and discriminate various emotions. Many
patients with PTSD have deficits in these areas. Trauma survivors, particularly
those with a history of childhood abuse, may lack basic emotion-regulation skills.
They tend to have difficulty regulating intense emotions and they may have difficulty recognizing and responding effectively to emotions (Tull, Barrett, McMillan,
& Roemer, 2007). The absence of these basic skills can impede trauma-focused
therapies. Cloitre, Koenen, Cohen, and Han (2002) noted that difficulty tolerating
and managing unpleasant emotions, higher likelihood of dissociation, and difficulty
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developing and maintaining a good working relationship are characteristics of both
childhood abuse survivors and patients who do not fare well in exposure-based treatments. In addition, survivors of childhood abuse were more likely than other patients
with PTSD to score high on measures of expressed and subjective anger, which, as
noted above, may complicate exposure therapy (Chard, Weaver, & Resick, 1997;
Franklin, Posternak, & Zimmerman, 2002).
When treatment is not proceeding smoothly, the therapist should attend to indicators of poor affect-regulation skills (Chard et al., 1997; Franklin et al., 2002). These
can include difficulty disentangling emotions, being overwhelmed by emotions for
long periods between therapy sessions, or dissociating in the face of moderately
intense emotion. Such patients may have trouble engaging with anxiety during
exposure therapy or may fail to extinguish anxiety during exposure. They also can
have trouble identifying relevant thoughts to challenge in cognitive restructuring.
Difficulties with trust and poor interpersonal skills that often are features of poor
affect regulation can result in problems maintaining an effective therapy relationship. This may in turn affect acceptance of the treatment rationale and willingness
to take the necessary risks in therapy, or result in interpersonal conflicts that distract
from the therapy activities.
Broadly speaking, the therapist can modify the patient’s skill level or modify the
treatment. Modifying the patient’s skill level usually entails adding treatment components that are designed to increase distress tolerance and the ability to experience
and manage emotions. Several approaches have provided affect-regulation skills
training before delivering CBT for PTSD (e.g., Chard et al., 1997; Cloitre et al.,
2002; House, 2006). Similarly, we have found that integrating components of dialectical behavior therapy (Becker & Zayfert, 2001) (Linehan, 1993b) or acceptance
and commitment therapy (Orsillo & Batten, 2005) can improve patient’s ability
to tolerate focusing on trauma and consequently may increase their likelihood of
completing treatment. Emotion-regulation approaches are grounded in theory and
research, though their specific benefits for enhancing treatment of PTSD awaits further research. Nonetheless, they offer the clinician constructive options for working
with challenging cases.
Working Through Psychosocial Crises
Emotional or pragmatic crises often arise during treatment and many patients with
PTSD lack adequate coping skills to manage them. For example, patients sometimes
lose their jobs, housing, or marriage, are notified of re-deployment to a war zone, or
experience a new trauma, such as an accident or assault in the course of treatment.
These crises can adversely affect treatment in two different ways. First, they may
interfere with session attendance or homework compliance. Patients may report that
they did not have time to complete assignments or come to session because they
were out looking for a job or trying to call their lawyer. Second, psychosocial crises
can divert session content away from interventions formulated to target symptoms.
Protocols for exposure and cognitive therapy address the symptoms that are thought
Avoiding Treatment Failures in PTSD
161
to cause patients’ difficulties with everyday stressors, but do not directly address
those stressors. A focus within session on those stressors therefore represents a
departure from the treatment plan.
Commonly, treatment protocols advise that clinicians respond to psychosocial
crises by noting the potential for treatment interference, explaining that decreasing
PTSD symptoms will improve ability to cope with the crisis and maintaining focus
on PTSD treatment (Riggs et al., 2006). This can be effective if the patient agrees
with the rationale, has adequate problem-solving skills, does not become emotionally overwhelmed, and is able to maintain focus on the therapy. However, many
PTSD patients lack the problem-solving skills to resolve crises and the affective
regulation skills to modulate the intensity of their emotional responses. As a result,
life problems can quickly escalate and derail treatment. Pre-treatment functioning
is an indicator of overall problem-solving ability and emotional stability that can
inform decision-making in this area. Patients who were not functioning well before
treatment often have difficulty maintaining trauma treatment focus under crisis conditions. It is sometimes necessary to suspend trauma-related treatment and provide
a brief course of training in problem-solving and affect-regulation skills, with the
clear message that these skills can be applied to the patient’s new or ongoing psychosocial crises in order to maintain focus on the trauma-related treatment goals
that will bring greater long-term emotional stability.
Substance Use Disorders
Rates of substance use disorders (SUDs) are higher among individuals with a history of trauma than in the general population (Chilcoat & Breslau, 1998; Kessler,
Sonnega, Bromet, Hughes, & Nelson, 1995), and rates of PTSD are higher among
individuals with SUDs (Greeley & Oei, 1999). The potential for substance use to
interfere with treatment of PTSD symptoms has been the subject of much theory
and research (Cloitre, Miranda, Stovall-McClough, & Han, 2005). The chemical
effects of the substance may prevent the patient from focusing attention on treatment
materials and experiencing arousal. Patients may use substances to avoid unpleasant thoughts or emotions associated with re-experiencing symptoms or trauma
treatment. Alcohol use has been related to negative outcome of anxiety treatment
(Keijsers, Kampman, & Hoogduin, 2001; van Minnen et al., 2002) and thus it is
not surprising that active substance dependence is a common exclusion criterion in
controlled trials of PTSD treatments.
The effect of substance use on treatment varies in relation to the severity of
the use and the function it serves. A thorough assessment of substance use, abuse,
and dependence, including the extent to which substances aid avoidance of traumarelated emotions, is key for developing a clinically useful PTSD case formulation.
The assessment information should help the therapist to determine the potential
for interference with PTSD treatment and whether specific substance use treatment should precede trauma-focused treatment. For a patient who is using daily and
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unable to work or maintain their activities of daily living, detoxification and intensive substance-abuse treatment should be initiated before trauma-focused treatment.
When patients have detoxified from substances and have maintained a period of
abstinence (many specialized PTSD programs require 30 days of sobriety before
admission), the case formulation approach may be employed to elucidate the relationship between PTSD and substance use and to assess the deficits (e.g., poor affect
regulation, minimal problem-solving skills) that place the patient at higher risk for
using substances as a way to cope. For patients in the early stages of recovery, there
are useful treatment approaches that combine the development of skills to maintain
sobriety in the face of trauma-related symptoms with early education on how trauma
and substances interact (Batten, 2009; Najavits, 2002).
Substance use need not be severe enough to warrant detoxification in order to
interfere with PTSD treatment. Even patients who work full-time and fulfill familial responsibilities may use substances as a way to decrease thoughts and emotions
associated with trauma. The substance use does not merit intervention, but it has
the potential to interfere with trauma-focused treatment. In many cases, traumafocused treatment can proceed by including discussion of the role of substance use
in the individual’s avoidance of trauma-related thoughts and emotions and monitoring substance use throughout treatment. Tom’s case is an excellent example
of this. His drinking caused few problems in his life, yet his therapist noted that
it could provide a means of avoiding uncomfortable beliefs and emotions when
completing therapy homework. During the education and rationale phase of treatment, Tom and his therapist discussed the function that his alcohol use served, and
Tom agreed not to drink for the duration of treatment. He also agreed to monitor
his urges to drink using a daily diary during treatment and to inform his therapist if his urge to drink increased. Although many clinicians strictly adhere to a
policy of achieving complete sobriety before addressing trauma, many individuals
are not able or willing to achieve complete abstinence before PTSD treatment, or
even afterward. Ongoing collaborative discussions around the role of substances in
managing PTSD symptoms will help the therapist guide the client toward optimal
decisions.
Titrating Engagement with Emotions During Exposure Therapy
Parameters of treatment can be modified to facilitate. As noted above, emotional
engagement is an important ingredient for successful outcome from exposure therapy. Yet over-engagement also can impede the progress treatment of therapy, as
some patients will be unwilling to continue exposure without experiencing some
relief of their distress. Failure of distress ratings to diminish across exposure trials
is predictive of poor outcome (Jaycox, Foa, & Morral, 1998). There are a variety
of reasons patients may over- or under-engage traumatic memories and emotions,
some of which have been described earlier (e.g., poor ability to regulate emotions,
efforts to avoid memories or the accompanying emotions, beliefs about the potential
consequences of experiencing emotions, such as losing control). One approach is to
Avoiding Treatment Failures in PTSD
163
initiate exposure as soon as possible and then problem-solve to remove any obstacles that may present during the procedure. An advantage of this approach is that
patients may experience reduction of distress more quickly, which can enhance their
confidence in the treatment. A disadvantage of providing exposure immediately is
that patients who have difficulty titrating affect are “set up” for failure, which is not
conducive to a good treatment experience (Lee, 2006). An alternate approach is to
assess thoroughly before initiating exposure and seek to eliminate obstacles before
beginning. The disadvantage here is that delay of symptom reduction may increase
likelihood of dropout. Indeed, Zayfert et al. (2005) found that patients who started
exposure therapy in a clinical setting were more likely to complete CBT for PTSD
successfully than patients who did not start exposure therapy.
Patients who under-engage typically present the trauma account with minimal visible or self-reported emotional arousal. Important and likely uncomfortable
details (e.g., what a soldier was thinking after he was shot; the initial penetration
during a sexual assault) may be missing entirely, and the account of the experience
may be brief. The patient may provide the “6 o’clock news” version of the trauma, a
short summary that glosses over anything difficult. There are a number of strategies
therapists can implement to increase engagement with trauma-related emotions so
as to maximize the likelihood of treatment success (Jaycox et al., 1998). Minimally,
the therapist may remind the patient of the rationale for exposure and the consequent
importance of engaging with the memory and related emotions. The therapist may
also modify the parameters of the exposure exercise, asking the patient to relate the
memory in the present tense, with eyes closed, and with a greater detail of events,
thoughts, and feelings. Asking questions during the exposure can increase focus on
particular details, thoughts, or emotions. Cognitive restructuring of thoughts about
fear of losing control of emotions can help the patient feel less threatened by the
task of engaging. Similarly, assessing for and targeting guilt, shame, or anger may
enable the patient to engage with the trauma memory more directly. For those who
are high in anxiety sensitivity (fear of fear), it can be useful to engage the patient
in interoceptive exposure exercises, such as hyperventilation, to expose the patient
to the physical sensations of fear independent of the trauma memory and stimuli
(Barlow & Cerny, 1988).
Patients who are over-engaged will report extremely high levels of anxiety during imaginal exposure and may express concern about the effects of experiencing
emotions at high levels. Over-engaged patients may also dissociate during imaginal exposure, causing them to lose engagement with the memory and the associated
emotions. The main goal in working with over-engaged patients is to establish and
maintain a sense of safety during exposure activities so that the patient is able to
access and engage the trauma memory. The therapist should emphasize to patients
that though distress (and PTSD symptoms) may increase in the early stages of treatment, it tends to decrease for most patients as treatment progresses and the increase
is symptoms does not mean they will not ultimately benefit (Foa et al., 2002; Nishith,
Resick, & Griffin, 2002). The therapist may also take steps to titrate anxiety, such as
instructing patients to keep their eyes open while recounting the trauma, interacting
verbally with them during exposure, beginning the exposure in written form, and
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dividing the memory into manageable segments. In some cases, it may be useful to
make a plan in advance that if the patient begins to “flash back,” the therapist will
gently touch them on the leg or shoulder to re-orient them. Once anxiety has extinguished under modified conditions, exposure can resume in its original form (e.g.,
verbally with eyes closed).
Summary
Cognitive-behavioral therapies have been shown to be efficacious for treatment
of PTSD. However, there are a number of obstacles that can interfere with the
implementation of evidence-based CBT for PTSD or that predict poor outcome
of treatment. Some of these obstacles can be overcome by providing patients with
skills to manage them, and others can be navigated by flexible application of existing treatment protocols. The case formulation approach is an important treatment
planning tool for clinicians faced with patients with multiple problems. A thorough
assessment of trauma history, PTSD symptoms, and comorbid problems informs
working hypotheses about the relationships among presenting problems. These
working hypotheses guide formulation of treatment plans, and continual assessment
of change during treatment may lead to revision of these hypotheses and adjusting the treatment plan accordingly. Clinicians should, whenever possible, adhere
as closely as they can to the structure of evidence-based CBT, while maintaining
flexibility to respond effectively to roadblocks to treatment success.
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Avoiding Treatment Failures in Social
Anxiety Disorder
Stefan G. Hofmann, J. Anthony Richey, Anu Asnaani, and Alice T. Sawyer
The Case of Paul
Paul1 was a 24-year-old white male. He was of medium build, attractive, and cooperative during the interview. He was well articulated but spoke very softly and avoided
eye contact with the interviewer. The main reason for which Paul sought help was for
debilitating and pervasive social anxiety that he had been experiencing since middle
school. Paul reported that he desired companionship but avoided any social contact
with other people for fear of being criticized or rejected. He even felt restraint when
interacting with his parents and other relatives. When asked why he was seeking
help, he noted that he wanted to move out of his parents’ home, get a job, have relationships, and lead a normal life. It was apparent that Paul showed a clear readiness
for change and had clear short-term and long-term goals for himself. However, he
viewed his competence to implement such changes as insufficient. Paul was offered
group treatment at the clinic, which is the standard treatment for social anxiety disorder. However, he refused to participate because he was too fearful of interacting
with other group participants.
Psychosocial History
Paul’s psychosocial history revealed that his social anxiety had interfered to a significant degree with his life. He reported that he dropped out of high school in tenth
grade when he was asked to give a presentation in front of his class. In order to avoid
this assignment, he ran away from home and spent the night in a local park. When
the police found him the next day, his parents told him that he did not have to return
to school. Since that time, Paul had been living at home with his parents. He did not
return back to school and did not see any of his classmates again.
S.G. Hofmann (B)
Department of Psychology, Boston University, Boston, MA, USA
e-mail: shofmann@bu.edu
1 This
is a real case, but the name of the patient and other identifying information was altered. A
detailed description of this case is given in Hofmann & Scepkowski (2006).
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_10,
C Springer Science+Business Media, LLC 2010
169
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S.G. Hofmann et al.
Paul described the relationship with his family as difficult. Both of his parents
were born and raised in Greece and immigrated to the United States when they were
in their twenties. Paul’s family spoke Greek at home and followed Greek traditions.
He described his father as politically conservative, domineering, authoritarian, and
over-involved, and his mother as submissive and conflict-avoidant. Paul reported
having two older sisters. He considered his second oldest sister to be his best friend.
He reported that he spoke to her once a week for a few minutes on the phone.
His family was unaware of the fact that he was seeking treatment for his social
anxiety.
In addition to social anxiety, Paul also reported that he felt depressed and that
he worried excessively about various minor matters. Paul stated that, due to his
problems, he had occasional thoughts about suicide but denied any intent or plan.
Paul had never received any psychological or pharmacological treatments.
Diagnostic Information
As part of the regular intake procedure, Paul underwent a structured diagnostic interview, the Anxiety Disorders Interview Schedule for DSM-IV (ADIS-IV, DiNardo,
Brown, & Barlow, 1994). A second interview by an independent clinician was conducted one week later. The two interviews yielded consistent results and senior
clinicians agreed with the diagnostic assessment. The ADIS-IV screens for all Axis
I mood and anxiety disorders and assigns a clinical severity rating (CSR) on a
scale from 0 (no distress/interference) to 8 (extreme distress/interference). A CSR
rating of 4 or higher marks the clinical threshold. Paul met the criteria for the
following Axis I diagnoses: Social Anxiety Disorder (Social Phobia), generalized
subtype (CSR: 8); Generalized Anxiety Disorder (CSR: 5); Depressive Disorder Not
Otherwise Specified (CSR: 5). Furthermore, he met criteria for Avoidant Personality
Disorder (CSR: 8) on Axis II and scoliosis (S-shaped side-to-side spinal curve) on
Axis III. No other patient at our center has ever received the maximum CSR ratings for both the social anxiety disorder and avoidant personality disorder (APD)
diagnoses. In addition, the raters coded problems related to the social environment and occupational problems on Axis IV and assigned a Global Assessment
of Functioning score of 45 (current and past year) on Axis V (serious symptoms or
any serious impairment in social, occupational, or school functions).
Case Conceptualization
During the interview, Paul made a number of remarks suggesting that he had a
distorted image of himself. Although his attractiveness was above average, he saw
himself as physically unappealing, socially inept, and inferior to others.
Paul’s case showed many prototypical features of social anxiety disorder (SAD).
Some of his concerns were focused on his physical appearance, which are often
associated with body dysmorphic beliefs. Although the diagnostic criteria for body
dysmorphic disorder were not specifically assessed, there is good evidence to
Avoiding Treatment Failures in Social Anxiety Disorder
171
assume that Paul would have met the diagnostic criteria. As a result of these concerns, he feared and avoided social contact, but at the same time greatly suffered
from social isolation. He also felt that he lacked the social competence and skills
required to improve his social situation. The resulting social isolation and withdrawal was associated with, and perhaps even caused, his depressive symptoms and
other anxiety symptoms. Due to the diagnostic overlap between SAD and avoidant
personality disorder (APD), it is not surprising that he also met criteria for APD.
In summary, Paul represented an extreme case of SAD that highlights many
commonly occurring examples of complications that might arise when treating
SAD. Specifically, he had a distorted and negative view of himself and he was
socially isolated and highly avoidant of social contact. At the same time, he greatly
suffered from social isolation, which was closely associated with his feelings of
depression. As a result, he showed features of body dysmorphic disorder, and met
additional diagnostic criteria for APD and depression. Despite these significant
complicating factors, Paul made remarkable improvement. In order to track Paul’s
progress, he was given the Social Phobia and Anxiety Inventory (SPAI; Turner,
Beidel, Dancu, & Stanley, 1989) at approximately every third session and at pretest, post-test, and 1-year follow-up. Turner et al. suggested that a SPAI (total)
cut-off score of 80 is optimal for identifying individuals with SAD among a sample of clinic patients with anxiety disorders. Figure 1 shows that the intervention
140
SPAI total scores (0–192)
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100
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60
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Fig. 1 Case of Paul. Paul’s treatment changes in the Social Phobia and Anxiety Inventory (total
score). Reprinted with permission from Hofmann and Scepkowski (2006)
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S.G. Hofmann et al.
led to a significant drop within the first 3 months of therapy (by session 11) from
the clinical to the non-clinical range. These gains were maintained at the 1-year
follow-up. Paul underwent a second diagnostic assessment at the end of treatment
by a blinded clinician as part of a regular clinic procedure. At that time he no
longer met any DSM-IV Axis I or II criteria. This case illustrates that, despite a
number of treatment complications that will be outlined below, SAD can be effectively treated with creative techniques if they specifically target these complicating
factors.
Psychological Interventions
Contemporary theories of SAD emphasize the role of cognitive processes in the
maintenance of the disorder (Clark, 2001; Leary, 2001; Rapee & Heimberg, 1997).
Cognitive-behavioral treatment (CBT) protocols based on this approach show a
number a similarities and notable differences. One of the first CBT protocols,
Cognitive Behavioral Group Therapy (CBGT) by Heimberg (e.g., Heimberg &
Becker, 2002), is an adaptation of Beck and Emery’s (1985) cognitive therapy
for anxiety disorders to SAD. This intervention is administered by two therapists
in 12 weekly 2.5-h sessions to groups comprised of six patients and consists of
several distinct but interwoven treatment components. In the first two sessions,
patients are taught the Beckian CBT model as applied to SAD, and are given
instructions in cognitive restructuring techniques. Specifically, patients practice
identifying negative cognitions (automatic thoughts), observing the co-variation
between anxious mood and automatic thoughts, examining the errors of logic,
and formulating rational alternatives to their automatic thoughts. The remaining ten sessions entail largely exposure exercises, in which patients confront
increasingly difficult feared situations such as public speaking (simulated in the
therapy group) while applying these cognitive restructuring techniques. Behavioral
experiments such as these are utilized to confront specific reactions to these
exposure experiences. At the end of each exposure-based session, the therapist
and group members agree on individualized assignments for exposure to similar real-life situations during the week. Patients also complete self-administered
cognitive restructuring exercises before and after each behavioral homework
assignment.
This method of intervention has stimulated a great amount of research interest. In
standardized protocols, CBGT has been shown to be at least as effective as the most
efficacious form of pharmacotherapy. On the other hand, however, there is clearly
still room for improvement. For example, in the most recent study on the efficacy
of CBGT, 133 patients with SAD were randomly assigned to phenelzine (Nardil, an
MAOI commonly used to treat SAD), Educational Support Group Therapy, a pill
placebo, or CBGT (Heimberg et al., 1998). After 12 weeks, both the phenelzine
(65%) and the CBGT conditions (58%) had higher proportions of responders than
pill placebo (33%) or Educational Support Group Therapy (27%), which served as
a psychotherapy placebo condition. The criterion for treatment response was based
Avoiding Treatment Failures in Social Anxiety Disorder
173
on a 7-point rating of change on the Social Phobic Disorders Severity Change Form
(Liebowitz et al., 1992). Patients rated as markedly or moderately improved were
classified as responders.
A recent modification of Heimberg’s CBT protocol is Comprehensive Cognitive
Behavioral Therapy (CCBT; Foa, 1994). This treatment protocol was included
as a treatment condition in a recently published clinical trial (Davidson et al.,
2004). The treatment protocol is derived in part from an earlier version of CBGT
(Heimberg & Becker, 2002) and combines exposure techniques, Beckian cognitive restructuring therapy, and social skills training. The intervention differs from
CBGT primarily in that it includes specific social skills training in addition to
the conventional cognitive restructuring exercises and exposure tasks. Furthermore,
the role-plays are shorter and the treatment is two sessions longer than CBGT.
The study by Davidson et al. suggests that Foa’s treatment shows efficacy rates
that are similar to CBGT. Specifically, the study randomized 295 patients with
generalized SAD to one of five groups: (1) fluoxetine, (2) CCBT, (3) placebo,
(4) CCBT combined with fluoxetine, or (5) CCBT combined with placebo. The
results showed that all active treatments were superior to placebo, and the combined treatment was not superior to the other treatments. The response rates in the
intention-to-treat sample (using the Clinical Global Impressions scale) were 50.9%
(fluoxetine), 51.7% (CCBT), 54.2% (CCBT/fluoxetine), 50.8% (CCBT/placebo),
and 31.7% (placebo). These findings are comparable to the clinical trials examining “traditional” CBT approaches (i.e., CBT protocols that are based on more
generic, Beckian-style CBT for anxiety disorders). Although the treatment efficacy
data were relatively modest, CBT was similarly effective than pharmacotherapy.
Interestingly, combining CBT and pharmacotherapy was not more effective than
monotherapy.
In an attempt to enhance the efficacy of the CBT approaches for SAD, some
investigators have more recently developed protocols that are designed to better
target disorder-specific factors of SAD that have been identified in experimental studies (Clark, 2001; Hofmann, 2007). One such treatment model is depicted
in Fig. 2.
According to this model, individuals with SAD are apprehensive in social situations in part because they perceive the social standard (i.e., expectations and social
goals) as being high. They desire to make a particular impression on others but
doubt that they will be able to do so (Leary, 2001), partly because they are unable
to define goals and select specific achievable behavioral strategies to reach these
goals (Hiemisch, Ehlers, & Westermann, 2002). This leads to a further increase in
social apprehension and increased self-focused attention (Clark & McManus, 2002;
Heinrichs & Hofmann, 2001; Hofmann, 2000; Hirsch & Clark, 2004; Woody, 1996),
which triggers a number of additional cognitive processes. Specifically, vulnerable
individuals exaggerate the probability and potential social costs involved in social
situations (Foa, Franklin, Perry, & Herbert, 1996; Hofmann, 2004). This is consistent with the model by Clark (2001), which assumes that individuals with SAD
assume that they are in danger of behaving in an inept and unacceptable fashion
and believe that this will result in disastrous consequences. In addition, the model
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High Perceived Social Standards
and Poorly Defined Social Goals
Social
Apprehension
Post-Event Rumination
Avoidance and Safety
Behaviors
Anticipation of
Social Mishap
Heightened
Self-focused Attention
Negative SelfPerception
High Estimated
Social Cost
Low Perceived
Emotional Control
Perceived Poor
Social Skills
Fig. 2 Treatment model. Psychological factors that maintain social anxiety disorder. Reprinted
from Hofmann (2008)
posits that individuals with SAD perceive little control over their anxiety response
in social situations (Hofmann, 2005; Hofmann & Barlow, 2002), hold a negative
view of themselves as social objects (Hofmann, Moscovitch, Kim, & Taylor, 2004),
and view their social skills as very poor or inadequate to master the social task. As
a result, the individual with SAD anticipates social mishaps and engages in avoidance and/or safety behaviors (Wells et al., 1995), followed by post-event rumination
(Mellings & Alden, 2000; Rachmann, Grüter-Andrew, & Shafran, 2000). This leads
to a positive feedback loop, leading to the maintenance and further exacerbation of
social avoidance and anxiety.
An unanswered question for the field is whether a particular focus on modification of social cost can boost treatment response beyond that seen in other protocols.
Comparative treatment trials have not yet been conducted to show the additive benefit with the same group of patients, but independent trials have shown particularly
promising effect sizes suggesting that more patients may be able to achieve remission with this approach. For example, Clark et al. (2003) developed an individual
treatment approach consisting of 16 sessions that primarily focuses on modifying
safety behaviors and self-focused attention, in addition to the conventional CBT
strategies. The Clark et al. trial randomly assigned 60 patients with generalized
Avoiding Treatment Failures in Social Anxiety Disorder
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SAD to one of three conditions: (1) cognitive therapy alone, (2) fluoxetine combined
with self-exposure, or (3) fluoxetine combined with placebo. Treatment efficacy was
measured by calculating a composite score that was based on six frequently used
self-report measures of SAD and a rating based on a structured clinical interview.
The results at post-treatment and 12-month follow-up assessments showed that cognitive therapy was superior to the other two conditions, which did not differ from
one another. The results showed that the uncontrolled effect size of the severity rating based on the clinical interview was 1.41 (pre-test to post-test) and 1.43 (pre-test
to 12-month follow-up) in the cognitive therapy group. Even stronger effects were
found for the composite score, which was associated with an uncontrolled pre–post
effect size of 2.14. Similar results were reported in an open-label pilot trial with ten
patients with SAD who received a 12-session group therapy with five participants
per group (Hofmann & Scepkowski, 2006). This intervention resulted in a substantial reduction of social anxiety with effect size estimates ranging between 1.54 and
2.37. These results suggest that it is possible to improve the treatment effects of
CBT by targeting cognitive variables that appear to be specific maintaining factors
for SAD and that have not been systematically addressed in more conventional CBT
protocols.
Potential Predictors of Poor Treatment Response
Generalized Subtype and Avoidant Personality Disorder
APD is an Axis II condition which is commonly comorbid with SAD and highly
overlapping in symptomatology with the generalized subtype of SAD. Studies have
found that both the generalized subtype of SAD and APD are associated with poor
overall psychosocial functioning, greater overall psychopathology, high trait anxiety, and depression (e.g., Boone et al., 1999; Brown, Heimberg, & Juster, 1995;
Herbert, Hope, & Bellack, 1992; Holt, Heimberg, & Hope, 1992; Turner, Beidel, &
Townsley, 1992). It has been suggested, therefore, that this additional diagnosis may
simply represent increasingly severe manifestations of social anxiety, which range
on a continuum from specific (nongeneralized) SAD, to generalized SAD without
APD, to generalized SAD with APD (Hofmann, 2000b; McNeil, 2001; Hofmann,
Heinrichs, & Moscovitch, 2004).
Whereas some studies support the notion that APD is a predictor of poor treatment response (Alden & Capreol, 1993; Feske, Perry, Chambless, Renneberg, &
Goldstein, 1996) other studies have not shown APD to be a significant moderator of treatment change (Brown et al., 1995; Dreessen & Arntz, 1998; Hofmann,
Newman, Becker, Taylor, & Roth, 1995; Hope, Herbert & White, 1995; Mersch,
Jansen, & Arntz, 1995; Van Velzen, Emmelkamp, & Scholing, 1997). Similar inconsistent results have been reported in studies investigating the generalized subtype as
a predictor of poor treatment outcome (Brown et al., 1995; Gorman, Liebowitz,
Fyer, Campeasa, & Klein, 1985; Liebowitz et al., 1992; Turner et al., 1992; Uhde,
Tancer, Black, & Brown, 1991).
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Depression
Depression is highly comorbid with SAD (Kessler, Stang, Wittchen, Stein, &
Walters, 1999), and there is evidence to suggest that a diagnosis of SAD increases
the risk of subsequent depression (Alpert et al., 1999; Brown, Campbell, Lehman,
Grisham, & Mancill, 2001; Stein et al., 2001). Furthermore, a study by Chambless
and colleagues found that a high level of depression is a predictor of poor SAD
treatment response (Chambless, Tran, & Glass, 1997). In contrast, however, Erwin,
Heimberg, Juster, and Mindlin (2002) did not observe a differential treatment
response of SAD patients with or without depression. Instead, the authors found
that SAD patients with comorbid mood disorders, but not comorbid anxiety disorders, were more severely impaired than those with no comorbid diagnosis both
before and after 12 weeks of CBGT. Moreover, a study by Moscovitch, Hofmann,
Suvak, and In-Albon (2005) found that changes in SAD mediate changes in depression during CBT for SAD. The role of comorbid depression in relation to SAD is
covered in more detail in Chapter 10.
Social Skills
The perception of one’s social skills and abilities appears to be an important component of perceived self-efficacy in SAD. Although it remains uncertain whether
socially anxious individuals are in fact deficient in any of their social skills (Clark
& Arkowitz, 1975; Glasgow & Arkowitz, 1975; Halford & Foddy, 1982; Hofmann,
Gerlach, Wender, & Roth, 1997; Rapee & Lim, 1992; Stopa & Clark, 1993), they
do tend to appraise their own performance in social situations more negatively than
non-anxious individuals, even when actual differences in performance are accounted
for (Alden & Wallace, 1995; Glasgow & Arkowitz, 1975; Rapee & Lim, 1992;
Stopa & Clark, 1993). These results and others call into question the value of social
skills training modules (Stravynski & Amado, 2001). Although social skills training seems to be effective in reducing social anxiety (Stravynski, Grey, & Elie, 1987;
Stravynski, Marks, & Yule, 1982), there is no clear evidence to suggest that it is
more effective than exposure therapy or cognitive-behavior therapy for reducing
social anxiety, even for individuals who were judged to have poor social skills
(Mersch, Emmelkamp, Bögels, & van der Sleen, 1989; Mersch, Emmelkamp, &
Lips, 1991; Wlazlo, Schroeder-Hartwig, Hand, Kaiser, & Münchau, 1990).
Core Elements of Treatment and Common
Sticking-Points in Therapy
One of the most important components of CBT is the therapy rationale itself.
Three aspects are important to convey: (1) the therapy is an active, goal-directed,
behavioral-based intervention to eliminate avoidance and reduce subjective distress;
(2) cognitive errors contribute to social anxiety; and (3) avoidance behaviors maintain social anxiety. The following brief dialogues will exemplify selected aspects of
the treatment.
Avoiding Treatment Failures in Social Anxiety Disorder
177
Motivation for Therapy
Treatment motivation is crucial for any exposure-based therapy of highly avoidant
individuals. In addition to establishing rapport with the patient and discussing
the treatment model, the first session also has an important motivational goal.
Discussing the treatment model, the role of avoidance for the maintenance of
SAD, and the importance of exposure practices can generate a great degree
of distress and increase the likelihood of avoidance tendencies and even treatment dropout. Therefore, it is important to “inoculate” the patient for avoidance
behaviors. In other words, it is often useful to prepare patients for situations in
the future when they will want to avoid exposure assignments, other homework
tasks, or even coming to sessions. In order to counter this tendency, the therapist should explain that not doing exposure practices in sessions and homework
assignments (i.e., tasks to be completed between sessions every week after the
second session) and missing sessions are all forms of avoidance behavior. For
example, the therapist might introduce this issue at the end of the first session as
follows:
T: Before we end this session, I would like to say something that I think is very
important. Avoidance has many faces. And sometimes it might be difficult
to recognize a behavior as avoidance behavior. This is partly because avoidance has developed into a habit; and habits occur on a subconscious level.
Avoidance behaviors are particularly hard to identify if you can give yourself
other reasons why you avoided. That way, you can avoid doing something
unpleasant and at the same time can tell yourself that you didn’t do it not
because of your anxiety, but because your car broke down, you had a deadline at work, or because your dog got sick. Your avoidance is a strong habit
and it will always be easy to find reasons why you can’t do it, some might
be more convincing to yourself and other people than others. But the bottom
line is: it is still avoidance. Every time you avoid, you are making a decision
against an independent and anxiety-free life and for a life that is controlled
by your anxiety. And every time you don’t avoid, you are courageous and
choose the hard-way with the goal to free yourself from your anxiety. I want
you to be fully aware of this. Patients I have worked with who succeeded
were the ones who were committed to getting better. I recommend you do
the same – nothing should be more important than coming to our sessions
and practicing the homework exercises.
Some patients may be resistant and hesitant to undergo therapy because they
believe that this is the way they are, and changing their social anxiety would
require fundamental changes in personality traits. The following dialogue illustrates
this issue:
T: Social anxiety, the fear of social situations, is something really interesting.
You are constantly confronted with social situations in your daily life. Just
think about how often you interact with people during your day. And yet,
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in the absence of treatment, social anxiety can persist for many years or
decades. What keeps this anxiety going? Why don’t people get used to it?
Do you have any ideas?
P: I am just very shy. I have always been.
T: People clearly differ in how shy they are. But shyness itself is not the problem. The problem develops when social anxiety interferes with your life and
when you can’t do things you want to do because of your fear of social situations. We discussed earlier the many ways in which social anxiety interferes
with your life. The goal of treatment is to make you feel more comfortable in
social situations so that you can do the things you want to do. So the goal is
not to change you as a person. Instead, the goal is to accept yourself the way
you are in order to feel less uncomfortable in social situations.
Challenging Cognitive Errors
A very common cognitive error that is often resistant to change is estimated social
cost. This refers to the belief that social mishaps would lead to disastrous consequences. The following dialogue exemplifies the Socratic method of cognitive
therapy to deal with this error:
P: But what if this unlikely event really does happen? What if I really do lose
my train of thought and my mind goes blank?
T: Yes, good point. So what if your mind really does go blank? What do you
think would happen?
R: This would be awful.
T: A real catastrophe?
P: Yes.
T: But what exactly would be so terrible about it?
P: It would be embarrassing!
T: Why would it be embarrassing?
P: Because I will make a fool of myself in front of other people.
T: What does “making a fool of yourself in front of other people” exactly mean?
What would happen?
P: They would laugh about me and think that I am a total loser.
T: How do you know what other people think of you? Do you have a crystal
ball?
P: What do you mean?
T: You are making a number of assumptions here that may or may not be correct. Interestingly, you choose out of many possible alternatives the one that
threatens your self the most. For example, you are assuming that if you lose
your train of thought, everybody will notice it, laugh at you, and think that
you are incompetent. This scenario would then elicit embarrassment in you.
If people don’t notice that you lost your train of thought or if they do, but are
not the least bit hostile, you wouldn’t have any reason to feel embarrassed
any more. Isn’t that right?
Avoiding Treatment Failures in Social Anxiety Disorder
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P: I guess so.
T: Furthermore, while this scenario is not completely impossible, it is not very
likely. It assumes that the social world out there is hostile and aggressive,
and that people are out to get you. But let’s assume for a moment that this
scenario actually does happen, and that you happen to speak in front of
an audience that consists of some very hostile people, and that you would
indeed embarrass yourself. Then what? Have you been in any embarrassing
situations before in your life?
P: Of course I have.
T: How many times?
P: Oh, many times. More than I can count.
T: And are you still alive?
P: (Laughs)
T: My point is that even if your mind does go blank, even if people notice that,
and even if they are in fact hostile and think that you are an incompetent
loser, which causes you a great deal of embarrassment, it is not a catastrophe. You have been embarrassed before, and so has everyone else. And life
will go on.
Eliminating Avoidance Behaviors
It is recommended to define avoidance as anything the patient does or does not
do that prevents him/her from facing his/her anxiety. This includes not entering
the feared situation, escaping out of the feared situation, distracting oneself, using
breathing techniques, or behaving in a way that makes oneself feel more comfortable
(which are termed as safety behaviors).
Exposure situations serve a number of different purposes, one of which is providing an opportunity to practice goal setting and re-evaluate social standards. For
this purpose, the therapist should discuss with the patient what the social expectations (standards) of a given situation might be, and should help the patient to
state at least one clear (e.g., behavioral, quantifiable) goal (e.g., asking a particular question). At the beginning, it is important to provide very clear instructions
about what the exposure task should look like. The therapist’s role during these
early exposures is similar to that of a movie director who provides the patient with
a clear script of his/her expected behavior. If the situation requires a complex social
interaction (e.g., returning an item to the same sales person minutes after it was
purchased) the therapist should clearly specify when a particular action should be
shown. For example, rather than simply instructing the patients to “return a book
minutes after you bought it,” the therapist should instruct the client to “purchase
the newest Harry Potter book, walk with it toward the exit door, and when reaching the exit doors, turn around, find the same sales person again, and ask for a
refund of this book by saying: ‘I want to exchange this book that I just bought
because I changed my mind.’ ” The goal of this task may be to say this particular
sentence.
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Effective situations for individuals with SAD differ from exposure situations
to treat other phobic disorders. First, it often requires performance of complicated chains of interpersonal behavior during exposure. Second, the SAD patient’s
specific anxiety-eliciting situations are not always “available.” For example, an agoraphobic individual may go for a walk away from home at almost any time, but
the patients with SAD may confront that feared staff meeting only once weekly.
Other situations may occur only sporadically and be beyond the individual’s realistic control. Therefore, in-session exposure, especially at the beginning of therapy, is
recommended. Public speaking or initiating and maintaining a conversation with a
stranger can be easily created in the session. Further along in treatment, it is recommended to conduct in vivo exposures outside the safe environment of the therapist’s
office. Later exposure practices should further specifically target estimated social
cost. Examples of in vivo exposure tasks to challenge this cognitive error are given
below. The patient should be instructed to conduct similar and more individually
tailored exercises as part of his/her homework assignments. A monitoring form will
aid the patient specifically to examine and challenge the perceived social costs and
probability associated with these situations. For example, the patient may be asked
to order a bagel, and then to “accidentally” drop it on the floor, and ask for a new
one (without paying for it) or to go to a local video store, rent a DVD, and immediately return it, saying “I forgot I don’t have a DVD player.” For a more extensive
account, see Hofmann and Otto (2008).
Flexibility for Dealing with Challenging Cases
The exposure assignments should be designed to be challenging for all patients.
With adequate motivation by the therapist, patients should be able to perform the
assigned exposure tasks, even if they significantly violate the patient’s perceived
social norms. Some patients, however, may feel unable to conduct the exposures.
In those cases, the therapist should show the adequate degree of flexibility and
modify the task accordingly. People who severely fear public speaking, for example, might answer simple questions that the therapist or some audience member
ask rather than give an impromptu speech, or they may be asked to simply read a
text paragraph in front of the audience. Conversely, the situation should be made
more challenging if the patient does not experience enough anxiety or discomfort.
For example, the patient may be asked to give a presentation about negative personality characteristics rather than a speech about their hobbies. Simple physical
exercises prior to the exposure task (e.g., push-ups) that induce intense physical
sensations and sweatiness can further heighten the anxiety during an exposure exercise. We believe the optimal level of anxiety during the anticipation phase of a
social task is between 5 and 7 on a scale from 0 (no anxiety) to 10 (extreme
anxiety).
Homework practices, and especially the lack thereof, are another significant
challenge to treatment. As part of the homework assignments, patients are asked
Avoiding Treatment Failures in Social Anxiety Disorder
181
to perform behaviors or place themselves in situations that were previously avoided
or tolerated only with excessive anxiety. If the patient repeatedly refuses homework
assignments, the therapist should discuss the importance and negotiate attainable
goals and practices. During these discussions, patients should be told that homework is a very important element of this treatment and that not doing the homework
is a form of avoidance. At the same time, successful exposure practices, or even
simple but honest attempts, should be rewarded by the therapist. Moreover, patients
should be asked to reward themselves by doing something special or buying something if they did engage in the exposure practice. Discussion of the homework is
an opportunity to reinforce successful behavior and for the therapists to identify the
parameters of the patient’s feared situations. In addition, it provides an opportunity
for the therapists to reinforce the model.
Summary
SAD is a common and debilitating disorder. Traditional CBT approaches have
shown reliable effects that are comparable to pharmacologic interventions and
superior to psychological and pharmacological placebo treatments. More recent
CBT protocols that have been specifically tailored to SAD demonstrated effects
that appear to be stronger, although comparative treatment trials are lacking.
Nevertheless, there is still considerable room for improvement. So far, empirical
studies have failed to reliably identify predictors of poor treatment response or treatment complications, such as the generalized subtype, avoidant personality disorder,
depression, and social skills. Instead, treatment complications may arise if patients:
(1) lack treatment motivation and are deficient in setting appropriate treatment goals;
(2) show cognitive errors that enhance social anxiety in response to actual or imagined social threat; and (3) exhibit avoidance strategies that lead to the maintenance
of social anxiety. It is recommended to flexibly tailor CBT approaches to the individual patient and idiosyncratic psychopathology in order to maximize treatment
efficacy and minimize or resolve treatment complications.
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Avoiding Treatment Failures in Generalized
Anxiety Disorder
Evelyn Behar and T.D. Borkovec
Resolving Treatment Complications in Generalized
Anxiety Disorder
Generalized anxiety disorder (GAD) first appeared as a diagnosis in the third edition
of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III; American
Psychiatric Association (APA), 1980). Since that time, programmatic research on
the nature of worry and GAD has led to advancements both in its diagnostic criteria
and in its treatment. With the publication of DSM-III-R (APA, 1987), the primary
defining symptom of GAD became excessive anxiety and worry about more than
one topic. Later, DSM-IV (APA, 1994) retained excessive worry as GAD’s cardinal
feature and further stipulated that the worry must be difficult to control. GAD is
highly comorbid with other Axis I conditions, particularly with other anxiety and
mood disorders (Kessler, 1997; Noyes et al., 1992). Thus, its pervasiveness in other
conditions makes the thorough understanding and successful treatment of worry an
important aspect of mental health care in general.
Although cognitive-behavioral treatments for GAD have been shown to be effective in treating this condition (Borkovec & Ruscio, 2001) and in reducing symptoms
of comorbid Axis I conditions (Borkovec, Abel, & Newman, 1995), cognitivebehavioral therapy (CBT) alone evidences only a 50% rate of high end-state
functioning among treated patients (Borkovec, Newman, Pincus, & Lytle, 2002).
Consequently, knowledge resulting from (a) research on predictors of treatment
responsiveness and (b) laboratory investigations on the etiology and maintenance
of GAD has been applied in attempts to increase the efficacy of traditional CBT
techniques. In this chapter, we will describe traditional cognitive and behavioral techniques, as well as more recent approaches incorporating emotional and
interpersonal therapy, mindfulness-based therapy, metacognitive therapy, emotion
regulation therapy, and therapy focused on increasing tolerance of uncertainty.
E. Behar (B)
University of Illinois, Chicago, IL, USA
e-mail: ebehar@uic.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_11,
C Springer Science+Business Media, LLC 2010
185
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E. Behar and T.D. Borkovec
Moreover, we focus on the resolution of complications in treatment by identifying
predictors of poor response to treatment and highlighting methods to increase
efficacy of treatment for those individuals.
Predictors of Response to Treatment
Knowledge regarding the individual differences that may enhance or compromise
responsiveness to treatment can assist in the development of treatment packages that are able to successfully treat a larger percentage of GAD patients.
Newman, Crits-Cristoph, Connelly Gibbons, and Erickson (2006) conducted a
review of the participant factors that predict responsiveness to treatment for anxiety. Among demographic variables, gender (Gould, Otto, Pollack, & Yap, 1997;
Tyrer, Seivewright, Ferguson, Murphy, & Johnson, 1993) and intelligence (Haaga,
DeRubeis, Stewart, & Beck, 1991) do not seem to be significant predictors of
treatment outcome for GAD patients. On the other hand, findings show that high
socioeconomic status predicts maintenance of treatment gains over 12 months following GAD treatment (Durham, Allan, & Hackett, 1997) and is associated with
less severe GAD symptoms during the treatment phase (Tyrer et al., 1993). Also,
research indicates that older patients (over 35 years of age) are less likely to drop
out of treatment (Edlund et al., 2002), suggesting that therapists treating younger
patients may want to pay special attention to building a strong alliance, addressing
and mending alliance ruptures, providing a believable rationale for treatment, and
addressing patients’ motivation difficulties in therapy.
Data on whether severity of GAD symptoms appears to be a predictor of treatment outcome are mixed. Although three studies suggested that patients with higher
self-reported anxiety (Butler & Anastasiades, 1988), assessor-rated anxiety (Butler,
1993), and clinician-rated global severity and number of symptoms (Yonkers, Dyck,
Warshaw, & Keller, 2000) at pre-treatment responded less well to therapy, a host of
other studies failed to find a relationship between outcome and symptom severity as
rated by assessor (Barlow, Rapee, & Brown, 1992; Butler, 1993), Hamilton Anxiety
Scale (Barlow et al.; Biswas & Chattopadhyay, 2001; Durham et al., 1997), or selfreport (Barlow et al.; Durham et al.; van den Brink et al., 2002). Research on whether
duration of symptoms, or chronicity, predicts treatment outcome is less equivocal.
Longer duration of GAD has been shown to predict worse outcome from treatment
(Biswas & Chattopadhyay, 2001; van den Brink et al.). Furthermore, the presence of
comorbid Axis I conditions seems to predict poor response to therapy. For example,
patients are more likely to maintain treatment gains if they lack a comorbid Axis
I diagnosis in general (Durham et al.) or comorbid dysthymia or panic disorder
specifically (Tyrer, Seivewright, Simmonds, & Johnson, 2001).
Certain cognitive variables have also been found to predict response to treatment
in GAD. Butler (1993) found that the degree to which ambiguous external information is interpreted as threatening predicts outcome in patients being treated with
CBT. Also, high internal locus of control predicts positive response to treatment
Treatment for GAD
187
following cognitive therapy for GAD (Biswas & Chattopadhyay, 2001). Together,
these findings suggest that cognitive therapy may be useful in the treatment of GAD
symptoms, particularly among patients with interpretive biases and external loci of
control.
Finally, several areas of research on predictors of treatment response converge
to suggest that interpersonal problems predict a poor response to treatment among
GAD patients. First, Borkovec et al. (2002) found that interpersonal problems
remaining at treatment termination predicted poor outcomes at post-therapy and
follow-up assessments. Second, personality pathology seems to play a role in
response to therapy. Sanderson, Beck, and McGinn (1994) found that patients with
Axis II diagnoses were more likely to drop out early from cognitive therapy for
GAD. Tyrer et al. (1993) reported that personality disorder traits were associated
with poorer response to cognitive therapy and self-help treatments among GAD
patients. Also, findings from longitudinal studies suggest that cluster B (Yonkers
et al., 2000) and C (Massion et al., 2002; Yonkers et al.) personality disorders are
associated with diminished likelihood of remission from GAD. Third, research on
the effects of social support converges with the above findings on interpersonal relationships. Durham et al. (1997) found that married (as opposed to single, widowed,
or divorced) patients are more likely to show sustained improvement following treatment for GAD, and that among married patients, high levels of marital tension are
associated with lower sustained improvement from treatment. These findings suggest that a focus on interpersonal functioning may be highly valuable in treating
chronic worriers who present with troubled relationships, personality pathology, and
limited social support systems.
Throughout the course of this chapter, we will highlight some of these and
other predictors of treatment response and, where appropriate, suggest methods for
treating individuals whose characteristics may make them less responsive to traditional cognitive-behavioral techniques. Also, as will be evident below, there are a
number of variations by which treatment can be targeted and delivered, focusing
alternatively on exposure interventions, cognitive interventions, and modification
of autonomic functioning. At the present stage of the literature, the best guidance is
that all of these strategies have efficacy, and when treatment resistance is confronted,
consideration of alternative strategies within the domain of these interventions is
warranted.
Theoretical Conceptualization of Worry
The avoidance theory of GAD is explained in detail by Borkovec, Alcaine, and
Behar (2004). Theoretical conceptualizations of GAD rest largely on Mowrer’s
(1947) two-stage theory of fear. Mowrer proposed that fear emerges via classical
conditioning and is maintained via operant conditioning in the form of negatively
reinforced behavioral avoidance of conditioned fear stimuli. Mowrer’s theory is the
foundation of traditional exposure-based treatments for anxiety disorders, which
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E. Behar and T.D. Borkovec
seek to decrease anxious reactions to feared stimuli by repeatedly exposing individuals to those stimuli while preventing avoidance responses that would otherwise be
negatively reinforced by temporary reductions in that fear.
According to the avoidance theory of worry, GAD differs from the other anxiety
disorders in a key way. Whereas all of the other anxiety disorders are often characterized by motoric avoidance of feared stimuli, GAD patients do not typically avoid
disorder-specific, discrete situations or stimuli. Instead, threat exists in the nonexistent future, and there is therefore no behavioral avoidance response at the worrier’s
disposal. To satisfy the need to take immediate action to cope with this threat in
the absence of behavioral options, patients utilize cognitive avoidance (trying to
come up with ways to prevent the bad outcomes or to prepare oneself for them) in
response to threatening material. As a predominantly verbal-linguistic (as opposed
to imagery-based) phenomenon (Behar, Zuellig, & Borkovec, 2005; Borkovec &
Inz, 1990), worry is remote from physiological and affective experience, and a
period of worrisome activity has an inhibitory effect on physiological reactivity
during subsequent anxiety-provoking tasks (e.g., Borkovec & Hu, 1990). Given
the central role of physiological reactivity to emotional processing (Foa & Kozak,
1986), worry’s inhibitory effects therefore are hypothesized to prevent successful
emotional processing of fear and thus preclude anxiety extinction.
Patients with GAD are stuck in a variety of non-adaptive, habitual, and nonflexible ways of thinking, behaving, and experiencing emotion. Our approach to treating
GAD stems from the cognitive avoidance conceptualization of worry, and from our
understanding of the specific cause-and-effect relationships that contribute to the
etiology and maintenance of these non-adaptive habits. Therapy techniques target
those relationships in order to maximize the efficacy of interventions. The overall
goal of these techniques is to replace automatic, anxiety-maintaining spirals with
more adaptive, flexible, and anxiety-incompatible responses. Therapists encourage
patients to repeatedly rehearse coping skills both in session and in their daily lives
so that these alternative responses become habitual. Initial coping skills provide
stepping stones for later therapeutic work. By loosening up their rigid, maladaptive
behaviors, cognitions, and emotions, patients create new, less threatening meanings
and develop more flexible ways of behaving, thinking, and feeling. As laboratory
investigations have led to increased knowledge about the nature of worry, the development of interventions for GAD has focused on targeting non-adaptive areas of
functioning for the GAD patient. The foundation of current cognitive-behavioral
treatment entails teaching patients to objectively observe, or self-monitor, their
physiological functioning, behavioral responses, cognitive processes (thoughts and
images), interpersonal behaviors, and emotional experiences. By providing patients
with interventions targeting many or all of these relevant response systems, the ultimate goal is to cause change within the whole, cohesive organism, so that patients
can achieve freedom from ruminative worrying, experience adaptive thoughts and
emotions, and have an enhanced ability to experience and process each moment
of their lives as it occurs in the present moment. Below, we discuss each of
these areas of functioning and describe the techniques designed to treat them
effectively.
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Self-Monitoring
The cognitive world of chronic worriers is rigidly focused on threat. Worriers spend
large amounts of time engaged in rumination about potential future catastrophes,
they are frequently detecting threat cues in their immediate environments (Bradley,
Mogg, White, Groom, & de Bono, 1999), and they often interpret ambiguous information as threatening (Mogg, Bradley, Miller, & Potts, 1994). As a result of their
attentional resources being spent predominantly on the detection of threat, worriers’
awareness of their present-moment reality is compromised. Furthermore, given that
the success of treatment in part depends on patients’ ability to attend to internal and
external states so that they can implement therapeutic techniques at the appropriate
moments, such non-adaptive patterns of awareness must be targeted as an initial step
in treatment.
The first step in treating non-adaptive awareness is to equip patients with selfmonitoring skills. In self-monitoring, the therapist helps the patient to learn to attend
to his/her internal experiences and external environments and to become familiar
with how different response systems interact with one another. Patients are asked to
notice all thoughts, emotions, behaviors, and physiological experiences surrounding
a particular situation and to note the consequences of these responses. By becoming more attuned to their automatic responses and how these responses relate to one
another and to external situations, patients can become familiar with how their anxiety spirals and where and how in the sequence they can intervene. Take, for instance,
the following exchange between a patient (P) and her therapist (T) after they established that one of the patient’s most common triggers for worry and anxiety was
waiting for her children to get home from school.
T: Adele, I’d like to help you get into the habit of being very aware of what
happens before, during, and after an intense worry episode like the one you
just told me about. If you’re comfortable doing so, close your eyes for a few
moments and try to imagine the scene you just told me about from yesterday.
Imagine yourself sitting at your desk in your office. It is 2:45 pm – about
15 min before your kids are due home. Tell me what you see in the image
before the worry sets in.
P: I can see my desk, and my computer. I can also see my telephone very
clearly; it almost seems to be the focus point of the picture I’m conjuring
up. I am trying hard to focus on the email I need to write and send out, but
my eyes just keep wandering to the telephone. It’s almost like I’m willing
the phone to ring. I want to know that the kids are safely in the house, and
that nothing bad has happened to them.
T: Good. Try to stay with that image as much as you can, and continue seeing
it in your mind’s eye as vividly as possible. Tell me what is going on for you
internally in the situation at that moment.
P: I feel myself getting very nervous, and starting to worry that something awful
has happened to the kids. I imagine my youngest child run over by a car. I
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T:
P:
T:
P:
pick up the phone and call the house to see if they’re home yet, but there’s no
response. I start to get even more worried and I call my husband, check the
local news online, and make sure I have the phone number to the elementary
school.
As you’re saying this, I can see how worried you become before
3:00 pm every day. You seem to go straight for the catastrophic thinking,
landing on all sorts of awful possibilities of what may have happened.
Tell me, as you’re thinking about this scene, what do you notice in
your body?
I can feel my shoulders and my back – they’re very tense, even here and now.
I also feel a knot in the pit of my stomach, and I notice myself remembering
all sorts of awful news stories about children who have been kidnapped or
run over. I feel guilty that I’m not picking them up from school myself. . .that
instead, I have a job and a life away from them.
OK, so physically, you feel tension and I can also see from here that you are
furrowing your brow and clenching your jaw. Your thoughts focus on your
quality as a mother and on thoughts of bad things happening to your kids.
Also, you mention that you engage in some checking behaviors to decrease
your worry – doing things like calling your husband. What do you notice as
a result of that? What does it feel like the moment you get off the phone with
him?
I feel better for about five seconds, because he seems to be calm and hasn’t
heard of any accidents, but I immediately just start to worry again when
I begin to think of all the other possible sources of information I haven’t
checked. I just get more and more tense. Then I look at the phone, and the
email I was trying to write, and start to worry all over again.
In this exchange, it is clear that the patient’s anxiety spirals out of control when
faced with this daily event. By imagining the scenario and the sequence of events
in this and similar situations, and by generating anxiety in the session to identify
specific events and reactions, the therapist can work with the patient to identify
how the patient’s anxiety develops from moment to moment. Therapists should
encourage their patients to catch the anxiety spiral early (in this patient’s case, the
therapist might ask her to monitor her internal state beginning much earlier in the
day in order to detect precisely when the first hint of worry and anxiety begins in
anticipation of the 3:00 pm call).
Therapists should also help patients to understand the causal relationships
between thoughts, feelings, and behaviors. In the exchange above, for instance, the
therapist might help the patient come to the realization that her anxiety is not merely
an effect of the fact that her children have to get themselves home safely. She is creating much of her own anxiety by her checking behavior, her catastrophic images,
her automatic thoughts, her physiological tensing reactions, and her attempts to distract herself by composing an e-mail. This may be especially useful for patients
who have a strong external locus of control and therefore may believe that there is
little they can do to change their patterns (a negative predictor of treatment response;
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191
Biswas & Chattopadhyay, 2001). By becoming aware of their own contributions to
their anxiety, they may be more likely to believe that they can exert control over it.
As part of self-monitoring, therapists should frequently ask patients to use a 0–
100 scale to rate the degree of tension, anxiety, and distress they experience moment
to moment in the session. When therapists see or infer an increase in a patient’s
anxiety as issues are being discussed, they can ask “What is your number now?” in
order to quickly gather information about shifts in the patient’s state. This allows
therapists and patients to more accurately identify precursors and consequences of
anxiety, as well as to identify early stages of the anxiety spiral. This scale is also used
later to assess in-session impacts of new techniques being deployed (e.g., applied
relaxation, generation of new cognitions).
Self-monitoring provides an introduction to patients about focusing on the
present moment. By attending to the immediate reality of the world around them,
they can observe themselves and their environments objectively. They learn to
accurately process information in the present and to open their awareness to this
information. As therapy progresses, patients are encouraged to begin observing all
of the information contained in the present moment, especially positive information.
In contrast to their usual attention to negative aspects of the environment, which
contributes to confirmatory biases that bad things will happen in the future (Faust,
1984), patients learn a more balanced processing of the present in which they can
flexibly choose whether or not they want to attend to negative elements. Making the
choice to attend to what actually exists frees them from their automatic responses
and promotes genuine experiences – a connectedness between the environment, the
self, and emotion. As discussed later, self-monitoring is also useful in teaching and
facilitating emotional processing. Patients learn to attend to and fully process all
emotions that occur in reaction to present-moment events. By generating perspectives that cultivate approach to daily life and joy in its engagement, patients are more
likely to process positive, value-directed information.
Relaxation Training
Unlike patients with other anxiety disorders, who show sympathetic activation when
confronted with feared stimuli, GAD patients show a suppression of sympathetic
activation during worry and during anxiety-eliciting stimuli following worry periods (Borkovec & Hu, 1990). Along with sympathetic reductions, worriers show
reductions in cardiovascular variability indicative of parasympathetic deficiency
(Hoehn-Saric, McLeod, & Zimmerli, 1989; Thayer, Friedman, & Borkovec, 1996)
as well as reduced EMG variability (Hazlett, McLeod, & Hoehn-Saric, 1994). The
only physiological elevation evident in GAD patients is in muscle tension (Hazlett
et al.). Both this muscle tension and the parasympathetic deficiency are addressed
in treatment by the use of applied relaxation training. Progressive muscle relaxation
(PMR) and slowed, paced diaphragmatic breathing are two powerful methods that
can help patients cultivate physiological and psychological states opposite to those
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induced by worry and anxiety, both throughout the day in order to reduce baseline
anxiety and in response to incipient anxiety spirals.
In PMR, patients are taught to tense and then let go of the tension in a variety of
muscle groups. Scripts for guiding patients through PMR are available (Bernstein,
Borkovec, & Hazlett-Stevens, 2000), and focus initially on 16 muscle groups that
are combined gradually over sessions. One of the goals patients and therapists work
toward is to eventually be able to induce a relaxed state without employing muscle
tension at all, but rather by merely recalling states of relaxation. PMR can help
patients develop greater ability to quickly decrease tension levels as soon as they
are detected within the anxiety spiral. Furthermore, PMR can help patients create
a pleasant present moment, which they can recall as they practice “letting go” of
tension, negative thoughts, and catastrophic images.
Patients are also trained in diaphragmatic breathing methods. Unlike PMR,
which requires patients to set aside time to complete the exercises, diaphragmatic
breathing can induce a relaxed state in a very short period of time. Slowed, paced
breathing through the diaphragm is compared in session to shallow, rapid chest
breathing. Therapists can use the 0–100 rating scale to communicate regarding
the degree of tension and anxiety patients experience during each type of breathing. Diaphragmatic breathing can be a powerful tool in demonstrating to patients
that they have the power to create positive physiological and emotional states in
themselves very rapidly and even during situations that previously elicited anxiety
and worry.
Finally, patients are taught to practice engaging in relaxing imagery and in meditational techniques for relaxation. They are encouraged to shift flexibly between all
of the relaxation techniques at their disposal so that they can use whichever techniques work best in specific circumstances, and as a way of encouraging a flexible,
non-rigid lifestyle.
One complication that may arise in treatment is that particular patients may
become increasingly anxious as a result of relaxation training. Research on
relaxation-induced anxiety (RIA) shows that patients who become anxious during
PMR show poorer responses to therapy (Borkovec, Mathews, Chambers, Ebrahimi,
& Nelson, 1987). For this reason, therapists are advised to look for signs of RIA
in their patients and to (a) continuously target (via PMR) those muscle groups
that induce RIA if repeated practice is leading to reductions in RIA, (b) focus primarily on those muscle groups that produce less RIA if symptoms of RIA persist
despite repeated practice, and/or (c) rely more heavily on diaphragmatic breathing
and relaxing imagery for patients who are made anxious by the tensing of muscles.
By practicing their relaxation skills twice per day for 10 minutes each time,
patients can develop the ability to intervene more successfully whenever stressful
or worrisome situations occur. By eliciting these calm states frequently throughout their daily lives, patients become increasingly familiar with this tranquil state,
reduce their background anxiety levels, and apply their relaxation skills upon detection of the earliest signs of impending anxiety and worry, including detection of
the absence of this relaxed state. Using self-monitoring to detect incipient anxiety, patients can implement their relaxation skills to interrupt anxiety spirals.
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193
Furthermore, by inducing calm states frequently throughout the day, patients have
the opportunity to attend to the positive present moment instead of over-attending
to potential threat.
Self-Control Desensitization
In self-control desensitization (SCD; Goldfried, 1971), the vivid imagery and relaxation skills patients learned previously are used in combination to rehearse their
coping responses. Patients are asked to vividly imagine a situation that causes them
to worry and experience high levels of anxiety. While vividly engaged in imagery,
the patient indicates to the therapist (e.g., by a raised finger) when he/she notices
actual anxiety cues beginning to occur. The therapist then encourages the patient to
continue imagining the anxiety-inducing scene, but also to vividly imagine deploying his/her relaxation skills in that scene. The patient continues engaging in this
imagery until anxiety dissipates, at which point the patient indicates to the therapist
(e.g., by lowering the raised finger) that anxiety is significantly reduced or absent. At
this point, the therapist has the patient continue imagining relaxing in the situation
for a little while longer so that the patient further experiences successful relaxation
in the midst of the situation. Finally, the patient is asked to terminate the image
and deepen the relaxed state. This procedure is repeated until anxious responses
decrease quickly upon imagery of using relaxation skills or until the initial anxious
image fails to elicit incipient anxiety cues in the first place.
Once patients begin to learn cognitive therapy techniques for dealing with their
anxieties and worries (described below), during subsequent SCD image presentations they can rehearse both relaxing themselves and shifting their perspectives to
more adaptive ones within the scene.
Stimulus Control
Stimulus control treatments are used for a variety of emotional problems, including
insomnia (Bootzin & Epstein, 2000), issues related to developmental disabilities
(e.g., Falcomata, Roane, & Pabico, 2007), and eating disorders (Linden, 1980).
Stimulus control treatment for worry developed in response to the fact that worry
can occur anytime and anywhere. Thus, worry is under poor stimulus control. It
becomes associated with countless external cues (e.g., time of day, physical location, contact with specific people), and this can in turn make worry especially
easy to elicit, given that individuals are likely to come into contact with at least
some of those external cues quite often. By teaching their patients stimulus control
techniques, therapists can help their patients gradually limit the number of environmental conditions that come to elicit worry. These techniques have been shown
to be effective for chronic worriers (Behar, Tishk, & Zalewski, 2002; Borkovec,
Wilkinson, Folensbee, & Lerman, 1983).
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Two variations on stimulus control treatment can be implemented with patients.
In the first, patients are asked to self-monitor throughout the day so that they can
detect anxiety cues as early as possible, and they are then instructed to postpone
worry to a later half-hour worry period. This half-hour “worry time” is established at a consistent time each day, in a consistent location. During this time,
patients can worry intensely to provide for some habituation, but later in therapy
they are encouraged to use this time instead to engage in effective problem-solving,
employ techniques they learn in cognitive therapy (described later), and use other
coping strategies they learn in treatment. This approach helps patients to develop
greater discriminative stimulus control so that (a) worry does not pervade their lives
throughout the day and (b) they are able to focus on employing effective coping
techniques for their worries in a structured, time-limited setting.
A second stimulus control technique involves having patients establish a “worryfree zone,” a time or place in which they will not worry, letting go of or postponing
the worry to just outside of that zone. Once the patients notice lessened worry in that
zone, they establish a second worry-free zone in some other place or time during
their day. They continue to add additional zones to gradually reduce the number of
situations that elicit worry and anxiety. When patients are in these worry-free zones,
they can employ self-monitoring, mindfulness techniques (e.g., Roemer, SaltersPedneault, & Orsillo, 2006), and any other therapeutic skills that help them remain
focused on the present moment.
Cognitive Therapy
As mentioned earlier, the use of cognitive therapy may be useful in the treatment
of GAD symptoms, particularly among patients with less adaptive cognitive styles
(e.g., those who have strong interpretive biases and who believe that their fate is
guided by external, as opposed to internal, circumstances). GAD patients’ responses
on the Dysfunctional Attitude Scale suggest that they have non-adaptive core beliefs
(Behar & Borkovec, 2002). Cognitive therapy for GAD (adapted from Beck, 1976)
focuses on identifying core cognitions about the self, the past, and the future. To
help identify these non-adaptive cognitions, patients are first encouraged to employ
self-monitoring to detect incipient anxiety cues, and to then record the thoughts
that preceded and followed those cues. By reviewing the themes that run through
these automatic thoughts, therapists and patients can collaboratively challenge and
modify those cognitions and the underlying beliefs that give rise to them. A primary goal of cognitive therapy for GAD is the generation of multiple perspectives.
By generating numerous possible interpretations of an event or predictions of the
future, patients can begin to loosen up some of their inflexible ways of thinking. It
can be helpful in the beginning to introduce the concept of multiple perspectives by
using emotionally neutral situations for brainstorming many ways of seeing the situation without regard for accuracy. Then the creation of multiple perspectives can be
applied to more emotionally relevant material. Take, for instance, the case of Adele,
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the patient who worried uncontrollably about her children’s safety while coming
home from school:
T: This exercise of writing down your thoughts was very helpful, because I think
it helped us identify what some of your knee-jerk reactions tend to be. You
– along with lots of people who struggle with anxiety – seem to fall into, as
you put it, “thinking traps” when things go wrong or when you’re worried
about something. If it’s OK with you, I’d like to try something out. . .a small
exercise. Are you willing to give this a shot with me?
P: Sure.
T: Great. Now, you’ve mentioned in the past that you are an avid runner.
P: Yes, I love running. Sometimes I think it’s the only thing that keeps me sane!
T: I’d like you to imagine that you haven’t run for ten consecutive days. Can
you play the part of an unbiased observer and list for me some reasons why
Adele hasn’t run in ten days?
P: Hmmm. . .you mean you want me to just come up with possible reasons?
T: Yes, that’s right. Just form some hypotheses, without worrying whether they
are accurate or likely or acceptable. I’ll contribute some too.
P: OK. Well, maybe Adele has been very busy. Or maybe she got shin splints
and her doctor told her to lay off for a couple of weeks.
T: Excellent. Maybe Adele has been sick and wants to recover fully before she
gets back into the swing of things.
P: Yeah, or maybe her kids have been ill and she hasn’t wanted to leave them in
the house alone while she goes out.
T: Maybe Adele is tired of running and wants to take a month or two off from
it. . .or maybe even more.
P: Or maybe the weather has been very bad and her treadmill is broken. Or
maybe she is trying to gain a few pounds if she is very thin.
T: Excellent. These are all wonderful possibilities that you’ve generated. Now,
can you do the same thing regarding the consequences of her not running?
Can you generate lots of perspectives about those?
P: Well, she may end up gaining too much weight from not exercising. Or she
may lose lots of muscle and have a hard time getting back into it. Or maybe
she’ll really benefit from the time off and wind up being a better runner
when she starts up again. Maybe she’ll enjoy spending the extra hour with
her children and never go back to it, or maybe she’ll start to feel depressed
and realize that she really needs it in her life.
T: OK, great. Thank you for doing that. You seem to be very comfortable generating lots and lots of ways of looking at one small event or situation. Let’s
shift our focus a bit now and do the same thing with one of your biggest
“thinking traps” from the worry records. You seemed to have lots of kneejerk negative thoughts about the day last week when you had to step out
of your office just before 3:00 pm when your colleague needed you to sign
something and you missed the phone call from your kids letting you know
they were home safely. Here in your worry record, you wrote, “I am a bad
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P:
T:
P:
T:
P:
T:
P:
T:
P:
T:
P:
T:
P:
T:
mother. . .If it had been an emergency I would not have been available and
something awful could have happened. . .My children may end up thinking
I am not there for them.” What I’d like to do now is have you again play
the part of the unbiased observer and generate lots of ways of looking at this
situation. Let’s not pass judgment on any of them, or worry too much about
whether they are right or wrong. Let’s just come up with lots of ways of
looking at it.
[Hesitating]. . .This is harder to do when it’s something I feel really strongly
about.
Yes, this is definitely tougher. Why don’t you start with one, and I’ll
contribute one too. Remember to take the stance of the casual, unbiased
observer; that may help you think about it more easily.
OK. Well, I guess I could make the obvious statement that Adele simply had
to step out for a minute, and that stepping out for a minute doesn’t make her
a bad mother.
OK, that’s good. How about this: By not being responsive to colleagues’
needs or by not signing things on time, Adele might be viewed as a less
competent worker, which may influence her job satisfaction and therefore
her ability to be emotionally present for her kids.
It’s also possible, of course, that Adele is a bad mother, and puts her work
before her kids’ safety.
Yep, that’s a fair one to bring up, certainly. Can you come up with another
one?
Hmm. Well, maybe by not always being immediately available, Adele’s kids
can learn to be more independent.
I’ve got one, too: Maybe the kids can leave a voice mail, and Adele will get
the message as soon as she returns to her office.
Or maybe something is wrong, but they can call back.
OK, I think we could probably come up with another dozen interpretations,
but let’s stop there for now. What was that experience like for you?
A little weird. Usually, when something like that happens, I just think of 3
or 4 really bad things that led up to it or that can come of it, and then I get
worried and start all of my usual behaviors of checking the news, calling my
husband, and getting frantic. This didn’t seem natural for me.
I can imagine that it would feel very foreign for something so emotional and
anxiety-provoking, and for someone who doesn’t generally follow that train
of thinking.
At the same time, though, I found myself believing some of those, you
know? Like. . .maybe it will make my kids a little more independent if I’m
not always there checking up on them.
Wow, we went from “I’m a bad mother if I’m not immediately available” to
“Maybe I’m a bad mother if I am always immediately available.” It’s almost
hard to know which is accurate. . ..they’re both kind of believable at some
level. But that is precisely the most important part of this exercise.
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P: I think I know what you’re getting at. Just because I have a knee-jerk reaction, doesn’t mean my knee-jerk reaction is right. I guess in some ways, there
is no way to know which reaction is the right one to have. Maybe they are
all a little right and a little wrong.
In this exchange, we can see that the patient’s rigid thinking begins to slowly
loosen up. She will undoubtedly need to practice this many times (including
rehearsals within SCD) before it can become more habitual. However, in this
instance, by completing the exercise only once, she was able to reach the conclusion that just because she has a thought, it does not mean that the thought is
accurate, and indeed that it is not possible to know which thoughts are accurate
or inaccurate. As cognitive therapy progresses and the patient becomes increasingly skilled at generating multiple perspectives, the therapist can help the patient
to choose useful perspectives among the various ones generated by assessing their
relative accuracy, their advantages and disadvantages in the patient’s life, and each
perspective’s impact on the patient’s emotional functioning.
Therapists can further aid cognitive change by employing the Socratic method to
challenge patients’ automatic thoughts, as well as a host of other traditional cognitive therapy techniques. For example, when patients are catastrophizing about the
outcome of a worry, repeatedly asking “What would be so bad about that?” can
help them identify the worst potential outcome of their worry. Therapists can help
patients come to the conclusion that even the realistic worst-case scenario is often
better than what they had anticipated, and that they have the skills to effectively
cope with negative outcomes. This can also be achieved through the use of worry
outcome diaries, in which patients record four things: their worries; what the outcomes of those worries are; whether the actual outcomes, when they occur, were
better, equal to, or worse than they had initially anticipated; and, in the case of worries that came true, how well they were able to cope with the outcome. As a result
of this technique, many patients find that the majority of their worries do not come
true, and when they do, patients are able to cope with the outcomes better than they
expected (Borkovec, Hazlett-Stevens, & Diaz, 1999).
One complication that may arise during cognitive therapy for worry is the
patient’s espousal of positive beliefs related to worrying. Specifically, many patients
report the beliefs that worrying actually makes it less likely that negative outcomes
will occur, that worry motivates them to take action, and that worrying prepares
them to cope with the worst-case scenario (Borkovec & Roemer, 1995). One cognitive technique that specifically targets such positive beliefs about worrying is the use
of ABAB single-subject designs. Adapted from Barlow and Hersen (1984), patients
employing ABAB designs are encouraged to engage in a task that typically engenders worrisome thinking while worrying and while not worrying and to rate their
anxiety and performance throughout the course of the exercise. The goal is for
patients to employ a scientific approach to evaluate whether worrying actually does
have positive effects on their performance or affects whether good or bad outcomes
eventually occur. When used in the Penn State GAD treatment program, patients
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have routinely reported that they are less anxious during the tasks when not worrying and are able to perform the tasks as competently and efficiently (often more so)
when they are not worrying compared to when they are worrying.
Another cognitive technique aimed at reducing positive beliefs about worry is
to conduct a cost–benefit analysis of worrying. Two possible foci of cost–benefit
analyses are to (a) help patients recognize the advantages of producing small reductions in negative affect resulting from worrying relative to the disadvantages of the
distress caused by worrying about events that infrequently occur and to (b) help
patients compare the likelihood of a worry actually coming true to the emotional
energy spent on that worry. To illustrate this latter technique, consider, again, our
patient who worries about her children’s safety after school:
T: We’ve talked a lot about your levels of worry between 2:30 and 3:00 pm every
day, and how distressing it can be for you. I imagine that half hour period
every day is just torture for you.
P: You said it – it’s pure torture. It’s like living through hell, imagining all the
terrible things that might be happening to my kids. Honestly, you would
think that if it’s so terrible a feeling, I’d be motivated to not worry so much!
T: Do you ever think that worrying is having some positive effect?
P: You know, it’s funny you should say that. I worry all the time, and nothing
has happened to them so far. So sometimes I’m afraid that if I stop worrying,
it’ll cause the bad stuff to finally happen. I’ve never really said that out loud
before. Geez, that really sounds crazy.
T: Actually, you’re not the first person to believe that worrying has some positive
effects. I wonder, though, if we were to really examine the effect of worry –
if we were to submit it to a bit of a cost-benefit analysis – how it would do.
P: What do you mean?
T: Well, let’s take your biggest worry – that on the way home, a car will hit your
son, since you say he’s sometimes absent-minded when crossing the street.
On a scale of 0–100, how likely do you think it is that a car will actually hit
him?
P: Probably about 2%.
T: How likely do you think it is that he’ll be killed as a result?
P: About 1%.
T: OK, so we’ve got a 1–2% chance that your worst worry will come true,
correct?
P: That sounds about right.
T: Now, if you had to estimate, again using our 0–100 scale, how upset you get
for that half hour each day, what number would you give it?
P: I’d say about a 90.
T: So it sounds like you’re investing 90% of your emotional energy on
something that is 1 or 2% likely to happen.
P: Oh boy [laughing]. That’s not good. That’s pathetic.
T: Well, let’s not pass too much judgment on it. Let’s just be unbiased observers
of this assessment.
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P: Can I play devil’s advocate?
T: Of course. Please. . .
P: Well, maybe the cost of my getting upset is, you know, much higher than
the likelihood of Joey actually getting killed in an accident. But if he did get
killed, well, I’d be upset at about a 300 out of 100. And if worrying helps to
fend that off, then getting upset at a 90 is worth it!
T: Ah, I see, so you’re saying that you’re more than willing to suffer at a level
of 90 every day for 30 min if it decreases the likelihood of suffering at a 300
for the rest of your life.
P: Yep.
T: Well, I can certainly see where you’re coming from. I wonder, though, if the
picture looks the same when we consider how realistic it is that the worry
is actually having a positive effect. Let me ask you this: How much do you
really believe that your worry is keeping him safe?
P: Hmm. Well, rationally, I know it’s not. It’s more of an emotional thing.
That makes me think of all the times you’ve said that just because we feel
something, doesn’t make it true.
T: Obviously, there are some potential pros and definite cons here to the worry.
Can you step away from the emotionality of it for a moment and evaluate it,
again, as an unbiased observer? What’s the verdict on this worry?
P: I think I know what you mean. Chances are, Joey will live to see adulthood whether I worry or not. Meanwhile, I’ll have been a mess for all those
years, all for no good reason. Because I bet if I magically stopped worrying
tomorrow, he’d be no worse off every day on the way home from school. I’ll
probably never see that 300, and meanwhile I’m giving myself a daily dose
of 90.
In this exchange, one can see how strongly the patient holds on to her positive
beliefs about worrying. She is willing to suffer each day for the sake of avoiding
much more intense negative emotions if her worst fear were to come true. However,
when the therapist asks her to conduct an assessment of how effective she thinks
her worry is in having positive effects, she comes to realize that the combination of
(a) daily suffering and (b) low likelihood of a pay-off resulting from that suffering
simply does not tip the scales in the direction of benefit over cost.
Interpersonal and Emotional Processing
Given the limitations of CBT in achieving high end-state functioning among a large
number of patients, clinical scientists have utilized knowledge gained from research
investigations to develop adjunct treatments for GAD that may increase the number
of individuals who benefit from therapy. One such finding is that chronic worriers
who present with troubled relationships, personality pathology, and limited social
support systems may not benefit as much from therapy, suggesting that attending to
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interpersonal problems may be a fruitful path to helping chronic worriers. Although
no specific studies on emotional deficits as predictors of treatment response exist,
extant research suggests that targeting the emotional lives of individuals with GAD
may be fruitful. For instance, alexithymia studies in GAD suggest that worriers
have trouble identifying and describing their emotions (Yamas, Hazlett-Stevens,
& Borkovec, 1997), and research on GAD patients’ reactions to emotions suggests that they are fearful of emotional experiences (Mennin, Heimberg, Turk, &
Fresco, 2005) and find emotions to be aversive (Turk, Heimberg, Luterek, Mennin,
& Fresco, 2005). As mentioned earlier, the avoidance theory of GAD posits that
worry is remote from somatic and emotional experience, and that worry’s inhibitory
quality precludes emotional processing of fear cues (Borkovec et al., 2004).
In interpersonal and emotional processing therapy (IEP; Newman, Castonguay,
Borkovec, & Molnar, 2004), therapists help patients improve their functioning in
two major areas, namely interpersonal relationships and the depth with which they
experience authentic, primary emotion. In interpersonal therapy for GAD, therapists
and patients together conduct a functional analysis of interpersonal behavior, paying
close attention to behaviors that increase or decrease the likelihood of fulfilling interpersonal needs and of maximizing the quality of their relationships with significant
others. The therapeutic relationship is also used as an important sample of patients’
behaviors in their everyday lives, and the therapist provides valuable, constructive
feedback on how a patient’s behavior impacts the therapist in the moment. Through
this feedback, patients learn about natural contingencies and have the opportunity
to practice new skills within a safe context in which the significant other (here,
the therapist) provides genuine feedback and positive regard. Patients then practice these new behaviors in their actual relationships and conduct assessments of
which behaviors are successful at helping them attain their goals and satisfy their
interpersonal needs.
In emotional processing therapy for GAD, therapists help patients to undergo
repeated exposures to emotional experiences. The goal is to help patients to become
increasingly comfortable with both positive and negative affect, which helps them
both to experience and express more authentic emotions in their lives and to identify
underlying interpersonal needs which facilitate the development of effective interpersonal behaviors. Therapists may employ several techniques from experiential
therapy to help patients to deepen their emotional experiences. For example, in the
empty-chair technique, the patient has the opportunity to communicate with a significant other (whom he/she can imagine sitting in the “empty chair”) regarding an
issue that may elicit strong emotions in the patient.
Researchers at Penn State recently completed an investigation examining the
effects of adding IEP therapy to CBT (CBT+IEP), as compared to CBT plus supportive listening (CBT+SL, where SL was used to control for various common
factors related to therapy). Preliminary analyses indicate that the addition of IEP
to CBT does not enhance efficacy of treatment as measured by most of the primary
outcome measures, although 24 months after treatment termination this combined
condition did evidence a significantly higher rate of high end-state functioning.
Treatment for GAD
201
Although these results prevent us from routinely recommending the use of IEP therapy with all GAD patients, these techniques may be useful for individual patients if
functional analysis of those patients’ behaviors indicates that these areas of functioning are maladaptive, contribute to the patient’s anxiety, and are appropriate targets of
intervention. Within this clinical trial, for example, it was found that patients who
had highly dismissive attachment styles assessed at pre-therapy and received the
IEP component had significantly better post-therapy and follow-up outcome than
all other patients, whereas those who did not have enmeshed relationships with
their primary care-giver in childhood did particularly well when IEP was part of
their treatment (Newman, Castonguay, Fisher, & Borkovec, 2008).
A further example is given below in the case of our patient, Adele, who is discussing with her therapist a common interpersonal pattern that the therapist has
noticed:
T: Adele, with your permission, I’d like to take a few moments to make an
observation about our interactions. It’s something that I’ve noticed over the
course of our meetings, and I’d like to bring it out in the open so that we can
discuss it. Sometimes when we’re talking about emotional issues in here –
whether it’s about your relationship with your mom, or your marriage, or
even about how you feel about your sister’s death – it sometimes almost
feels like you’re not completely “here.”
P: I don’t understand. You’ve asked me to talk about those things, and
I have.
T: Yes, you definitely have, and I know it’s been hard for you to discuss some of
those tough issues. Maybe I’m not being very clear about what I mean. . .let
me try harder, with a more concrete example. Last time, about halfway
through our session, I thought there was a moment when we had a “disconnect” of sorts. The way I remember it – and please speak up if you think
I’m not doing it justice, or misremembering it – you were talking about your
sister’s death. At some point, you sort of shifted to a different topic. . .I think
we somehow started talking about the political elections. . .and I tried to redirect the conversation back to talking about your sister. I couldn’t tell exactly
what had happened, but it felt from my end that you had become frustrated
with me. And, thinking about it later, I realized that in twelve sessions we’ve
always briefly mentioned your sister’s death, but we’ve never really discussed
it in detail. The truth is, this is an enormous part of your emotional life, and
I don’t know much about it. The topic seems to be a slippery one, and we
seem to often lose our hold on it.
P: Well, you know, talking about her is really hard.
T: I can only begin to imagine just how hard it is. Did you feel that I was being
too pushy last time?
P: It’s not just that. I mean. . .sometimes I think about her, and I just. . .I miss
her a lot. Talking about her is hard, because it makes me remember her and
miss her. She was my closest friend, and it sometimes feels like I can’t find
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E. Behar and T.D. Borkovec
T:
P:
T:
P:
T:
P:
T:
P:
T:
P:
T:
P:
anyone who understands me the way she did. [Patient getting choked up,
with tears in her eyes.]
You know, there is something about sibling relationships that’s really special.
Siblings, in many ways, are our first friends.
Yeah. You know, I look at my kids sometimes and watch them playing or
fighting or negotiating something, and it’s kind of funny to see them like
that. [Patient brightens up a bit.] The other day, Joey and Hannah were
watching cartoons, and I could hear them laughing from the other room.
They’ve gotten really into this new cartoon on TV, and they wait all day
until 5 pm to watch it. My husband had the brilliant idea of using it as a
reward or punishment, and I don’t think he’s had this much power over them
in ages!
Adele, I’d like to bring us back to chatting about your sister. I can’t help but
feel again like we’ve slipped away from that topic. I know it’s hard to focus
on, but I just can’t help but notice that when we go there, you seem to run
away.
[Pause. . .] I’m afraid to think about her. I’m afraid it’ll be just like the year
after her death, when she was all I could focus on.
I can understand that. It must be a scary feeling. I can tell that you loved
your sister a lot.
[Crying openly now.]
Tell me what you’re feeling right now.
So many things. Love, sadness, longing, anxiety, guilt. I’m thinking about
my wedding, when she went out of her way to make everything so special
for me. I’m thinking about the birth of my first child, when she held my hand
in the hospital room as I pushed. I’m thinking about all the times she got on
a train to come see me when I needed her, and all the times I went down to
Virginia when she needed me. I’m thinking about our coffee dates, and the
time we went to see the Phantom of the Opera and she got sick in the theater
and how funny we thought it was later [laughing, crying]. I wish she could
be here now, so that I could show her how similar my daughter is to her. I
miss her so much. . ..
[silent]
Sometimes I just can’t believe she’s gone. Sometimes I wish it could have
been me instead of her. But other times, I’m relieved it wasn’t me, because
I have kids and she didn’t. But I feel so guilty that I even think that. I can’t
even believe I just said it. I hate myself for thinking it.
Adele, let’s try to stay with that for a moment. Tell me more about that
feeling of guilt. I know it’s hard, but please try.
You know, I wasn’t even there for her when she died. I could have gotten
there sooner, but I was just so wrapped up in my own life. Meanwhile, my
little sister was dying. And now that she’s dead, I feel relief that it wasn’t
me! Relief! It’s a disgusting thing for me to feel. I just feel so. . .dirty when
I think that. How can I think that, when she deserved to live? I feel so guilty.
I’m awful.
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203
T: It sounds like you have two big emotions here. On the one hand, you love
your sister and miss her dearly. On the other hand, you feel guilt over your
relief that it wasn’t you.
P: I feel so overwhelmed by all of this. I miss her. I miss her so much. I wish I
could see her right now, but I still feel so guilty. [Crying harder for a couple
of minutes.]
T: You know, Adele, even though this has been really hard for you to focus on,
I think this is the most genuine I’ve ever seen you be in here. You feel much
more real to me right now.
P: I spend so much time avoiding feeling like this that I sometimes forget how
much I miss her.
In the above exchange, the therapist began by discussing an interpersonal issue,
namely the loss of a loved one and the possibility that the therapist had caused a
rupture in the therapeutic alliance by trying to have the patient talk about this highly
emotional event. The discussion elicited an emotional reaction from the patient,
who quickly became avoidant of that path of discussion and any emotional engagement. Notice how the therapist gently redirects her, while pointing out the pattern
she notices and encouraging the patient to label her emotions and stay with the
emotional experience. The therapist also points out the patient’s apparent conflicting emotions, and reinforces the patient’s genuine expressions of emotion. Notice
also how the therapist relates this genuine emotional moment to a real interpersonal
issue between the two of them, namely that the patient’s emotionality and openness
has made their relationship itself more genuine (“You feel much more real to me
right now”). For a detailed description of emotional processing techniques in the
treatment of GAD, the reader is referred to Newman et al. (2004).
Future Directions
There remains important work to be done in the quest to develop effective treatments
for GAD that benefit larger numbers of patients. Recently, several investigators have
drawn on existing GAD research to suggest specific strategic approaches to treating
chronic worry. First, individuals with GAD find uncertain or ambiguous situations to
be less tolerable relative to individuals without GAD (Dugas, Gagnon, Ladouceur, &
Freeston, 1998). Indeed, “intolerance of uncertainty” reliably distinguishes individuals with GAD from non-anxious individuals (Ladouceur, Blais, Freeston, & Dugas,
1998). Dugas and his colleagues have developed an intervention to specifically target intolerance of uncertainty. Thus far, evaluations of this intervention in both an
individual (Ladouceur et al., 2000) and group (Dugas et al., 2003) therapy format
suggest that this treatment evidences significant improvements over a waiting-list
condition. Future evaluations employing comparisons against active control groups
will help to further inform the potential value of targeting this area of functioning in
the lives of individuals with GAD.
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Second, the metacognitive model of GAD (Wells, 1995, 1999, 2004) proposes
that when individuals engage in worry, negative beliefs about that worry are engendered, leading them to engage in worry about the worry process (or “meta-worry”).
This meta-worry is hypothesized to produce a number of ineffective coping strategies aimed at reducing worry, such as reassurance seeking, checking behaviors,
thought suppression, distraction, and avoidance of potential worry-inducing situations (Wells, 1999, 2004). Metacognitive therapy for GAD focuses on the use
of behavioral experiments and examination of the evidence to modify beliefs that
worry is uncontrollable, that it is dangerous, and that it has positive consequences. In
an open trial investigating the effects of metacognitive therapy for GAD, 10 patients
showed significant improvements at post-treatment on measures of worry, anxiety,
and depression (Wells & King, 2006). As pointed out by the authors, controlled
investigations of metacognitive therapy are needed to evaluate its potential unique
contribution to the treatment of GAD.
Third, the emotion dysregulation model of GAD (Mennin, Turk, Heimberg, &
Carmin, 2004) posits that individuals with GAD (a) experience emotions more
intensely than do others (Turk et al., 2005); (b) have a poorer understanding of
emotions than do others; (c) show greater negative reactions to emotions relative to most people; and (d) use ineffective strategies to regulate their emotions,
thereby leaving them in even worse emotional states. A therapeutic intervention
based on the emotion dysregulation model is currently being developed by Mennin
(2004), and combines elements of traditional CBT for GAD with treatment components specifically targeted to address problems with deficits in emotion regulation.
A focus on emotion dysregulation in GAD contains hope for increasing the efficacy of traditional CBT, and future controlled outcome investigations will surely
provide valuable information on the nature of the emotional lives of individuals
with GAD.
Finally, Roemer and Orsillo (2002, 2005; Roemer et al. 2006) have drawn
upon Hayes’ work on experiential avoidance (Hayes, Wilson, Gifford, Follette, &
Strosahl, 1996) to expand the theoretical framework in which GAD is conceptualized. Roemer and Orsillo reiterate the avoidance theory’s view of worry as cognitive
avoidance of physiological and emotional experience, and further argue that individuals with GAD fear losing control of their emotions and that they are less mindful of
internal and external events relative to individuals without GAD. They also stress the
importance of attending to patients’ core values in treatment as a way of enhancing
intrinsic motivation and intentional action. Thus, their treatment for GAD incorporates traditional CBT approaches combined with efforts to reduce fear of emotions
and experiential avoidance through the use of mindfulness- and values-based therapy (Roemer & Orsillo, 2005). In a recent open trial of this treatment, 16 patients
evidenced significant improvement in GAD severity and self-reported symptoms of
anxiety, depression, and fear/avoidance of internal experiences (Roemer & Orsillo,
2007). Future controlled investigations of mindfulness-based therapy for GAD hold
promise for informing the nature of worry and approaches to its treatment.
Finally, additional research aimed at identifying predictors of treatment responsiveness will be crucial to future efforts to devise techniques that can make GAD
Treatment for GAD
205
treatment successful for a greater number of patients. For example, research on specific emotion-related variables may elucidate whether emotional processing therapy
techniques may be beneficial for specific types of patients (e.g., those who display
deficits in expressions of negative or positive affect, or those who display deficits
in processing highly arousing emotions). As researchers identify specific individual
factors that make patients more or less responsive to therapy, treatment packages
can eventually help larger numbers of chronic worriers.
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Avoiding Treatment Failures
in Specific Phobias
Georg W. Alpers
Treatment Complications in Specific Phobias
When systematic research on phobias began, fears related to specific objects or
situations were still called “simple phobias” (see Marks, 1969), a term that misleadingly implied that these phobias were of low severity. In fact, specific phobias
can incur serious life impairment, in the range of other mental disorders (Becker
et al., 2007). Since the introduction of DSM-IV (American Psychiatric Association,
1994), they are listed by the preferable term specific phobias (see Hofmann, Alpers,
& Pauli, 2009).
Specific phobia is characterized by intense and persistent fear cued by exposure
to, or anticipation of, a clearly discernible and circumscribed object or situation
such as certain animals or insects, blood/injury/injection (BII), natural environmental events (e.g., thunder), or other stimuli (e.g., vomiting, contracting an illness).
Although adults with phobias realize that these fears are irrational, they avoid
confrontation in order to avoid triggering panic or severe anxiety. If the fear is
confronted, it is common to experience emotional discomfort and marked autonomic, respiratory, and endocrine reactivity (Alpers, Abelson, Wilhelm, & Roth,
2003; Alpers & Sell, 2008; Alpers, Wilhelm, & Roth, 2005). Some symptoms are
specific to certain fears, such as body sway, which is closely associated with fear of
heights (Alpers & Adolph, 2008; Hüweler, Kandil, Alpers, & Gerlach, 2009).
The DSM-IV (APA, 1994) lists five discrete subtypes of specific phobias: (1)
animal type: if the fear is cued by animals or insects; (2) natural environment type:
if the fear is cued by objects in the natural environment, such as storms, heights, or
water; (3) BII type: if the fear is cued by seeing blood or an injury or by receiving
an injection or other invasive medical procedure; (4) situational type: if the fear is
cued by a specific situation such as public transportation, tunnels, bridges, elevators,
G.W. Alpers (B)
Department of Psychology, University of Würzburg, Würzburg, Germany
e-mail: alpers@psychscience.org
This work was supported by a grant to Georg W. Alpers from the German Ministry of Research
and Education (BMBF FKZ 01GV0617).
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_12,
C Springer Science+Business Media, LLC 2010
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flying, driving, or enclosed places; and (5) other types: if the fear is cued by other
stimuli (including choking, vomiting, or contracting an illness, fear of falling, and
children’s fears of loud sounds or costumed characters).
Previous studies estimated the lifetime prevalence of specific phobias to be
between 1% and 19% of the population. More recent data suggest that the lifetime and 12-month prevalence rates of specific phobia are about 13% and 9%,
respectively (Becker et al., 2007; Kessler et al., 2005; Kessler, Chiu, Demler, &
Walters, 2005; Stinson et al., 2007). These data suggest that specific phobia is the
most common form of anxiety disorder. Prevalence rates are generally higher in
women than in men (ratios vary between 2:1 and 4:1 from study to study) with
much variance between subtypes of phobias (Becker et al., 2007; Bourdon, Boyd,
Rae, & Burns, 1988; Curtis, Magee, Eaton, Wittchen, & Kessler, 1998; Fredrikson,
Annas, Fischer, & Wik, 1996; Stinson et al., 2007). The highest prevalence rates
have been found for specific animal phobias in women and claustrophobia in men
(Curtis et al., 1998). Prevalence rates also differ with ethnicity; the rates of specific phobias are almost twice as high in African-American individuals (Eaton,
Dryman, & Weissman, 1991; Stinson et al., 2007). Considerable variation in prevalence rates can be found between cultures worldwide (Good & Kleinman, 1985;
Shen et al., 2006).
Impairment has been found to strongly correlate with the number of phobic
symptoms a patient experiences (Curtis et al., 1998). In addition to the high prevalence of multiple phobias, comorbidity with other mental disorders is high: 84%
of all phobic patients have one or more comorbid disorders. Aside from other
anxiety disorders, affective disorders and substance-related disorders are common
(Kushner, Krueger, Frye, & Peterson, 2008). The phobia more often preceded (in
57% of the cases) the comorbid disorder (Magee, Eaton, Wittchen, McGonagle, &
Kessler, 1996). In spite of the high prevalence and considerable impairment, only
8% reported treatment specifically for specific phobia (Stinson et al., 2007).
The Origin of Specific Phobias
Rachman (1977) suggested that there are three routes to develop a phobia: First, by
classical conditioning due to a traumatic experience in a specific situation or in the
presence of a specific object; second, by vicarious learning; and third, by instruction
(usually the parents) or information (e.g., the media). Empirical data suggest that
specific phobia develops following a traumatic experience in 36% of the cases, the
observation of fearful behavior or observation of a trauma to others in 8%, and the
instruction by others in 8%. This means that about 50% of the phobic patients do not
recall how or why they developed the phobia (Kendler, Myers, & Prescott, 2002).
A number of longitudinal studies clearly demonstrate the link between traumatic
experiences, such as traffic accidents or episodes of unexpected panic, and the later
development of a specific phobia (Blaszczynski et al., 1998). Although these data
show that some phobias date back to aversive experiences, this does not explain why
certain classes of typical cues (e.g., spiders and snakes) often elicit phobic reactions
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despite rarely inflicting harm, while others often inflict harm (e.g., knives) but are
rarely feared. This seeming paradox can be explained if one assumes that the typical
phobic cues are prepared fear stimuli (Seligman, 1971). Indeed, several experiments
consistently confirmed that fear responses conditioned to typical fear cues are more
resistant to extinction (Mineka & Öhman, 2002). Also, vicarious learning of fear
responses that has been documented for laboratory-reared monkeys who learned to
avoid snakes from a model (Mineka, Davidson, Cook, & Keir, 1984) seems to be
preparedness for evolutionary relevant fear cues (Cook & Mineka, 1989).
Based on the resistance to extinction documented for experimentally acquired
responses, the preparedness hypothesis has been widely accepted and entered almost
every textbook on biological and on abnormal psychology, although evidence for
other characteristics of preparedness (ease of acquisition, irrationality, and belongingness) is much more limited (McNally, 1987). The basic premise of the theory
that preparedness helps to protect humans from dangerous predators has recently
been questioned for a common specific phobia, i.e., spider phobia (Gerdes, Uhl, &
Alpers, 2009).
In humans learning avoidance behavior from models (Gerull & Rapee, 2002)
and fear acquisition by instruction (Field & Lawson, 2003) seem to be particularly
important routes to the development of anxiety. Moreover, it has been shown in
longitudinal studies that experience with certain challenges such as heights or water
is needed to unlearn certain inborn fears (Poulton & Menzies, 2002).
Theoretically, the characteristic avoidance behavior phobic patients display can
be explained by the two-factor model (Mowrer, 1947). This model assumes that
classically conditioned fear stimuli elicit a fear response that is then reduced
or ameliorated by the instrumental avoidance behavior. The conclusion that this
dysfunctional avoidance helps to maintain the fear response can be extended to
fears acquired through other routes than classical conditioning. Aside from these
learning-based considerations of how phobias may be acquired, there is strong evidence for a significant genetic disposition to acquire an anxiety disorder (Kendler,
Neale, Kessler, Heath, & Eaves, 1992).
Differential Diagnosis and Comorbidity
A challenge to adequate differential diagnosis is the fact that anxiety disorders
are highly comorbid (Brown, Campbell, Lehman, Grisham, & Mancill, 2001;
Stinson et al., 2007). However, structured interviews such as the Anxiety Disorders
Interview Schedule for DSM-IV and adequate training in its application lead to
good diagnostic accuracy and interrater reliability for specific phobias (Brown, Di
Nardo, Lehman, & Campbell, 2001). Although most subtypes of phobic disorder
can also be differentiated reliably (Fyer et al., 1989), a major difficulty is the diagnostic distinction of phobias and panic disorder. With the exception of phobias of
the animal type, panic disorder patients – especially those with marked agoraphobia
– often fear typical phobic cues such as heights, invasive medical procedures, public transportation, or contracting illness. Moreover, patients with specific phobias
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often experience panic attacks with marked physical symptoms during exposure
to the feared cues, especially in the situational subtype (Ehlers, Hofmann, Herda,
& Roth, 1994; Lipsitz, Barlow, Mannuzza, Hofmann, & Fyer, 2002). Symptoms
of these situational panic attacks markedly overlap with typical symptoms experienced by panic disorder patients (Craske, 1991); for example, the symptom profile
of the phobic fear of enclosed places is most similar to that of panic disorder and
the fear of enclosed places is frequent in panic disorder patients. A further complication arises because the phobias trace back to a spontaneous panic attack in many
patients (Himle, Crystal, Curtis, & Fluent, 1991). In spite of these similarities, phobic fear and panic disorder are clearly distinguished by most theoretical accounts
because they are either uncued (i.e., as seen in panic disorder) or cued (i.e., as seen
in specific phobia) (Barlow, 2002).
Gold Standard for Therapy: Exposure
A systematic review of treatment studies published between 1960 and 2005 shows
that research has been conducted on the usefulness of systematic desensitization (or
imaginal exposure), in vivo exposure, cognitive therapy, for a multitude of different specific phobias and applied tension for BII phobia specifically (Choy, Fyer, &
Lipsitz, 2007). The limited data on medication are disappointing (Choy et al., 2007).
Although some textbooks still recommend systematic desensitization (Wolpe,
1962) as the typical strategy for the treatment of phobias, today, the gold standard
for the treatment of specific phobias clearly is exposure therapy unaccompanied by
relaxation instruction. Response to in vivo exposure has proven to be superior to systematic desensitization in several direct comparisons (Choy et al., 2007). The effects
of exposure are generally not limited to behavioral changes but extend to improvement in cognitive measures of fear as well (Booth & Rachman, 1992). Figure 1
illustrates extinction of self-reported fear and heart rate within and across repeated
exposure sessions in a claustrophobic patient.
Efficacy of Exposure
A recent meta-analysis systematically compared the efficacy of different strategies used to treat specific phobias (Wolitzky-Taylor, Horowitz, Powers, & Telch,
2008). Data from 33 randomized treatment studies were compared. First, exposurebased treatment approaches produced large effect sizes relative to no treatment
(wait list). Second, exposure also outperformed placebo conditions and alternative
active psychotherapeutic approaches (e.g., relaxation training). Third, in vivo exposure with the phobic cue also outperformed alternative forms of exposure therapy
(e.g., imaginal exposure, virtual reality) at post-treatment. There are now several
well-established manuals providing self-help materials as well as support and information for the clinician (e.g., Barlow & Craske, 1994; Bourne, 1998, 2005). In vivo
exposure is often conducted in a graded fashion, beginning with a relatively mild
challenge and progressively moving upward on the hierarchy of fearful cues.
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Fig. 1 Self-reported fear (subjective units of distress, SUD) and heart rate (HR) in one selected
patient in the course of the six exposure sessions. The patient was 52 years of age. His HR at quiet
sitting after session 6 was 64 bpm. His scores on a claustrophobia questionnaire (CLQ, Radomsky,
Rachman, Thordarson, McIsaac, & Teachman, 2001) changed from 57 before to 28 after the sixth
session (with permission from Alpers & Sell, 2008)
A review of studies using in vivo exposure therapy reported that between 80%
and 90% of treatment completers were able to complete the behavioral avoidance
task, a measure of clinically significant change, at the end of treatment (Choy et al.,
2007). The difference between treatments was sometimes as large as 25% of completers being able to touch a snake after systematic desensitization versus 92% after
in vivo exposure (Bandura, Blanchard, & Ritter, 1969). Importantly, there has been
no evidence for symptom substitution. Instead, the gains obviously generalized to
other domains, even to those not addressed during exposure treatment (Götestam &
Götestam, 1998).
Follow-up assessments of in vivo exposure were gathered for several specific
phobias with periods ranging from 6 months to 14 months. In general, treatment gains are either maintained or further improved over time (Choy et al.,
2007). However, superiority of in vivo exposure to alternative approaches was
less pronounced in some studies at follow-up than at the post-treatment assessment following exposure therapy (Wolitzky-Taylor et al., 2008). For both findings
(the increasing effects and the decline of treatment-specific differences) a possible
explanation may be that even moderate therapeutic improvement may motivate all
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patients to engage in self-guided in vivo exposure so that they can improve further. On the other hand, some patients who were successfully treated with in vivo
exposure may cease to self-expose after treatment has terminated and may return to
some of their avoidance behavior. In the clinical setting, this needs to be assessed in
booster sessions on an individual basis. The few studies that examined very longterm outcomes call for caution. Lipsitz and colleagues reassessed symptoms 10–16
years after treatment and found considerable rates of relapse (Lipsitz, Mannuzza,
Klein, Ross, & Fyer, 1999).
Interestingly, very brief exposure treatments have garnered substantial support.
For example, Öst and coworkers have demonstrated that prolonged exposure can
be successful even if there is only one extended session (usually between 2 h
and 4 h) with a therapist (Öst, 1989). The effectiveness has been demonstrated
most clearly for small animal phobias (Gotestam, 2002; Hellstroem & Oest, 1995;
Koch, Spates, & Himle, 2004; Thorpe & Salkovskis, 1997) and flying phobia
(Öst, Brandberg, & Alm, 1997). However, in the meta-analysis mentioned before
(Wolitzky-Taylor et al., 2008), multi-session treatments marginally outperformed
single-session treatments on domain-specific questionnaire measures of phobic
dysfunction, and moderator analyses revealed that more sessions predicted more
favorable outcomes.
Although it is often assumed that some phobias may be more difficult to treat
than others, effect sizes for the major comparisons of interest were not moderated
by the type of specific phobia in the meta-analysis (Wolitzky-Taylor et al., 2008).
Interestingly, the meta-analysis also revealed that placebo treatments were significantly more effective than no treatment, which suggests that patients with specific
phobias are moderately responsive to placebo interventions.
Although beyond the scope of this chapter, it should be mentioned that phobias
are common in children as well. Although their characteristics often differ from
those in adults, there is some overlap. Because phobias start early in life, and pose
a risk for developing a second mental disorder, and because of the chronic duration,
the need for treatment in childhood and adolescence is obvious (Becker et al., 2007).
Exposure in vivo is also the treatment of choice for small animal phobias in children
(Muris, Merckelbach, Holdrinet, & Sijsenaar, 1998).
Core Elements of CBT
Cognitive Preparation or Psychoeducation
Most treatment approaches for specific phobias include some form of psychoeducation, but the core CBT strategy to overcome phobic fear is unanimously some
variant of exposure and response prevention. In this context, psychoeducation has
the purpose of introducing the therapeutic rationale, and typically addresses the
nature of (non-clinical) fear and its protective function. It usually also involves a
review of the individual’s risk assessment in a given situation and some cognitive
restructuring if this assessment seems to be exaggerated. Then, the principles of
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fear acquisition and extinction are reviewed, with the purpose of raising motivation and clarifying expectations for the exposure therapy to follow. Together, these
aspects of psychoeducation are sometimes summarized as cognitive preparation.
Significant predictors of treatment success are credibility of the treatment rationale
and the motivation for psychotherapy in general (e.g., Öst, Stridh, & Wolf, 1998;
Southworth & Kirsch, 1988).
Exposure to Fear Cues
In the preparation for exposure therapy, patients are asked to identify and arrange
cues that evoke undue fear from the least to the most frightening. Starting at a cue
representing moderate fear, patients are asked to gradually expose themselves to
the cue, usually for up to an hour or more at a time, allowing ensuing feelings and
thoughts to occur without escape, and to continue the exposure until these feelings of discomfort subside. Such homework is frequently assigned on a daily basis.
Exposure may be conducted with or without a therapist (e.g., Öst et al., 1998) and/or
guided by appropriate self-help books or computer systems (e.g., Kenwright, Marks,
Gega, & Mataix-Cols, 2004). Phobic cues are frequently live situations or objects,
but when difficult to arrange, pictures, film material, or computer animations (see
Virtual Reality) or imaginal stimuli may be used. A number of studies now suggest
that virtual reality may be effective in flying and height phobia, but this needs to
be substantiated by more controlled trials (Choy et al., 2007; Krijn, Emmelkamp,
Olafsson, & Biemond, 2004; Wolitzky-Taylor et al., 2008).
A Case Example: Treating Spider Phobia
Jen, aged 35, consulted a therapist for her severely handicapping and inexplicable
fear of spiders. She had never really liked spiders and her fear had intensified over
the years. Whenever she saw a spider she panicked helplessly and felt frozen in
place. Her heart raced, her palms sweated, and she felt embarrassed because she
depended on other people because of this fear. She avoided walking across a lawn
or going into her basement or garage lest she encountered spiders there. Having
unsuccessfully tried to prevent spiders entering her home, she was about to move
elsewhere. Jen was told her symptoms were typical of a phobia and that she could
endure them for long enough to get used to whatever was frightening her. Even the
mere thought of looking at a spider evoked extreme fear and disgust. In therapy, she
learned to open a book with pictures of spiders in the therapist’s office. She took the
book home and made herself touch the pictures with her fingers. Next, she looked at
a spider in an empty glass jar for at least 30 min without her usual attempt to remove
it or turn away from it. Jen was encouraged to do exposure without her usual subtle
avoidances that stopped her experiencing the fear fully and getting used to it. Thus
she examined the spider and her own reactions in detail, she was fascinated at not
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being overwhelmed by fear. Her distress decreased during each exposure session
and across repeated such sessions. She became more confident exposing herself to
spiders at home. After 10–50 min weekly sessions and several hours of practice at
home she touched a large spider and let it crawl across her palm. When she had
accomplished this, she expressed doubt that her family would actually believe what
she had just done, and the therapist spontaneously decided to take a few pictures
of how she handled the spider. She was proud and happy to take home her therapy
graduation pictures. Jen then cleaned out her garage, kept a spider in a jar in her
kitchen, and went to bed without checking for spiders. Improvement continued at
follow-up 8 weeks later.
Factors that May Interfere with Exposure Success
Treatment Engagement
As in CBT for panic disorder with or without agoraphobia (see Sanderson & Bruce,
2007), lack of engagement in behavioral exposure or non-compliance is the most
important reason for sub-optimal treatment response in phobia therapy as well. For
example, compliance with self-exposure homework during weeks 0–8 predicted
more improvement 2 years later (Park et al., 2001). An older and relatively small
study suggests that positive interaction (“warm therapist behavior”) contributes to
better adherence (Morris & Magrath, 1979). Even in completed treatments, negative cognitions have been identified as a predictor of poor treatment response
(Rachman & Levitt, 1988; Shafran, Booth, & Rachman, 1993). Accordingly, cognitive interventions should be considered to address possible negative expectations,
as a strategy to reduce drop-out and to improve outcome. It is important to point out
that patients who fail to improve with one treatment, for example, relaxation training, retain a strong chance of responding after subsequent crossover to exposure
therapy (Park et al., 2001).
Duration of Exposure
Generally, clinicians strongly emphasize that exposure sessions need to be of adequate duration to result in a reduction of fear across sessions. Exposure appears to
be more effective as the patient is given more time to experience the reduction of
anxiety in the presence of the phobic cue. For example, exposure was found to be
more effective when no anxiety was experienced for at least 1 min compared to a
condition where exposure was ended when the highest level of anxiety was reached
(Marshall, 1985). Likewise, longer exposure results in more fear extinction than
shorter exposures even if the total duration of exposure is held constant (Stern &
Marks, 1973; but see de Silva & Rachman, 1984). Several studies with fixed durations (e.g., 30 min) of exposure have also been found to be effective independent of
fear levels (e.g., Alpers et al., 2005); the most crucial aspect of these repeated brief
exposures may be that patients are taught that they will have to return to exposure
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soon after the first exposure has terminated, even if it was terminated at a relatively
high level of anxiety.
Multiple Phobias
When more than one situation or object is feared, which is quite typical (Hofmann,
Lehman, & Barlow, 1997; Stinson et al., 2007), patient and therapist need to decide
which fear to target first. If too many issues are targeted at the same time it may be
difficult for the patient to monitor gradual change in the course of the intervention.
As such, one recommendation is that extinction should be clearly observable in the
course of exposure exercises with one situation before targeting the next task.
Often, there are several distinct facets to one specific phobia. For example, in
some cases with driving phobia it makes a big difference whether the patient is
the driver or a passenger (Alpers et al., 2005; Ehlers et al., 1994). Exposure exercises will have to target these specific circumstances; the patient will have to be the
driver or the passenger. Similarly, if patients with such a specific phobia experience
panic attacks while driving, they may be very concerned that these attacks might
impair their ability to drive. Here, cognitive restructuring will have to address these
risk estimations (see below). On top of this, the car is a confined space that cannot
be left at any time, that is, claustrophobia may make things worse. As indicated
above, this aspect can be targeted separately. While driving, the driver might be
exposed to unpleasant temperatures or lighting conditions or dizziness – intolerance
of unpleasant bodily experiences, i.e., anxiety sensitivity may contribute to symptom development. Specific interventions targeting interoceptive exposure (Antony,
Ledley, Liss, & Swinson, 2006) may be indicated to treat fear of bodily sensations.
Also, while driving one is exposed to being far away from home when driving long
distances – a typical agoraphobic challenge that can be the topic of a homework
exercise even when the patient is not prepared to drive yet. When there are different facets to a specific phobia, the different circumstances and conditions need to
be thoroughly explored and evaluated. Any case formulation will have to take these
patient-specific factors into account.
When Other Unpleasant Emotions/Sensations Come into Play
Disgust. Although the characteristic emotional experience in phobias is fear upon
exposure to the phobic cue, some cues may also elicit the distinct emotion disgust
(Davey, 1994; Woody, McLean, & Klassen, 2005), which seems to change with therapy on different gradients (Smits, Telch, & Randall, 2002). Disgust also decreases
during exposure treatment. However, in one study, the decline of disgust ratings was
found to lag behind that of fear ratings in a direct comparison (Smits et al., 2002).
Interestingly, disgust levels at pretreatment did not moderate the level of fear activation or fear reduction during treatment in this study. Although an experimental
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analysis seems to indicate that disgust does not have a strong influence on the return
of fear (Edwards & Salkovskis, 2006), the observation that not all emotions extinguish at the same rate may be relevant for treatment. The goal of exposure may not
only be to reduce fear but also to reduce the level of other unpleasant emotions.
Nausea. Nausea is frequently related to anxiety disorders (Haug, Mykletun, &
Dahl, 2002). More specifically, the fear of vomiting can make it difficult for a patient
to expose herself to fear-provoking cues. Research with patients who are specifically afraid of vomiting (i.e., emetophobia) suggests that this fear may be closely
related to the fear of losing control, and that vomiting phobia reflects this underlying problem (Davidson, Boyle, & Lauchlan, 2008). Such a fear of losing control
should be explored and targeted by specific cognitive interventions which are aimed
at increasing the tolerance of uncertainty (see Keefer et al., 2005; Robichaud &
Dugas, 2006). There is evidence from a few case reports that also other worries
about gastrointestinal problems, such as being afraid of having diarrhea (Hedberg,
1973) or excessive need to urinate (Myers, MacKinnon, & Corson, 1982), have been
successfully treated with behavioral interventions. Physical therapy with vestibular rehabilitation exercises may benefit phobic patients with vestibular dysfunctions
(Jacob, Whitney, Detweiler-Shostak, & Furman, 2001).
Lightheadedness/Fainting. Related to disgust and nausea is the fear of BII.
Patients with BII phobia often faint when exposed to the relevant cues (Dahlloef
& Öst, 1998; Sarlo, Buodo, Munafo, Stegagno, & Palomba, 2008). This particular
psychophysiological pattern has been addressed in a specific intervention, applied
tension (Öst, Fellenius, & Sterner, 1991; Öst, Lindahl, Sterner, & Jerremalm, 1984;
Öst & Sterner, 1987).
Shame. Patients with a specific phobia can feel utterly debilitated as a consequence of their fear. They are dependent on family members and friends. In many
cases they have to tailor their job search around conditions allowing them to avoid
whatever they are afraid of. As in cases of social anxiety disorder, the focus of
maladaptive cognitions can be placed on the consequence of public scrutiny and
subsequent negative evaluation (“I’m going to make a fool of myself”). Some treatment strategies can also result in embarrassment (e.g., riding an elevator up and
down for extended periods of time or staying in small fitting rooms while other people rush through the department store). This needs to be addressed when exposure
is planned or it may result in undue insecurity or early cessation of prolonged exposure. Importantly, the patient needs to be aware of the different emotions aroused in a
given situation (i.e., claustrophobic fear versus embarrassment because the exercises
may draw passengers’ attention).
When Skill Deficits Accompany the Phobia
Longstanding phobias (with onset in childhood) – phobias of animals, the natural
environment, and BII type often start in childhood while most situational phobias
usually start in early adulthood (e.g., Becker et al., 2007; Lipsitz et al., 2002) –
may have prevented development of appropriate skills for the phobic situation.
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For example, individuals with longstanding fears of dogs may not have developed skills for appropriately interacting with animals, and may require training
in how to approach, touch, or interact with an animal (e.g., Rentz, Powers, Smits,
Cougle, & Telch, 2003). Similar considerations are apt for driving fears, where the
therapist should remain vigilant to poor driving habits which may both increase
the fearfulness and the actual risk of the driving experience (see Taylor, Deane, &
Podd, 2007).
When Anticipation Is Worse than Exposure
The maladaptive cognitions associated with the phobias tend to be future-oriented
perceptions of danger or threat (e.g., what is about to happen, what will happen).
This sense of danger may involve either physical threat (e.g., having a heart attack)
or psychological (e.g., anxiety focused on embarrassment). In addition, these cognitions tend to focus upon a sense of uncontrollability over the situation or symptoms
of anxiety.
Related to the issue of risk assessments is the fact that anticipatory anxiety is
often worse than fear during exposure. A striking overprediction of fear before the
exposure compared to the limited increase in fear during the exposure itself has
frequently been observed (Alpers & Sell, 2008; Johansson & Oest, 1982; Rachman
& Bichard, 1988).
In a study with a height exposure task in a theme park we showed that, for all
participants, fear, dizziness, and body sway were increased during exposure (Alpers
& Adolph, 2008). However, anticipated fear most reliably predicted body sway during exposure. In addition, persons scoring high on trait fear of heights anticipated
and experienced more fear during exposure, but this relationship was not found for
any objective measure.
Attending to overestimations in the likelihood of catastrophic events is one way
of addressing these anticipatory fears. A focus on danger or harm is most frequently
associated with the natural environment and situational subtypes (Lipsitz et al.,
2002). Patients with a fear of flying may overestimate the risk of plane crashes,
those with claustrophobia may exaggerate the risk of suffocation in an elevator, and
those with the specific phobia of driving are often concerned with their own ability
to drive. To help with anticipatory anxiety, patients may be asked to research facts
about the feared situation prior to the initiation of exposure. This information is then
applied in a cognitive-restructuring format to help patients generate more accurate
expectations prior to exposure.
When Patients Use Cognitive Avoidance During Exposure
Even if patients agree to pursue exposure, this strategy may sometimes fail to result
in a sizable extinction of fear responses. One reason is related to cognitive avoidance during exposure. Theoretically, avoidance or distraction should result in less
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extinction (Foa & Kozak, 1991, 1986; Rodriguez & Craske, 1993). This is supported by studies that found less treatment response in patients who were distracted
from experiencing the full extent of fear during exposure (Grayson, Foa, & Steketee,
1982; Kamphuis & Telch, 2000; Mohlman & Zinbarg, 2000) or more return of fear
(Haw & Dickerson, 1998). However, the detrimental effects of safety behavior (subtle avoidance strategies designed to reduce fear during exposure) have not always
been replicated (Antony, McCabe, Leeuw, Sano, & Swinson, 2001; Milosevic &
Radomsky, 2008).
In a recent study with claustrophobic patients it was evident that those who were
encouraged to use safety behaviors during exposure showed significantly more fear
at post-treatment and follow-up relative to those encouraged to focus and reevaluate
their core threats during exposure (Sloan & Telch, 2002). Particularly during imaginal exposure, safety behavior is frequent and linked to poorer outcome (Rentz et al.,
2003). Thus, patients should be instructed not to use subtle avoidance strategies and
to fully experience the symptoms and feelings provoked by exposure.
Vigilance to Threat
Eysenck’s (1992) hypervigilance theory proposes that anxious people scan their
environment excessively and broaden their attention span when searching for a
fear-relevant stimulus and narrow it while that stimulus is processed. This hyperactive alarm system may lead to frequent and intense false alarms in fearful subjects
(Becker & Rinck, 2004). The subsequent narrowing of attention may explain why
patients have difficulties to disengage attention from spider distractors before moving on to the target. In contrast to several theoretical accounts, there is little evidence
that attentional engagement to phobic cues actually occurs automatically (Alpers
et al., 2009). Instead, patients with a spider phobia seem to have a deficit in disengaging their attention from spider cues (Gerdes, Alpers, & Pauli, 2008; Gerdes,
Pauli, & Alpers, 2009). Under naturalistic conditions, phobic patients have also been
shown to scan their environment for threatening stimuli (Lange, Tierney, ReinhardtRutland, & Vivekananda-Schmidt, 2004). Although specific interventions to address
the dysfunctional allocation of attention are not yet available outside of the laboratory (see Mathews & MacLeod, 2002), patient behavior should be closely observed
and observations such as excessive scanning should be addressed.
When Self-Report Is Not Predictive of Emotional Processing
Assessing verbal report during treatment is often not enough to assess emotional
activation. Multiple response theory states that phobic fear is reflected in autonomic nervous system activation, self-report, and avoidance behavior (Lang, 1968).
Despite the positive reaction this statement has created with theorists (e.g., Foa
& Kozak, 1991), physiological measurement is often neglected, partly because its
contribution of useful and unique information has not been convincingly documented. However, in a recent study we documented that although claustrophobic
Specific Phobias
221
patients are activated both in self-report and in physiology while being exposed to a
fear-related situation such as a small confined space, measuring heart rate can provide incremental information (Alpers & Sell, 2008). Although initial fear activation
during exposure as indicated by self-report is not predictive of therapeutic change,
higher heart rate responses to exposure correlate with more therapeutic change
from before to after exposure treatment. Thus, whenever possible, physiological
measurements should be consulted to monitor the effects of exposure treatment.
Enhancing Memory of Success
The return of fear in successfully treated patients is often thought of as a process
similar to reinstatement of extinguished fear in the conditioning model (Bouton,
2002). To aid retention of exposure across the multiple contexts in which a phobic
cue may be experienced in the future, extinction training in multiple contexts may be
important (e.g., for animal work see Gunther, Denniston, & Miller, 1998). A superiority of variable context exposure training can also be observed in therapy with
humans, especially in longer-term follow-up assessments (Vansteenwegen, Vervliet,
Hermans, Thewissen, & Eelen, 2007; for review see also Craske et al., 2008). Hence,
variability in the way in which exposure is conducted (in different settings, at different times of day, with and without therapist accompaniment) may aid longer-term
fear reduction.
Also, there are now data suggesting that pharmacological cognitive enhancers
(e.g., d-cycloserine) may increase the efficacy of exposure-based interventions in
specific phobias (acrophobia Ressler, Rothbaum, Tannenbaum, Anderson, Graap,
Zimand et al., 2004). Exposure therapy combined with d-cycloserine resulted in significantly larger reductions of acrophobia symptoms on all main outcome measures.
Promising initial findings have also been reported for the augmentation of exposure therapy for claustrophobia with yohimbine, another putative cognitive enhancer
for extinction learning (Powers, Smits, Otto, Sanders, & Emmelkamp, 2009).
However, whether such adjunctive treatment with putative memory enhancers can
help reduce the rate of treatment non-response to CBT has not been systematically
evaluated.
Conclusion
It is appropriate that specific phobias are no longer called simple phobias. Specific
phobias are highly prevalent and they can result in significant life impairment. The
multitude of different fears and the considerable level of comorbidity imply that
treatment needs to be individually tailored. There are several etiological pathways
to the development of specific phobias and the individual’s learning history should
be considered for treatment. Exposure and response prevention is the gold standard
for treatment. Variants of this treatment approach have proven to be highly effective
with lasting effects on multiple levels of responses (self-report, physiological reactivity, and behavioral avoidance). The specific ways in which exposure is conducted
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likely influences the robustness of outcome. This chapter attended to factors that
need to be considered in planning and for adequate exposure situations, sufficient
frequency, and duration of exposure exercises. Possible treatment complications,
when other emotions come into play and when risk assessments call for specific
interventions, were highlighted.
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Stern, R., & Marks, I. (1973). Brief and prolonged flooding. A comparison in agoraphobic patients.
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Stinson, F. S., Dawson, D. A., Chou, S. P., Smith, S., Goldstein, R. B., Ruan, W. J., et al. (2007). The
epidemiology of DSM-IV specific phobia in the USA: Result from the national epidemiologic
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Taylor, J. E., Deane, F. P., & Podd, J. V. (2007). Driving fear and driving skills: Comparison
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Part III
Treatment Complications
in Special Populations
Resolving Treatment Complications
Associated with Comorbid Depression
Christen M. Deveney and Michael W. Otto
The Impact of Comorbid Depression on Treatment for Anxiety
Brad is a 30-year-old male who presents to the clinic with complaints of frequent, intense,
unexpected panic attacks as well as symptoms of major depression. Following a functional
analysis of his symptoms, Brad and his therapist agree to an initial treatment focus on
panic disorder. As treatment progresses, and despite understanding the treatment model and
reporting motivation for conducting exposure exercises, Brad has difficulty completing his
exposure homework. He reports that it is hard for him to gather the motivation to conduct
the exposures without help from his therapist and only manages to practice one exposure
per week. He considers this to be a sign that he is a “failure.” During treatment sessions
he sits slouched in his chair with a sad expression on his face. Brad sighs and says that he
is considering stopping treatment, because “it isn’t working.” This thought quickly spirals
into a series of thoughts about how he will never get better and will never be able to support
himself” so he will have to return home and live with his parents or live on the street.”
This coincides with a week of frequent and intense panic attacks, significant anticipatory
anxiety and avoidance, as well as an exacerbation of depression symptoms – including
passive suicidal ideation.
Brad’s case effectively represents some of the issues encountered by clinicians
in the treatment of comorbid anxiety and mood disorders. The choice to initiate a
treatment focus on the anxiety disorder, if it is the primary source of distress and
disability, rather than the depression is well supported by the treatment literature.
In many cases, the empirical literature suggests that cognitive behavioral therapy (CBT) for anxiety disorders is resilient to comorbid depression. There is also
evidence that depression symptoms improve with treatment of a primary anxiety
disorder (see below). Nonetheless, as illustrated by Brad’s case, there are treatment challenges introduced by the depression. Depression has been associated with
increased clinical severity and therefore may require additional treatment sessions
and/or additional treatment strategies to fully address all anxiety and depression
symptoms. Depression may influence motivation for treatment in general as well
as the perceived ability to complete specific assignments and may change the evaluation of treatment progress. Also, depression brings with it waxing and waning
M.W. Otto (B)
Department of Psychology, Boston University, Boston, MA, USA
e-mail: mwotto@bu.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_13,
C Springer Science+Business Media, LLC 2010
231
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symptoms that may demand attention therapeutically, ranging from variable levels
of distress in session to the importance of monitoring and intervening with suicidal
ideation.
In the sections that follow, we will review the nature and impact of depression
comorbid with anxiety disorders. We will also address treatment modifications that
can be important for treating anxious individuals who have comorbid depression.
The Impact of Comorbid Depression
Comorbidity between anxiety and major depressive disorders (MDDs) is associated
with greater severity of anxiety symptoms. For example, increased panic disorder severity, help seeking, role impairment, and symptom persistence have been
routinely observed among patients with panic disorder and comorbid major depression relative to non-comorbid individuals (e.g., Brown, Antony, & Barlow, 1995;
Joormann, Kosfelder, & Schul, 2005; McLean, Woody, Taylor, & Koch, 1998;
Roy-Byrne et al., 2000. Elevated panic symptoms frequently remain after treatment among individuals with higher depression scores (e.g., Keijsers, Hoogduin,
& Schaap, 1994). Symptom severity was also higher in a social anxiety disorder and comorbid major depression group relative to social anxiety disorder
alone and social anxiety disorder and comorbid anxiety disorder comparison
groups (Erwin, Heimberg, Juster, & Mindlin, 2002). At times, it appears that
the driving force behind this increased clinical severity may reflect an increase
in general anxiety rather than elevations in symptoms related to specific anxiety
disorders. For example, general anxiety, but not disorder-specific symptoms, was
more severe among individuals with primary obsessive-compulsive disorder (OCD;
Overbeek, Schruers, Vermetten, & Griez, 2002) or social anxiety disorder (Turner,
Beidel, Wolff, Spaulding, & Jacob, 1996) and comorbid depression relative to a
non-depressed group.
Depression is also associated with an intensification of anxiety-related cognitions. For example, social anxiety disorder with depression was associated with
even more marked negative evaluations of social performances than a non-comorbid
group (Ball, Otto, Pollack, Uccello, & Rosenbaum, 1995; Wilson & Rapee, 2005
see also Bruch, Mattia, Heimberg, & Hoit, 1993). A similar relationship has
been noted for somatic sensation fears among panic disorder patients with comorbid depression relative to a non-comorbid group (Otto, Pollack, Fava, Uccello &
Rosenbaum, 1995).
Another impact of comorbid depression is reduced motivation for treatment.
Marks (1987) reported reduced motivation to engage in treatment or complete
self-directed exposures among anxiety patients with comorbid depression. Also,
two studies found an association between decreased post-traumatic stress disorder (PTSD) treatment adherence and pretreatment depression scores (e.g., Bryant,
Moulds, Guthrie, Dang, & Nixon, 2003; McDonagh et al., 2005; c.f. Resick, Nishith,
Weaver, Astin, & Feuer, 2002). One source of this adherence difficulty may be
the negative attitudes and self-evaluations that are endemic to depression. As discussed by Telch (1988), depressogenic cognitions should be expected to impact
Comorbid Depression and Anxiety Treatment
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evaluations of success following exposure exercises. For example, an individual
with social anxiety disorder and comorbid depression may be more likely to judge
his/her exposure performance in the context of larger depressogenic beliefs (e.g., “I
wasn’t perfect in the exposure, which is just one more sign of my worthlessness”).
In addition, failure to recognize the positive outcome of an exposure exercise (e.g.,
“I just did something very difficult and my worst fears did not happen”) may minimize the safety learning considered to be essential for the successful resolution of
anxiety symptoms. These depressive cognitions may limit treatment gains by reducing patients’ expectations or ability to learn from anxiety treatment interventions
(Safren, Heimberg, & Juster, 1997).
Another independent effect of depression on adherence may be via an impact on
problem solving. Stress management and problem solving appears to be reduced
by depression, and may lead patients with depression to feel that much more overwhelmed by stressors. As a result, homework assignments, which by their nature
are stressful, may be perceived as an unmanageable burden and therefore avoided.
Finally, symptoms such as anhedonia in combination with sad mood and decreased
energy may reduce motivation for the benefits that exposure therapy can bring
– the ability to engage in more personal, social, and role activities. Hence, the
“vision” of what successful anxiety treatment may bring in terms of enhanced
functioning may be both less salient and less important for individuals with severe
depression.
Increased symptom severity, increased negative cognitions, and decreased willingness and ability to engage in treatment-related as well as pleasurable activities
may all combine to reduce an individual’s ability to engage in anxiety treatment.
Missed appointments and low motivation have been associated with poorer treatment outcome (Dugas et al., 2003; Tarrier, Sommerfield, Pilgrim, & Faragher,
2000), even in studies where comorbid major depression itself did not impact treatment outcome (Tarrier et al., 2000). Hence, clinicians should be prepared to work
harder to help patients with depression engage adequately in treatment.
Impact of Comorbid Depression on Anxiety
Treatment Outcome
A critical issue for consideration is the degree of impact comorbid depression has
on anxiety disorder treatment outcome. In the following section we review the existing literature for panic disorder, social anxiety disorder, OCD, and PTSD. Although
there are some equivocal findings for each diagnostic group under consideration,
overall there is evidence that CBT for anxiety disorders is often robust in the
presence of comorbid depression.
Panic Disorder
Empirical investigations of the impact of comorbid depression upon CBT for panic
disorder have been the most extensive (see Mennin & Heimberg, 2000 for review)
and indicate that CBT for panic is frequently resilient to comorbid depression.
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Despite some mixed findings, it appears as if neither pretreatment depression
symptom severity (e.g., Beck Depression Inventory scores; Başoğlu et al., 1994;
Black, Wesner, Gabel, Bowers, & Monahan, 1994; Jansson, Öst, & Jerremalm,
1987) nor the presence of a diagnosable mood disorder (Barlow, Gorman, Shear, &
Woods, 2000; Brown et al., 1995; Kampman, Keijsers, & Hoogduin, 2008; Laberge,
Gauthier, Cote, Plamondon, & Cormier, 1993; Maddock & Blacker, 1991; McLean
et al., 1998; Wade, Treat, & Stuart, 1998) reduces the efficacy of CBT for panic
disorder. Similarly, the presence of a comorbid mood disorder at pretreatment does
not appear to influence panic relapse (Otto, Pollack, and Sabatino, 1996). The durability of CBT for panic disorder extends to more naturalistic settings as CBT for
panic disorder was not markedly influenced by the presence of major depression,
despite the greater clinical impairment among the comorbid group, as evaluated
in a German community clinic (Joormann et al., 2005). Consistent with our prior
discussion of increased symptom severity among individuals with comorbid depression, the literature indicates that despite greater symptom severity at baseline in the
comorbid group, individuals with panic disorder and comorbid depression are able
to make similar treatment gains as compared with individuals with panic disorder
only (McLean et al., 1998).
Despite these promising outcomes, some studies have linked pretreatment major
depression to poorer acute outcome (Başoğlu et al., 1994; Maddock & Blacker,
1991; Steketee, Chambless, & Tran, 2001) as well as increased panic symptoms and
decreased social adjustment over a long-term period (Noyes et al., 1990). There is
less evidence for a relationship between treatment outcome and pretreatment depression severity scores (e.g., Başoğlu et al., 1994). Accordingly, we are left with the
conclusion that in many cases, CBT for panic disorder is robust over the long term
in the face of comorbid depression (see Mennin & Heimberg, 2000 for review). Yet,
given the initial starting and ending severity differences, more treatment may be
required to bring patients with comorbid depression to the desired outcome.
Social Anxiety Disorder
As with panic disorder, several clinical trials indicate that the presence of comorbid depression does not have a marked impact on treatment outcome for social
anxiety disorder (e.g., Van Velzen, Emmelkamp, & Scholing; Turner et al., 1996).
The strongest evidence comes from a study by Erwin et al. (2002), who indicated
that individuals with social anxiety disorder exhibited similar rates of improvement, regardless of whether they had comorbid major depression. These findings are
echoed by a recent meta-analysis by Lincoln and Rief (2004) which indicated that
treatment outcome for social anxiety disorder did not differ depending on whether
comorbid major depression was permitted or excluded from the clinical trial. Indeed,
effect sizes for the two groups were virtually identical (d = 0.091 for studies including comorbid major depression and d = 0.92 for studies excluding comorbid major
depression; Lincoln & Rief, 2004).
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Despite these promising results, two studies indicate that pretreatment depression is associated with poorer treatment outcome for social anxiety (Chambless,
Tran, & Glass, 1997; Scholing & Emmelkamp, 1999). In the Chambless et al.
(1997) study, pretreatment depression scores predicted negative treatment outcome
beyond that of other measures of anxiety and anxious apprehension. However, pretreatment depression scores may be most related to early measures of treatment
outcome, as there was no relationship between pretreatment depression and outcome
at an 18-month follow-up assessment in the study by Scholing and Emmelkamp
(1999). Accordingly, given the compelling findings from the meta-analysis, clinicians can be at least moderately confident that outpatients with social phobia
and depression will have the opportunity to improve to similar degree as outpatients without comorbid depression, especially when assessed over a long-term
period.
OCD
Empirical investigations of the impact of depression on treatment outcome for OCD
are more limited than for panic or social anxiety disorders, yet there are some similarities with the preceding literature. As with other anxiety disorders, comorbid
depression has been associated with higher OCD symptom scores both before and
after treatment relative to non-comorbid individuals (Abramowitz & Foa, 2000).
Yet this increased severity does not appear to hinder the ability of individuals with
comorbid major depression to make equivalent gains in treatment as compared with
their non-comorbid counterparts (e.g., Abramowitz, Franklin, Street, Kozak, & Foa,
2000; Abramowitz & Foa, 2000). Indeed, two studies suggest that OCD treatment
efficacy was not affected by the presence of pretreatment depression (Abramowitz
& Foa, 2000; Orloff et al., 1994), and pretreatment depression scores did not differ
between treatment completers and noncompleters in at least one study (Franklin,
Abramowitz, Kozak, Levitt, & Foa, 2000).
This small literature does include some evidence suggestive of a negative impact
of depression on OCD treatment outcome. Steketee et al. (2001) reported that
the presence of comorbid depression has an adverse effect on post-treatment and
6-month follow-up outcome. Work by Abramowitz et al. (2000) suggests that
treatment gains are limited among individuals with severe (relative to mild or moderate) depression. Finally, a recent meta-analysis associated comorbidity (including
depression) with reduced treatment effect sizes (Rosa-Alcázar, Sánchez-Meca,
Gómez-Conesa, & Marín-Martínez, 2008). Although this literature is somewhat
mixed, several studies indicate that individuals with OCD and comorbid depression can benefit from CBT for OCD and that comorbid depression is unrelated to
treatment compliance. Much less confidence is appropriate when treating an individual with severe depression, as this may be related to poorer outcome. Additional
research is necessary in order to clarify the influence of comorbid depression upon
CBT for OCD.
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PTSD
As with OCD, empirical investigations of the impact of comorbid depression on
treatment outcome for PTSD are limited. Several studies indicate that the presence of comorbid depression is unrelated to PTSD treatment outcome (Ehlers,
Clark, Hackmann, McManus, & Fennell, 2005; Gillespie, Duffy, Hackmann, &
Clark, 2002; Tarrier et al., 2000) and treatment attrition (e.g., Resick et al., 2002),
although additional treatments sessions may be required to attain the same clinical outcome (Gillespie et al., 2002). A negative impact of comorbid depression
on treatment outcome for PTSD is documented in three studies. Taylor et al.
(2001) noted that higher pretreatment depression scores were associated with partial relative to full response to CBT, and two studies related decreased treatment
adherence with increased pretreatment depression scores (e.g., Bryant et al., 2003;
McDonagh et al., 2005; c.f. Resick et al., 2002). Together, the evidence suggests
that response to CBT for PTSD may not be affected by the presence of comorbid
major depression, although additional treatment sessions or particular attention to
patient engagement in treatment may be required in order to maximize treatment
outcome.
Conclusions from the Treatment Outcome Literature
In an effort to clarify the scope of our chapter, the following limitations are important to note. First, the literature reviewed above concerned treatment for populations
with a primary anxiety disorder and secondary depression. Primary depression
may negatively impact treatment for secondary anxiety more substantially than
our review above suggests. Indeed, several of the studies excluded individuals
with depression that was severe enough to require hospitalization, re-emphasizing
the secondary nature of the depression considered in the studies reviewed above.
Second, anxiety disorders are frequently comorbid with bipolar disorder, yet treatment outcome studies concerning the impact of bipolar depression on anxiety
treatment are lacking in the published literature. Consequently, this review focused
on the effects of unipolar depression on anxiety treatment. Third, many of these
studies reviewed above included small sample sizes that may be underpowered
to detect small influences of comorbid major depression on treatment outcome.
Therefore, while it is possible that depression has a small effect on anxiety treatment
outcome, it is unlikely to have a marked negative impact upon treatment response in
this population. Finally, no studies examined whether the duration or early onset of
depression predicted anxiety treatment outcome. Given the evidence that depression
chronicity is a predictor of poor outcome in depression treatment studies (Keller
et al., 1992; Stewart et al., 1989), it is possible that individuals with early onset
of recurrent depressive episodes may exhibit lower treatment responses to CBT for
anxiety and later-onset comorbid depression may have a negligible effect on anxiety
treatment. Therefore, additional research is necessary before definitive conclusions
Comorbid Depression and Anxiety Treatment
237
can be drawn about the exact nature of the relationship between comorbid MDD and
anxiety treatment outcome. What is clear is that despite increased symptom severity before and after treatment, treatment gains need not be limited by the presence
of a comorbid mood disorder, but these patients may require additional attention in
treatment.
Impact of CBT for Anxiety Disorders
on Depression Symptoms
One particularly promising finding is that in many cases depression symptoms
appear to resolve significantly following anxiety treatment with CBT. For example, the percentage of individuals with panic disorder who met criteria for
comorbid depression (MDD and dysthymia) decreased from 18% to 6% following panic treatment (Tsao, Mystkowski, Zucker, & Craske, 2002). Significant
decreases in the percentage of individuals meeting criteria for MDD have also
been observed following CBT for PTSD (Blanchard et al., 2004; Resick &
Schnicke, 1992).
Depression severity reductions have also been observed across several anxiety populations including panic disorder (Joormann et al., 2005; Öst, Thulin, &
Ramnerö, 2004; Tsao et al., 2002), social anxiety disorder (Joormann et al., 2005),
generalized anxiety disorder (GAD) (Borkovec & Costello, 1993; Ladouceur et al.,
2000; Öst & Breitholtz, 2000), and OCD (Rosa-Alcázar et al., 2008). Indeed, almost
all studies of PTSD indicate a significant decrease in depression severity scores
following CBT (e.g., Bryant, Harvey, Dang, Sackville, & Basten, 1998; Bryant
et al., 2003; Cloitre, Koenen, Cohen, & Han, 2002; Ehlers et al., 2003; 2005;
Foa et al., 1999; Marks, Lovell, Noshirvani, Livanou, & Thrasher, 1998; Paunovic
& Öst, 2001; Resick et al., 2002; Resick & Schnicke 1992, see Foa, Rothbaum,
Riggs, & Murdock, 1991 and McDonagh et al., 2005 for failures of CBT to reduce
depression scores to a greater degree than a wait-list control group). Two studies
suggest that the impact of CBT for anxiety disorders on depression symptoms is
dramatic. Moscovitch, Hofmann, Suvak, and In-Albon (2005) indicated that social
anxiety symptom improvement mediated 91% of subsequent depression symptom
improvement and one meta-analysis suggests that CBT for (GAD) reduced depression symptoms to a greater degree than pharmacotherapy (Gould, Otto, Pollack, &
Yap, 1997). Therefore, the majority of studies indicate that CBT for anxiety disorders results in a reduction of comorbid depression, even when depression symptoms
are not a target of treatment.
Given research suggesting that the addition of CBT specifically aimed at reducing depression after the conclusion of anxiety treatment successfully reduces
remaining depressive symptoms (Woody, McLean, Taylor, & Koch, 1999), augmenting treatment with a booster session focusing on depression may be implemented for those individuals whose depression scores are not alleviated by CBT
for anxiety. In addition, some evidence suggests that anxiety interventions that
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target cognitive restructuring may result in greater depression severity reductions
than interventions that rely on exposure interventions (Bryant et al., 2003; Harvey,
Bryant, & Tarrier, 2003). Consequently, a therapist may choose a treatment protocol that emphasizes cognitive restructuring as well as exposure interventions for use
with comorbid patients.
There are a number of ways in which common treatment elements for anxiety
and depression may facilitate symptom reductions in both disorders. For example,
although negative thinking patterns in anxiety often involve fears of catastrophic
consequences and are distinct from the more self-punitive thoughts observed in
depression, the cognitive restructuring skills typically employed in CBT provide
patients with skills to identify, evaluate, and modify maladaptive negative thinking styles more generally. Training individuals to treat their thoughts as ideas to
be considered and evaluated rather than taken as fact may facilitate a reduction in
maladaptive responses to both anxiogenic and depressive thoughts. For example,
restructuring negative automatic thoughts common in social anxiety disorder (“I
will stumble over my words and look like an idiot”) requires similar techniques
as restructuring negative thoughts associated with MDD (“I am unlovable”). As
a result, depression-related thoughts, and therefore depression symptoms, may be
reduced following anxiety treatment.
Treatment for anxiety and depression encourages a systematic approach toward
symptom reduction and re-engagement with the world. In anxiety, the creation
of fear hierarchies and gradual conduct of exposure exercises encourage patients
to decrease avoidance behavior. Increased engagement in pleasurable activities
is a core component of CBT and behavioral activation treatments for MDD
(Jacobson, Martell, & Dimidjian, 2001). It is possible that the reduction of
avoidance behaviors following anxiety treatment promotes active engagement
in meaningful and pleasurable activities thereby ameliorating both anxiety and
depressive symptoms. For example, a panic patient’s increasing comfort using
public transportation or driving long distances following exposures may result
in increased visits to friends and family. The patient’s increased social engagement may then decrease depressive symptoms associated with loneliness and
isolation.
Finally, anxiety and depression are both characterized by effortful suppression and avoidance of emotional experiences (Campbell-Sills, Barlow, Brown, &
Hofmann, 2006). Several treatment strategies for anxiety encourage patients to
experience, acknowledge, tolerate, and accept their affective states and negative
thoughts while continuing to strive toward their goals (e.g., Barlow, Allen, &
Choate, 2005; Hayes, Strosahl, & Wilson, 1999; Otto, Powers, & Fischman, 2005).
Exposure exercises for OCD encourage tolerance and observation of anxious states
in order to view the extinction process and learn that rituals are not necessary in
order for anxiety to decrease. To the extent that an acceptance of emotions represents a general treatment factor that encourages more adaptive responses to marked
affective states (Barlow et al., 2005), reductions in depression symptoms may result
following the acknowledgement of negative affect and associated thoughts. These
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skills may be translated to other situations and emotions, leading to a reduction in
both anxiety and depressive symptoms.
Treatment Considerations for Comorbid Anxiety
and Depression
Although it is unlikely that comorbid major depression will routinely prevent an
individual from benefiting from anxiety treatment, the literature suggests that clinicians should expect some costs associated with the presence of a mood disorder
at least some of the time. For example, clinicians should anticipate that individuals
with comorbid anxiety and depression will exhibit higher symptom severity scores,
may have poorer motivation, and may exhibit thinking patterns that exacerbate their
anxiogenic thoughts and interfere with treatment compliance. Consequently, we
turn to a discussion of several treatment considerations that may help clinicians
to maximize successful outcome with comorbid populations.
First, both the patient and the clinician should consider that additional treatment
sessions may be required due to the presence of greater pre- and post-treatment clinical severity among individuals with comorbid conditions. In addition, treatment of
one disorder may fail to address the comorbid condition at all or to resolve symptoms completely. Some studies have used additional sessions as a successful way
of addressing the increased symptom severity likely to be present in comorbid populations (e.g., Gillespie et al., 2002), but additional protocols or strategies for the
comorbid illness may be required.
Second, an initial decision on treatment ordering is necessary when addressing comorbid conditions. As long as the anxiety disorder is primary (the primary
source of distress and disability), we routinely recommend attending to this disorder first as was done in the case example that opened this chapter. However,
because treatment adherence is greatest when participant expectations and treatment
methods are aligned (Eisenthal, Emery, Lazare, & Udin, 1979; Schulberg et al.,
1996), it is important to elicit information about the patient’s most pressing concerns and treatment goals. Developing a collaborative relationship with the patient
and conducting a thorough analysis of the relationship between symptom clusters
may facilitate treatment ordering decisions. For example, if a patient’s depression
primarily results from repeated panic attacks that interfere with her social and occupational abilities, she may benefit most significantly from initial treatment of panic
disorder. Depression symptoms may resolve naturally as panic symptoms subside
and as skills learned in CBT for panic are translated to her depression symptoms.
Additional treatment for MDD may be considered if her mood symptoms remain
elevated following successful panic treatment. On the other hand, if a patient’s
depression is severe enough to hinder her ability to conduct or benefit from the exposure exercises, treating the depression symptoms first using cognitive restructuring
and behavioral activation may lead to a more optimal outcome. See the following
case descriptions for an example.
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Box 1 – Case Examples
Case #1: Sally arrives at the clinic requesting treatment for panic attacks
occurring daily for the past 10 years. Some of her panic attacks occur out
of the blue, but some are triggered by reminders of prior traumatic events
resulting in a diagnosis of PTSD. The frequency of her panic attacks and
PTSD symptoms has led to a lengthy and severe depression over the past several years and she has been unable to work and take care of many household
responsibilities. After some conversation, it appears as if Sally’s depression
primarily stems from the impairment caused by her frequent and intense panic
attacks. In addition, Sally and her therapist believe that some of the skills associated with panic disorder treatment may be translated into future treatment
for PTSD. Consequently, they agreed to target panic symptoms first, PTSD
second, and depression third, with regular assessments of symptoms in each
domain throughout treatment. Sally responded well to CBT for panic disorder, noting a decrease in both trauma-uncued and trauma-cued panic attacks
over time. As the frequency of panic attacks decreased, Sally was able to
function more effectively at home and noticed an improvement in her social
relationships which helped to ameliorate her depressive symptoms. Further,
Sally reported a decrease in anxiety in response to trauma-related situations
due to increased coping skills as well as enhanced motivation to begin PTSD
treatment as a result of her successful treatment for panic disorder.
Case #2: Jill arrives at the clinic requesting treatment for frequent obsessions
and compulsions. Jill spends up to 6 hours/day completing complex rituals and
is unable to work. She reported having difficulty with depression throughout
her life and is currently experiencing a marked period of sad mood, anhedonia, poor energy, decreased appetite, psychomotor retardation, difficulty
concentrating, and passive suicidal ideation. Jill and her therapist evaluate the
relationship between Jill’s OCD and depressive symptoms and it appears as
if Jill’s depression sometimes occurs independently of her OCD symptoms,
but the onset of the current depressive episode began after a marked increase
in compulsions and the resulting loss of her job. Consequently, Jill and her
therapist believe that Jill’s current MDD symptoms are the result of the recent
OCD exacerbation and they agree to target OCD symptoms before turning
to address her depression. However, Jill had difficulty completing exposure
exercises in session, frequently remarking that she “isn’t strong enough” and
that “treatment won’t work for me.” In addition, Jill was unable to complete homework exercises, reporting that low energy and motivation made
it hard for her to purposefully challenge her anxiety. Because Jill’s depressive symptoms were making it difficult for her to complete and learn from
the exposure exercises, Jill and her therapist agreed to change the focus of
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treatment and address Jill’s depressive symptoms. Following behavioral activation and cognitive restructuring interventions, Jill’s depressive symptoms
remitted somewhat and she resumed OCD treatment. Once Jill’s marked MDD
symptoms no longer interfered with her ability to conduct exposure exercises
and her behavioral activation exercises provided her with opportunities to benefit from naturally occurring exposures, Jill experienced significant symptom
relief from repeated exposure exercises and the resulting habituation. This
success, in turn, further alleviated her remaining depressive symptoms.
The research literature suggests that Jill (Case #2) would likely benefit from OCD
treatment despite the presence of depression symptoms. However, given the impact
of depression on treatment compliance, Jill and her therapist adjusted their treatment
plan when it was clear that Jill’s comorbid depression was influencing her ability to
perform the homework exposures necessary for maximum treatment benefit. It is
possible that similar changes in treatment emphasis may help individuals whose
depression is impeding treatment progress to a significant degree. However, therapists will frequently encounter more subtle interference in daily sessions that can
negatively impact treatment goals. For example, comorbid depression frequently
results in the display of tearfulness or obvious low mood in session, whereas anxiety and avoidance may be more likely to occur outside of session and away from
a clinician’s immediate observation. Signs of in-session distress are often powerful and can lure a therapist into addressing these symptoms at the expense of the
anxiety treatment. Deciding whether to respond to in-session distress or focus on
the larger treatment goals is a difficult process. Returning to the initial functional
analysis of symptoms developed in collaboration with the patient may help the therapist to focus on the long-term goals relative to the patient’s short-term distress.
For example, a therapist may be tempted to use cognitive restructuring techniques
to challenge the negative thoughts (e.g., “I will never have friends”) of an individual with social anxiety and MDD, taking away time available during the session to
devote to exposures. Yet, the patient may benefit most from participating in exposure exercises designed to help him reduce his social anxiety and facilitate his ability
to develop social networks. These exposure exercises may also provide him with an
opportunity to challenge the maladaptive thoughts that help to perpetuate his negative mood. Given prior evidence that depression symptoms resolve following social
anxiety treatment (e.g., Moscovitch et al., 2005), it may be in the patient’s best
interest to minimize attention to his in-session distress and actively promote the
techniques that will move him toward his long-term goals. The one exception to
this principle is when suicidal ideation or intent arises. Regular assessment of suicidal ideation is a must in comorbid patients and, when present, may well redirect
therapeutic interventions to safety issues. Cognitive therapy emphasizing cognitive
restructuring and problem solving is efficacious for those at suicidal risk (Berk,
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Henriques, Warman, Brown, & Beck, 2004; Brown et al., 2005) and should be considered as part of an integrated treatment approach when serious suicidal ideation is
confronted in comorbid patients.
Third, a recent study found that a brief motivational interviewing intervention
prior to treatment for panic disorder, social anxiety disorder, or GAD increased
engagement with CBT and resulted in improved outcome (Westra & Dozois, 2006).
Consequently, attention to engaging the participant in treatment as a means of combating low motivation among anxiety patients regardless of comorbidity appears
worthwhile. In order to promote engagement with the treatment, we recommend
encouraging homework compliance, taking care to clearly write down all homework assignments, systematically review homework progress at each session, and
emphasizing the crucial nature of at-home practice. Similarly, although treatment
gains are always applauded, extra attention is given to early treatment gains to help
maintain a client’s motivation for treatment and facilitate the ability of patients to
link their efforts with demonstrable changes in their symptom and abilities.
Fourth, because low motivation and energy can make it more difficult for individuals to fully utilize CBT strategies, extra attention is paid toward preparing patients
for mood-specific cognitive biases and ways that they can challenge those biases.
For example, we attempt to give patients a vivid example of the powerful effects of
moods on thought patterns by examining how easily our beliefs are manipulated in
movies. Although we may know that the movie sequel starring the main character is
already being filmed, the ominous music and seemingly insurmountable obstacles
during the movie climax contribute to a temporary conviction that the main character is doomed. Negative affect common to depression and anxiety can function like
the background “mood music” present in these films and can increase the likelihood
that we will believe negative and false ideas that would be evaluated differently in
neutral or pleasant mood states. Therefore, thoughts can feel true during times of
marked depressed mood. However, “feeling” more believable does not increase the
actual accuracy of those beliefs. Thoughts about one’s inability to manage anxiety during depressed moods can be discussed in this framework. Psychoeducation
is paired with cognitive restructuring and coping skills designed to neutralize the
negative thought that interferes with treatment progress. Practicing this skill before
patients encounter such negative thoughts during exposure exercises may help the
patients reap the benefits of these exercises to a greater degree.
Fifth, negative thinking styles characteristic of depression may impair a patient’s
ability to learn from exposure exercises and to acknowledge treatment progress (e.g.,
“this isn’t working”; “I won’t get better”). Consequently, practicing the recognition
of and coping strategies for these thoughts during the session can have significant benefit for the patient when they encounter these thoughts on their own or
during exposure exercises. For example, negative thoughts about treatment (e.g.,
“this won’t work”) are likely to interfere with the individual’s willingness to conduct an exposure and a therapist may benefit from identifying and restructure this
thought early in treatment (e.g., “I don’t know if this will work but it can’t hurt to
give it a try”). Therefore, when the patient has the initial thought that treatment
won’t work outside of the session, s/he may already have a ready and adaptive
Comorbid Depression and Anxiety Treatment
243
response to the thought which may promote compliance with exposure homework.
Challenging negative thinking styles in advance may be of particular importance when addressing long-standing depressive cognitions related to core beliefs
(e.g., “I am a failure”). Hofmann and Otto (2008) addressed this issue in a recent
treatment manual. They discuss the case of Bob, a client with social anxiety disorder and comorbid depression whose negative self-statement, “I am a failure,” was
impeding treatment of his social anxiety disorder and did not respond to traditional
cognitive therapy strategies. The therapist chose to use an exposure-based technique
in order to help neutralize these negative thoughts and promote progress in social
anxiety treatment. Selected text from this portion of the manual is reproduced below.
Box 2 – Using Exposure Principles to Target
Maladaptive Beliefs
Therapist: Given how long you have been rehearsing that line, “I am a failure,” I am not going to try to directly break the habit of your saying it. But I
do want you to know that it does not serve you well; as long as you buy into
that thought, it keeps you stuck in your current position, making it hard for
you to learn new ways of interacting socially. So, while respecting the power
of your habit in saying, “I am a failure” to yourself, I am also going to ask you
to help this phrase lose its current meaning. I want it to becomes a phrase that
can no longer push you around emotionally or stand in your way of developing more social comfort. Starting today in session, I am going to ask you to
exposure yourself to this thought (“I am a failure”) by saying it over and over
to yourself aloud. I want you to listen to yourself say this statement and, as
you hear it, realize that this thought has traditionally pushed you around and
made it harder for you to reach your goals. I want you to say it to yourself and
let it lose some of its meaning. . .
Below are some of the examples of thoughts that went through Bob’s head as
he was reading the phrase:
I am a failure (boy, that is a nasty thought, generally makes a person feel
lousy)
I am a failure (yep, this is what I say to myself to make myself feel bad)
I am a failure (pretty negative. . . this is my habit)
I am a failure (I will just need to get bored with hearing this)
I am a failure (yep, this is what I say over and over again)
I am a failure (getting boring)
I am a failure
I am a failure
I am a failure (yep, I use this thought to really screw myself over)
I am a failure
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C.M. Deveney and M.W. Otto
I am a failure (time to really get bored with this)
I am a failure
I am a failure (time to take away all meaning from this thought)
I am a failure
I am a failure
I am a failure
I am a failure (here I go again with this old, negative thought)
I am a failure
I am a failure . . .
Reproduced with permission from Hofmann, S.G., & Otto, M.W. (2008).
Cognitive behavioral therapy for social anxiety disorder. New York:
Routledge, pp 117–118.
Finally, earlier in this chapter we discussed the similarities between systematically addressing items on a fear hierarchy and gradual participation in activities
designed to increase behavioral activation. Both of these strategies emphasize
systematic exposure to healthy behaviors that increase reinforcement and reduce
avoidance. As individuals gradually increase their participation in activities that
constitute a meaningful life, depression and anxiety symptoms should be reduced,
indicating that these strategies may allow a therapist to target both symptom clusters successfully (Hopko, Lejuez, Ruggiero, & Eifert, 2003). For example, Hopko,
Lejuez, and Hopko (2004) recently applied behavioral activation strategies to the
treatment of an individual with comorbid panic disorder and depression (Hopko
et al., 2004). Successful progression through a hierarchy of depression and anxietyrelated behaviors ranked by level of ease was associated with a corresponding
reduction in both symptom clusters. Consequently, when working with a population with anxiety disorders, we encourage the scheduling of activities that will help
boost pleasant mood and encourage the patient to conduct exposure exercises.
Concluding Comments
Because comorbidity rates between anxiety and depression are high in the research
literature (e.g., Kessler et al., 1996) and clinical practice (e.g., Brown, Campbell,
Lehman, Grisham, & Mancill, 2001), our goal in this chapter was to address the
impact of depression comorbidity upon the treatment of anxiety disorders and to
review strategies to resolve problems associated with this comorbidity. Fortunately,
it appears as if the efficacy of CBT for anxiety disorders is not significantly reduced
by the presence of MDD. Ability to engage in treatment and make treatment gains
appears unaffected by the presence of MDD and depression symptoms are often
significantly reduced by treatments targeting anxiety disorders. Yet the empirical
literature also highlights several subtle ways in which comorbid depression may
Comorbid Depression and Anxiety Treatment
245
influence anxiety treatment (e.g., increasing symptom severity, influencing motivation, decreasing ability to learn from exposure exercises). Therefore, we offered
several suggestions to help minimize the smaller effects that comorbid depression
may have upon treatment for anxiety disorders. We hope that these suggestions will
allow clinicians to work effectively with challenging populations.
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Resolving Treatment Complications
Associated with the Presence of Comorbid
Personality Disorders
Matthew K. Nock, Tara L. Deliberto, and Michael Hollander
Eva, a 36-year-old Hispanic woman, presented to an outpatient clinic for the treatment of social anxiety disorder (SAD). Eva was referred by her psychoanalyst, whom
she had been seeing four times per week for the past two years, because the analysis
did not appear to be improving her SAD and he believed cognitive-behavioral therapy (CBT) may be indicated. During his first meeting with Eva the CBT clinician
conducted a structured diagnostic interview for Axis I disorders, which confirmed
the presence of SAD as well as comorbid major depressive disorder. No assessment of Axis II disorders was performed given the case was referred as “a pretty
straightforward SAD case” and the initial interview did not disconfirm this (nor did
it try). The interview suggested that Eva’s depression was secondary to her SAD,
as the negative automatic thoughts and other depressive symptoms she experienced
seemed largely to result from her lack of engagement in pleasurable activities and
her failure to have any social interactions outside of those that were completely necessary at work. Eva was referred to cognitive-behavioral group therapy for SAD,
but refused to participate in a group because “I’ve had great difficulties with other
women in the past. Men are always very attracted to me, and women get angry as a
result, and I don’t want to participate in group therapy at this time because I don’t
want all of that to get in the way of my treatment.” Eva began once weekly CBT
for SAD, which initially proceeded just as planned. She attended each session on
time and was very organized in session – creating a binder for all of her treatmentrelated materials, writing out a detailed homework list at the end of each session,
and completing most of her homework assignments each week. However, several
complications arose after the first few sessions. During the first in vivo exposure
exercise, Eva became extremely upset. She cried for 15 minutes and made numerous
self-critical statements such as “I’m so stupid!. . .I don’t deserve to get better!. . .No
one will ever be with me!” The intensity and duration of Eva’s responses were much
stronger than expected given the situation. A follow-up with Eva by the clinician
revealed that Eva had been experiencing extremely intense responses to stressful
M.K. Nock (B)
Department of Psychology, Harvard University, Cambridge, MA, USA
e-mail: nock@wjh.harvard.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_14,
C Springer Science+Business Media, LLC 2010
251
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events for many years. Moreover, she reported using non-suicidal self-injury for the
past 15 years in order to help regulate this intense affect, as well as to convey to
others how distressed she was feeling. Eva also reported the daily experience of
intense anger toward others, feelings of emptiness and abandonment, and paranoid
thoughts that other people were plotting against her at work. The clinician used the
next session to conduct a thorough diagnostic assessment of Axis II disorders, which
revealed the presence of borderline personality disorder and paranoid personality
disorder.
How might the presence of these comorbid personality disorders introduce complications in the treatment of Eva’s SAD? What things should the clinician consider
in conducting ongoing assessment in this case? What can the clinician do to manage
and/or ameliorate Eva’s personality disorders while also providing effective treatment of her Axis I disorders? The purpose of this chapter is to (a) describe the
nature of personality disorders, (b) review the extent to which personality disorders
are comorbid with anxiety disorders, (c) discuss treatment complications that can
arise when comorbid personality disorders are present, and (d) describe ways in
which clinicians can resolve these complications.
The Nature of Personality Disorders
A personality disorder is “an enduring pattern of inner experience and behavior that
deviates markedly from the expectations of the individual’s culture, is pervasive and
inflexible, has an onset in adolescence or early adulthood, is stable over time, and
leads to distress or impairment” (American Psychiatric Association [APA], 1994,
p. 629). The DSM-IV includes 10 personality disorders grouped into three overarching clusters. Cluster A includes paranoid, schizoid, and schizotypal personality
disorders – all characterized by odd or eccentric thoughts, feelings, and behaviors.
Cluster B includes antisocial, borderline, histrionic, and narcissistic personality disorders – all characterized by dramatic, emotional, or erratic thoughts, feelings, and
behaviors. Cluster C includes avoidant, dependent, and obsessive compulsive personality disorders – all characterized by anxious or fearful thoughts, feelings, and
behaviors.
Although personality disorders have existed as formal diagnoses since DSM-III
(APA, 1980), their rate of occurrence in the community has been unknown until
recently. Several recent surveys indicate that personality disorders occur in approximately 9.1–15.7% of adults in the community (Crawford et al., 2005; Lenzenweger,
Lane, Laranger, & Kessler, 2007; Samuels et al., 2002). The largest and most representative survey reporting on the prevalence of personality disorders in the United
States, the recently completed National Comorbidity Survey – Replication (Kessler
& Merikangas, 2004), provides the most recent and representative rates of Cluster
A (5.7%), Cluster B (1.5%), and Cluster C (6.0%) disorders (Lenzenweger et al.,
2007).
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Although all clinicians are quite familiar with personality disorders in general,
it is instructive for the current purposes to acknowledge several important issues
that can arise when working with clients with personality disorders. First, many
clinicians have negative thoughts and feelings about people with personality disorders. Such individuals are often viewed as being hostile, uncooperative, and
manipulative (Bowers & Allan, 2006; Potter, 2006). Although empirical work on
personality disorders suggests that these are often difficult conditions to treat, it
is important to remember that not all clients with a personality disorder share the
undesirable qualities listed above. It may be helpful to remember that many of the
behavioral patterns displayed by those with personality disorders are the result of
both biological predispositions and earlier learning experiences (e.g., Siever, 2005;
Ehrensaft, Cohen, & Johnson, 2006).
Perhaps more importantly, the conceptualization about what it means to “have”
a personality disorder has changed recently as a result of new research on
this topic. There is emerging evidence that personality disorders are not all
categorical entities but in some cases represent extreme points on a continuum or dimension of personality traits or characteristics that we all possess
(Guay, Ruscio, Knight, & Hare, 2007; Haslam, 2003; Trull & CDurrett, 2005;
Westen & Shedler, 1999). Conceptualizing personality disorders in this way has
great intuitive and clinical appeal and may help clinicians and the public better
understand the experiences and behaviors of those diagnosed with a personality
disorder.
Often, clinicians’ preconceived notions about what characterizes people diagnosed with a personality disorder can negatively influence the treatment offered. A
common error is to confuse the intention of a client’s behavior with the effect the
behavior has on the clinician. Consider the following interaction between a clinician (T) and his supervisor (S) in which the clinician came to supervision clearly
frustrated by his client (P).
T: Once again P did not do her homework. In our last session I clearly told her
exactly what to do for homework and even worked on getting a commitment,
and then did some troubleshooting.
S: OK. What happened when she came in for the next session?
T: What always happens, she didn’t follow through. It’s so clear that she is purposely sabotaging the treatment as a way of just holding on to her relationship
with me.
S: Perhaps. Did you speak with her, though, about how difficult the homework might be for her? Is it possible that this is why she has not done her
homework?
T: I think it’s a given that the homework is tough. It’s homework. I don’t think
we need to belabor that point. She is just being a typical Borderline who
doesn’t want to get better.
S: It may be that her presentation is not atypical for someone with BPD.
It also sounds, though, like you may be responding like “a typical
therapist.”
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The supervisor went on to suggest that the clinician might be confusing his
understandable frustration as being caused by the client’s deliberate lack of followthrough; however, it was clear that an element was missing in the treatment. Instead
of placing blame on the client, one must take the view that the treatment must be
modified. Specifically, it might be useful for the clinician to accept how emotionally
challenging the homework is going to be for the client and offer validation regarding
the difficulty level of the assignment.
A second important issue that can arise when working with patients with
personality disorders is that although personality disorders are often thought
of as life-long or at least long-term conditions, recent research examining the
stability of these disorders suggests they are much less persistent than previously assumed. Results from the Collaborative Longitudinal Personality Disorder
Study indicate that although personality disorders are generally more persistent
than Axis I disorders and maladaptive trait constellations that characterize specific personality disorders tend to persist over time, the majority of clients who
meet criteria for a personality disorder at initial assessment fail to meet criteria when followed up 12 or 24 months later (Grilo et al., 2004; Shea et al.,
2002).
The fact that personality disorders are not necessarily intractable by nature suggests that their remission may be facilitated, and their probability of re-occurrence
reduced, by psychological intervention. Indeed, results from the NCS-R suggest that
approximately 39.0% of those with a personality disorder report receiving treatment
of some kind in the past year, with the rate much higher for Cluster B (49.1%) than
Cluster A (25.0%) or Cluster C (29.0%) (Lenzenweger et al., 2007). What is less
clear, however, is how and why people with personality disorders come to present
for treatment.
Comorbidity of Personality Disorders and Anxiety Disorders
In our experience it is relatively rare for people to present for treatment with a chief
complaint of a personality disorder. Instead, personality disorders are often revealed
at the initial assessment or during the course of treatment for some other disorder.
Prior research in this area suggests that personality disorders are significantly more
likely to be present among those with an Axis I mental disorder of any kind and
the odds are highest for those with mood and anxiety disorders. Indeed, those with
an anxiety disorder are approximately seven times more likely to have a personality
disorder than those without an anxiety disorder; and despite the apparent overlap
between anxiety disorders and Cluster C personality disorders, the odds are higher
for Cluster B (OR = 8.4) than Clusters C (OR = 4.0) or A (OR = 2.5) (Lenzenweger
et al., 2007). Moreover, examination of the odds of having a personality disorder
among each type of anxiety disorder reveals that the highest odds of personality
disorder are seen among those with SAD (OR = 9.9) and panic disorder (OR = 8.0)
(Lenzenweger et al., 2007). While these data are from a nationally representative
survey, data from both outpatient and inpatient clinical samples also indicate that
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personality disorders are fairly common among those with an anxiety disorder (29–
35% of outpatient cases and 89% of inpatient cases), although the highest rates of
personality disorders in such settings appear to be for Cluster C rather than Clusters
B and A (Sanderson, Wetzler, Beck, & Betz, 1994; Skodol et al., 1995).
It is important to consider the ways in which comorbidity between anxiety disorders and personality disorders may arise; a case conceptualization of the relation
between the presenting disorders based on the client’s psychological history can
help guide assessment and treatment decisions. There are many different ways in
which comorbidity may arise in any particular case (Kessler & Price, 1993). It
could be that the presence of anxiety disorders during childhood leads to maladaptive behavioral patterns (e.g., avoidance of others, excessive fears or concerns) that
interact with contextual factors to produce personality disorders. In contrast, these
disorders could share a common etiologic pathway and overlapping symptom presentations. For instance, multiple studies demonstrate significant overlap between
SAD and avoidant personality disorder (e.g., McGlashan et al., 2005), both of which
are characterized by persistent and impairing social inhibition and fear of negative
evaluation, and some have suggested that they are actually different conceptualizations of the same disorder (Johnson, Cohen, Kasen, & Brook, 2006; Ralevski,
sanislow, & Grilo 2005).
Another example of comorbid disorders with potentially shared etiology is seen
in the overlap of post-traumatic stress disorder (PTSD) and panic disorder with borderline personality disorder (BPD). Prior research has consistently demonstrated
strong relations between these two anxiety disorders and BPD (see Lenzenweger
et al., 2007; McGlashan et al., 2005; Shea et al., 2004), and each of these disorders has been associated with the occurrence of abuse during childhood (e.g., Latas,
Starcevic, Trajkovic, & Bogajevic 2000; Ozkan & Altindag, 2005). It may be that
early abuse leads to the increased likelihood of factors such as hyperarousal, numbing, and re-experiencing of earlier traumatic events, with the experience of these
symptoms meeting criteria for PTSD; the experience, misinterpretation, and fear of
them leading to a diagnosis of panic disorder; and the experience and maladaptive
behavioral reaction to them leading to a diagnosis of BPD (e.g., Kaplow, Dodge,
Amaya-Jackson, & Saxe, 2005; Lilienfeld & Penna, 2001; Pollack et al.,1996; Yen
et al., 2002).
Although the etiology of mental disorders is quite difficult to determine in
even the most methodologically rigorous research studies, let alone in uncontrolled
clinical settings, the careful assessment and development of a working case conceptualization about the relations between anxiety and personality disorders is strongly
advised in treating clients who may display features of both classes of disorders. The
following case vignette highlights the importance of having a case formulation that
includes an understanding of the ways personality disorders and anxiety disorders
may have a synergistic effect on each other:
Christie presented for treatment with two significant complaints. First, she
reported having a number of failed relationships with men that often led to her
withdraw for weeks at a time from the expectations of her daily life. Second,
she complained that her anxiety was seemingly ever present but worsened when
she withdrew. On several occasions her withdrawal led to her losing friendships
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and jobs. A series of analyses of antecedents and consequences of Christie’s
maladaptive behaviors in relationships elucidated a pattern in which she would
quickly become dependent on the men with whom she was with, and then would
begin to worry excessively that they would leave her. Her worry often caused her to
be overly demanding and needy, and she would often become furious when she felt
that the man was pushing her away. Her angry responses to her boyfriends led to
the dissolution of the relationship. This ineffective interpersonal style is often characteristic of people with BPD. Christie reported that as she began to get over her
failed relationship her anxiety would begin to rise, just when she started to imagine
re-engaging in relationships and other social activities. By description, her anxiety
had the quality of SAD in which she dreaded making phone calls and applying to
jobs and attending social functions. Examinations of her anxiety in the context of
her more global behavioral patterns led her to discover several dysfunctional core
beliefs, including that she perceived she was doomed to this pattern of relating and
that she was defective and weak.
Complications Associated with the Presence of a Comorbid
Personality Disorder
Greater clinical severity. The first potential complication to consider in treating
clients with an anxiety disorder who have a comorbid personality disorder is that the
presence of the latter has been associated in some studies with significantly greater
clinical severity and chronicity of the anxiety disorder and with great functional
impairment (e.g., Ozkan & Altindag, 2005; Skodol et al., 1995). These findings
suggest that the identification of a personality disorder among a client with anxiety
should signal to the clinician that such a client may have greater impairment than
typically seen among anxiety disorders clients, and conversely that the observation
of more extreme symptom presentation and impairment in a client with an anxiety disorder should prompt an assessment of personality disorders if not already
completed.
On balance, several studies have failed to find a difference in the severity of
anxiety disorders between those with and without a personality disorder (e.g., Grant
et al., 2005; Sanderson, Wetzler, Beck, & Betz, 1994) and also have reported that
much of the impairment observed among those with personality disorders is largely
accounted for by the presence of an Axis I disorder. Thus, the data appear to be
somewhat mixed on whether those with a comorbid personality disorder will present
with greater clinical severity. However, what is perhaps most important to consider is
whether a comorbid personality disorder will interfere with or complicate treatment
in some way.
Poorer response to treatment. A second important consideration is that those
with a comorbid personality disorder have been reported to have a poorer response
to the treatment of their Axis I disorder. For instance, Mennin and Heimberg (2000)
reviewed nine studies of the treatment of panic disorder in which some participants
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had a comorbid personality disorder and reported that two-thirds of these studies
showed that the presence of a personality disorder was associated with a worse
clinical outcome. Similarly, Pollack and colleagues (1996) reported that in the
cognitive-behavioral treatment of 100 outpatients with panic disorder, 59% of those
without a comorbid personality disorder achieved at least a two-month period of
remission, while this was true for only 29% of those with a personality disorder. The
relation between a comorbid personality disorder and poorer treatment outcome has
been found in other anxiety disorders beyond panic disorder. For instance, Berger
and colleagues (2004) found that the presence of a comorbid personality disorder
was associated with a poorer and slower response to treatment. More specifically,
the likelihood of a favorable response to cognitive group therapy and/or paroxetine was twice as high among those without a comorbid personality disorder. Poor
response also has been shown in other studies in the context of SAD and generalized
anxiety disorder (e.g., Massion et al., 2002).
Here too, however, other studies suggest the issue is slightly more complex.
Some have reported that although clients with a comorbid personality disorder have
greater clinical severity to begin with, they experience as much clinical change over
the course of treatment as those without a comorbid personality disorder (Dreessen
& Arntz, 1998). An important direction for researchers to focus on is determining
why individuals with an anxiety disorder might have less favorable treatment outcomes in the presence of a comorbid personality disorder. Some research suggests it
is not the presence of a specific personality disorder per se, but the presence of maladaptive, avoidant, and paranoid beliefs that may lead to poor outcomes (Kuyken,
Kurzer, DeRubeis, Beck, & Brown, 2001). Also, it is common for people with a
personality disorder to conceptualize their problems as being indicative of a character flaw or weakness rather then as a psychological problem to be solved. This
belief may make people with personality disorders skeptical that psychotherapy can
be beneficial. With a better understanding of how and why personality disorders
might limit treatment effects, clinicians can aim their treatment at these factors in
an attempt to maximize treatment effects.
Premature termination of treatment. Another potential complication is that
clients with a personality disorder may be more likely than others to terminate treatment prematurely; however, those remaining in treatment may improve just as much
as others (Persons, Burns, & Perloff, 1988; Sanderson et al., 1994). The specific reason for premature termination among people with a personality disorder may vary
depending on the disorder present. For instance, people with a comorbid avoidant
personality disorder may have an excessive fear of criticism and ridicule from
others, including their clinician, which may increase the likelihood of treatment termination (Greenberg & Stravynski, 1985). Those with BPD also have shown rates
of treatment attrition that are twice as high as those without BPD. This may be
due to BPD-related problems such as conflicts that can arise in the client’s relationship with the clinician, concerns about abandonment by the clinician, or concerns
about treatment being too intense or inflexible (Chiesa, Drahorad, & Longo, 2000).
When treating a client with comorbid anxiety and BPD or dependent personality
disorder, it is critical that the clinician be alert to issues pertaining to problems with
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dependency. Treatments are often ended precipitously either because the client cannot tolerate their dependency on the clinician or because the clinician finds the client
too demanding. These are only a few of the ways in which a comorbid personality
disorder may lead to premature termination, and this possibility is one the clinician
should keep in mind over the course of the intervention.
Greater likelihood of self-injurious thoughts and behaviors. The most important
potential complication to consider in treating those with a comorbid personality disorder is that the presence of personality disorders is associated with a significantly
higher likelihood of self-injurious thoughts and behaviors (SITB; Duberstein &
Conwell, 1997; Isometsa et al., 1996; Linehan, Rizvi, Shaw Welch, & Page, 2000).
This is true of personality disorders in general and also is true in the context of Axis
I anxiety disorders. Anxiety disorders are independently and significantly associated
with both suicidal thoughts and suicide attempts (e.g., Kessler, Borges, & Walters,
1999). Further, prior research has shown that among those with an anxiety disorder,
the presence of a personality disorder is associated with significantly higher impulsiveness and suicidal thoughts and behaviors (Starevic, Bogojevic, Marinkovic, &
Klien, 1999; Zlotnick et al., 2003).
Anxiety disorders and SITB have both been conceptualized as attempts to escape
from aversive cognitive and emotional states (Barlow & Craske, 2000; Hawton,
Cole, O’Grady, & Osborn, 1982; Nock & Prinstein, 2004, 2005), and the presence of
a personality disorder may signal the existence of especially strong emotion reactivity and increased impulsiveness or irritability (depending on the personality disorder
in question), which could together significantly increase the likelihood of SITB. In
addition, non-suicidal self-injury (NSSI) can have the effect of being a very potent
negative reinforcer (e.g., Nock & Prinstein, 2004). It can function as an effective,
but maladaptive, short-term solution to the experience of aversive internal states.
Consequently, the presence of this behavior may interfere in the between-session
practice components of a behavioral intervention.
Resolving Treatment Complications
Assessment of personality disorders. The first thing one must consider clinically in
attempting to resolve treatment complications related to the presence of a comorbid
personality disorder is whether such a disorder is present at all. There are a number of interview-based and self-report measures of personality disorders, some of
which also assess non-diagnostic personality traits that may be of interest clinically.
Although a comprehensive review of these measures is beyond the scope of this
brief chapter, we review some of the most commonly used measures here. Those
interested in more detailed information on the assessment of personality disorders
should consult sources dedicated to this topic (e.g., Widiger, in press).
Perhaps the most commonly used interview-based measure of personality disorders is the Structured Clinical Interview for DSM-IV Axis II Disorders (SCID-II;
First, Gibbon, Spitzer, Williams, & Benjamin, 1995). The SCID-II is a 119-item
semi-structured interview that assesses the presence of each of the 10 personality
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disorders one symptom at a time. It takes approximately a half hour to an hour
to administer and with a trained interviewer yields reliable Axis II diagnoses. The
strengths of the SCID-II are that it is based directly on the DSM-IV, it is fairly
straightforward to use, and it can be easily and flexibly modified for clinical purposes. For instance, if a single personality disorder is detected at pre-treatment, the
clinician can re-administer only that module repeatedly over the course of treatment,
or at the end of treatment, rather than the entire SCID-II interview. Some things to
consider, though, are that the SCID-II requires fairly extensive training to be administered and scored correctly, and this training may not be accessible or desirable for
all clinicians.
Other interview-based measures to consider are the Personality Disorder
Examination (PDE-R; Loranger, Susman, Oldham, & Russakoff, 1987) and the
Structured Interview for DSM-IV Personality Disorders (SIDP-R; Pfohl, Blum,
Zimmerman, & Stangl, 1989). The PED-R takes approximately two and a half hours
to administer and the SIDP-R takes anywhere from an hour to an hour and a half to
administer. Although the PED-R takes a relatively longer period of time, it is especially accurate in deriving dimensional scores (Beck, Freeman, Davis, & Associates
2004). Both interviews have demonstrated reliability; however, training for these
interviews is imperative.
Where semi-structured diagnostic interviews of personality disorders are not
feasible or are less desirable, diagnostic measures can be administered in a selfreport format. Many clinicians and researchers find this approach most practical
because training to administer the questionnaire is not required and questionnaires
take less time to complete than interviews. Although evidence suggests that selfreport measures of personality disorders result in over-diagnosis (Zimmerman,
1994), there is insufficient evidence supporting that one format, interview or selfreport, should be preferred over the other. Questionnaires such as the Millon
Clinical Multiaxial Inventory (MCMI-III; Millon, Millon, & Davis, 1994) and
the Personality Diagnostic Questionnaire-Revised (PDQ-R; Hyler & Reder, 1988)
are just a few of the most widely used self-report measures of personality
disorders.
Several self-report measures of personality traits also may be of great clinical use, such as the Schedule for Non-adaptive and Adaptive Personality (SNAP;
Clark, 1993) and the Dimensional Assessment of Personality Pathology-Basic
Questionnaire (DAPP-BQ: Livesley, 1990). Clinician-rated assessments also are
available, such as the Shedler-Westen Assessment Procedure (Westen & Shedler,
2007), which are slightly more time-intensive but provide a unique means of quantifying clinicians’ experience of clients’ normal and pathological personality traits.
In addition, measures such as the Personality Belief Questionnaire (PBQ; Beck
& Beck, 1991) and the Schema Questionnaire (SQ; Young & Brown, 1994) have
been created specifically to assess cognitive dimensions present in specific personality disorders and thus may be particularly useful in the context of CBT (Beck
et al., 2004).
Assessment of self-injurious thoughts and behaviors (SITB). Another important
issue for the clinician to consider is the assessment of SITB among clients with a
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comorbid personality disorder. Comprehensive guidelines for assessing suicide risk
have been outlined in detail (AACAP, 2001; APA, 2003; Jacobs, 1999), and several recent papers describe the evidence-based assessment of SITB (Nock, Wedig,
Janis, & Deliberto, 2008) as well as practical recommendations for conducting risk
assessments (Bryan & Rudd, 2006; Joiner, Walker, Rudd, & Jobes, 1999; Kleespies
& Dettmer, 2000). Given both the likelihood that clinicians will encounter potentially self-injurious individuals and the limited training in the assessment of SITB
currently provided in most training programs (Kleespies et al., 2000), we strongly
suggest consulting these sources on suicide assessment. For the current purposes,
we will outline some of the key points to consider below.
First, it is essential to carefully assess the presence of SITB, which can include
suicide ideation, suicide plans, suicide attempts, and suicide death – all involving
an intent to die on the part of the individual. SITB also include non-suicidal SITB –
in which intent to die is not present (e.g., repetitive self-cutting, suicide gestures).
It is important to distinguish between suicidal and NSSI, as well as between selfinjurious thoughts and behaviors, as research has demonstrated that these different
constructs have different base rates and correlates (Kessler, Berglund, Borges, Nock,
& Wang, 2005; Nock & Kazdin, 2002; Nock & Kessler, 2006), as well as different responsiveness to treatment (G. K. Brown et al., 2005; Linehan, Armstrong,
Suarez, Allmon, & Heard, 1991a). In clinical practice, ascertaining the differences
between suicidal and non-suicidal behaviors is often a matter of asking the right
questions. Clients often know when their self-injurious behavior is in the service of
affect regulation (helping them to calm down from painful emotional experiences)
and when the behavior is specifically designed to end their lives. A direct inquiry
often helps the clinician make this determination, and of course further assessment
of the behavior is always in order to confirm this finding.
Second, the assessment of SITB can best inform one’s case conceptualization if
it goes beyond the measurement of the presence of SITB to assess the factors that
may have led to the initiation and maintenance of SITB. SITB are multi-determined
behaviors and the range of factors that may influence their occurrence is extremely
broad; however, the strongest risk factors are the presence of prior SITB and the
presence and accumulation of mental disorders. Beyond these factors, it is often very
useful to assess the specific antecedents and consequences of SITB episodes in order
to better understand the specific factors or processes influencing their occurrence
(e.g., Nock & Prinstein, 2004, 2005). Several reliable and valid measures are freely
available that can guide the assessment of the presence of a wide range of SITB,
as well as the factors that influence them, such as the Suicide Attempt Self-Injury
Interview (SASII; Linehan, Comtois, Brown, Heard, & Wagner, 2006) and the SelfInjurious Thoughts and Behaviors Interview (Nock, Holmberg, Photos, & Michel,
2007). These and a broader range of measures of SITB are described in great detail
elsewhere (G. K. Brown, 2000; Goldston, 2000; Nock, Wedig, Janis, & Deliberto,
2008).
Third, the treatment of SITB should be guided by the information obtained from
the assessment of the presence and determinants of the SITB. Prior studies have
failed to demonstrate that treating mental disorders (e.g., major depressive disorder)
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decreases SITB. However, several treatments targeting SITB directly have proven
efficacious at decreasing the occurrence of these behaviors (e.g., G. K. Brown et al.,
2005; Linehan, Armstrong, Suarez, Allmon, & Heard, 1991b; Linehan, Comtois,
Murray et al., 2006). In addition to targeting SITB directly, it is important to continue to assess SITB over the course of treatment in order to measure treatment
effects, as well as to manage the risk of SITB over the duration of the intervention.
Case formulation. One of the most important steps in resolving treatment
complications associated with the presence of a comorbid personality disorder is
determining how that personality disorder fits into the clinician’s conceptualization
of the development and maintenance of the client’s mental disorders and functional
impairment. Many valuable sources are available that provide great detail about a
cognitive therapy conceptualization of personality disorders (e.g., Beck et al., 2004;
Young, 1994) and we can only scratch the surface of such issues here. It is assumed
that the pervasive and persistent thoughts, feelings, and behaviors that characterize personality disorders are developed through the interaction of genetic/biological
predispositions and significant environmental events (see Goodman, New, & Siever,
2004; Siever, 2005). Through these interactions, individuals may learn to process
information and view themselves, others, and the world in inaccurate and dysfunctional ways. More specifically from a cognitive perspective, a person can develop
core beliefs that influence the way they subsequently attend to, encode, and process information, as well as how they respond behaviorally in different situations.
For instance, a person who develops a core belief of “I will be hurt by others” or
“Others are harmful and cannot be trusted” may ultimately behave in ways that are
consistent with a diagnosis of avoidant or paranoid personality disorder.
Several of the personality disorder measures reviewed above, such as the PBQ
and SQ, may be particularly useful for this purpose as they provide information
about specific dysfunctional beliefs that could be targeted in treatment. Obtaining
information about the beliefs a client holds, and how these beliefs may influence
their personality disordered behavior, as well as their Axis I disorder, can enhance
clinical understanding of this behavior and will be extremely useful in guiding treatment as well as in providing information about treatment effectiveness. For instance,
if a client is avoiding others because she firmly believes all others will ultimately
hurt her, this information: 1) may help the clinician understand and more accurately
predict this client’s behaviour, and 2) provides a specific target for cognitive therapy. Furthermore, the intensity and frequency of such beliefs and thoughts offer a
baseline that can be used to measure change over the course of treatment.
Ordering of target behaviors in treatment. Regardless of the case conceptualization, it is essential that the first target of treatment be decreasing and ultimately
eliminating any SITB that are present. This is the case for both ethical and clinical reasons, as it is in direct opposition to the role of the clinician as a healer to
focus on less severe behaviors while a client directly and deliberately engages in
self-injury. In addition, if self-injurious behavior serves as a means of decreasing
anxiety, the treatment will have little traction if this behavior is not the top priority. If SITB are not present, then the clinician should focus on behaviors that
might interfere with treatment such as attendance and adherence, followed by those
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that are most impairing or believed to be the primary problem that the client is
currently experiencing. Such a structure for organizing treatment targets has been
proposed in much greater detail by Linehan (1993) in discussing the treatment of
BPD and serves as an excellent model for all treatments where SITB and treatmentinterfering behaviors may arise. It is notable that the clinician should actively assess
each of these areas and make decisions about the ordering of treatment targets as
often times when SITB are present they are not the chief complaint of the client, or
even desirable treatment targets.
Treating personality disorders in the context of treating Axis I disorder. As in
CBT focused on treating any disorder, whether an Axis I disorder, Axis II disorder,
or a problem not addressed in the DSM-IV, it is important to identify target behaviors and define them as clearly, specifically, and objectively as possible. In addition,
applying what is currently known about the principles of behavior change to modify
these targets is essential. The cognitive-behavioral principles, strategies, and practices used to treat Axis II pathology are quite similar to those used to treat Axis I
disorders. For instance, after a thorough assessment, the clinician provides information about the personality disorder(s) present, describes a cognitive-behavioral
model of the disorder(s), and outlines the proposed treatment plan. In addition, the
clinician develops a case conceptualization and shares this with the client in an effort
to work collaboratively toward the agreed-upon goals of treatment.
In attempting to change cognitions and behaviors associated with a personality disorder, the clinician uses the same cognitive strategies as in the treatment of
Axis I disorders, such as identifying and labeling dysfunctional beliefs, examining the evidence for these beliefs, and generating and evaluating more balanced
beliefs. Particularly helpful in the treatment of personality disorders, especially
given their pervasive and persistent nature, is the identification of the client’s core
beliefs related to their personality disorder. As an example, consider an exchange
between Eva and her clinician in which they attempt to uncover the core beliefs that
may be contributing to her paranoid personality disorder:
P: I did only part of my homework assignment for this week. I attended the
pottery class in an attempt to meet other people. . .but I didn’t introduce
myself to anyone or start-up any conversations, so I guess I completely blew
this one.
T: That’s great that you went to the class! That is really wonderful! So let’s talk
a bit about what happened at the class. Did you remember that your goal for
this assignment was to introduce yourself to one person in the class?
P: I’m not an idiot. Of course I did.
T: OK, great. So thinking back to when you were actually in the class. . .did you
try to introduce yourself to anyone?
P: No.
T: What thought did you have when you remembered that that is what you were
planning to do?
P: I thought: ‘This class is mostly women. This sucks. I don’t want to talk to
any of these women.’
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T: OK, I see. And why didn’t you want to talk to any of them?
P: Because I knew they would be mean to me.
T: What would it mean if they were mean to you?
P: That they are just like all other women. . .ALL women are mean to me.
T: And what does it mean if all women are mean to you?
P: That I can’t trust ANY women. . .they are NOT to be trusted!
T: And what does it mean if no women are to be trusted?
P: Everyone is trying to hurt me and they always will.
In addition to purely cognitive strategies, the clinician should incorporate behavioral exposures and experiments in which the validity of the client’s dysfunctional
beliefs can be tested. For instance, drawing from the exchange described above,
the clinician might ask Eva to complete a homework assignment for the following
week in which she makes predictions about how others are likely to behave if her
dysfunctional beliefs are correct (and write these down on her homework sheet or
diary card). The client then should test these predictions by following through with
her behavioral exposures and recording the actual behaviors of others, ultimately
comparing what she observed to what she expected. In this way, the clinician uses
the same cognitive and behavioral strategies to simultaneously target the Axis I
(SAD) and Axis II (paranoid personality) disorders. While doing this, the clinician should of course be carefully measuring change in all of the target problems
over the course of treatment in order to evaluate the effectiveness of the treatment
provided. This is especially important given that although there is evidence supporting the cognitive-behavioral treatment of personality disorders, in many cases
the use of these techniques to treat comorbid personality disorders is akin to providing “off-label” treatment of the evidence-based approach. The provision of truly
evidence-based treatment requires careful measurement of the target behavior in
each and every case (Nock, Goldman, Wang, & Albano, 2004).
Addressing additional complications. As mentioned above, the presence of
comorbid personality disorders may be associated with problems with poorer treatment attendance, adherence, and the therapeutic relationship. Such problems can
arise for many different reasons, and the clinician working with clients with comorbid personality disorders should be prepared for this possibility and should attempt
to determine the potential source of the difficulties. One way to conceptualize such
complications is to consider whether they may be generated primarily by the client,
the treatment itself, or the clinician.
Clients may experience treatment as being too demanding or not appropriate
for the problem for which they are presenting. Similarly, many clients have low
expectations for treatment or are not particularly motivated to participate in treatment. Each of these problems may be especially pronounced among clients with
a comorbid personality disorder (Chiesa, Drahorad, & Longo, 2000) and should
be assessed directly by the clinician. Measures have been developed specifically
for assessing potential barriers to treatment participation that are freely available to
clinicians (e.g., Kazdin, Holland, & Crowley, 1997; Kazdin, Holland, Crowley, &
Breton, 1997). Moreover, brief interventions have been developed that are designed
264
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to enhance clients’ treatment motivation and participation in treatment, many of
which are also freely available to clinicians (e.g., Nock & Kazdin, 2005). These
assessments and interventions have been designed for quick and easy use (e.g., 5–
10 min of assessment and 5–45 min of intervention in total) and we would encourage
clinicians working with clients with a comorbid personality disorder to incorporate
these into their regular practices.
Treatments for anxiety disorders can be quite distressing (e.g., “You’re afraid
of germs? Let’s take a look at this road kill I have in my desk!”), and this may
be especially problematic for those with a comorbid personality disorder who may
have problems regulating one’s emotional and behavioral experiences. These issues
can be infinitely complex; however, we believe the best advice is for the clinician
to (a) think carefully about how the client’s personality disorder may influence their
experience of the treatment, (b) assess this directly either by raising it with the client
or through behavioral observation in sessions, and (c) modify the intervention to
account for these difficulties. For instance, we described above how Eva’s symptoms
of borderline and paranoid personality disorder interfered with her ability to engage
in exposure exercises both in and out of sessions. If left unchecked, these factors
could have continued and ultimately led to treatment being persistently ineffective
(and unimplemented in the case of her failure to complete homework exposures),
to her dropping out of treatment prematurely, or to the clinician becoming confused
and frustrated with her ongoing failure to complete treatment assignments.
Clinicians may experience clients with a personality disorder as being hostile,
uncooperative, and manipulative, as mentioned earlier (Bowers & Allan, 2006;
Potter, 2006). The presence of a comorbid personality disorder clearly can introduce
many treatment complications and can arouse negative thoughts and feelings in the
clinician, and it is important for the clinician to address these thoughts and feelings
using the same strategies that they teach their clients. For instance, Linehan’s (1993)
treatment for BPD requires consultation team meetings in which clinicians meet
on a weekly basis and among other things provide each other with objective feedback, direction, and support. Similarly, Beck and colleagues (2004) propose using a
“Clinician’s Dysfunctional Thought Record” to identify, evaluate, and correct dysfunctional thoughts that can arise about the client, the treatment, or the clinicians
themselves. The same practices and techniques that can be used to change clients’
behaviors often work just as well when directed at the clinician.
Conclusion
As we have discussed, personality disorders often co-occur with anxiety disorders,
and their presence can introduce complications including greater clinical severity,
poorer attendance and adherence to treatment, increased likelihood of SITB, and
potentially worse clinical outcomes. Given the clinical and methodological complexities involved in studying the treatment of anxiety disorders in the context of
comorbid personality disorders, clinical research has not, will not, and should not
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aim at studying the treatment of the seemingly infinite number of combinations
of anxiety and personality disorder constellations. Instead, the clinician should
use what is currently known about the evidence-based assessment of anxiety and
personality disorders, cognitive-behavioral case conceptualization, and evidencebased treatment (involving careful and continuous assessment of key outcomes) in
order to resolve treatment complications associated with the presence of comorbid
personality disorders.
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Resolving Treatment Complications
Associated with Comorbid Anxiety
and Substance Use Disorders
Elizabeth K. Reynolds, Matthew T. Tull, Idit Shalev, and C.W. Lejuez
The associations between anxiety disorders and substance use disorders (SUDs)
have received significant attention in recent years. This is appropriate both because
of the growing literature suggesting the presence of comorbidity and possible
causal and functional linkages across these disorders, and because this attention
is encouraged by clinical demand for treatment options for these patients. Indeed,
the comorbidity of these conditions creates a wealth of challenges for practitioners.
According to McGovern, Xie, Segal, Siembab, and Drake (2006) “when it comes
to providing services to persons with co-occurring disorders, addiction treatment
providers may find themselves lost between the vague and the overly particular. This makes research-to-practice translations even more difficult than usual”
(p. 267). Accordingly, the goal of this chapter is to identify and discuss complications in the treatment of an anxiety disorder with a comorbid SUD1 . Following
a review of the links between anxiety disorders and SUDs, we report key issues
from assessment through treatment including the emergence of integrated treatments that focus on concurrently addressing a comorbid anxiety disorder and SUD.
Finally, we provide two illustrative case examples. Throughout this chapter, we
acknowledge that the lack of available research on this topic often prevents specificity within either anxiety disorders or SUDs. As such, we will focus more on
broad connections across disorders, but also attempt to address specificity where
appropriate.
C.W. Lejuez (B)
Center for Addictions, Personality, and Emotion Research, Department of Psychology,
University of Maryland, College Park, MD, USA
e-mail: clejuez@psyc.umd.edu
1 It
is of note that we will limit our review to alcohol and illicit drugs, to the exclusion of cigarette
smoking. Clearly, anxiety and cigarette smoking are highly comorbid. Although there is a clear
need to understand the role of anxiety in the development of smoking and the exacerbation
of anxiety that may result from smoking, the current chapter is focused more on complications that an SUD might cause in the treatment of anxiety beyond merely exacerbating the
symptoms.
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_15,
C Springer Science+Business Media, LLC 2010
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Link Between Anxiety Disorders and Substance Use Disorders
Studies consistently find that individuals with an anxiety disorder diagnosis are at
heightened risk for a comorbid SUD. Reiger, Rae, Narrow, Kaelber, and Schatzberg
(1998), in analyzing cross-sectional data from the Epidemiological Catchment Area
(ECA) study, found that the 12-month prevalence of a SUD among individuals with
an anxiety disorder was 15%. Although epidemiological studies tend to find higher
prevalence rates for alcohol use disorders (alcohol abuse and/or dependence) than
for drug use disorders, prevalence rates for both types of disorders are elevated in
the context of an anxiety disorder when compared to individuals without an anxiety
disorder diagnosis (Conway, Compton, Stinson, & Grant, 2006; Grant et al., 2004).
In regard to alcohol use disorders specifically, Grant et al., 2004 in examining the
National Institute on Alcohol Abuse and Alcoholism’s National Epidemiologic
Survey on Alcohol and Related Conditions (NESARC) Wave 1 data obtained
from a nationally representative sample of 43,093 individuals, found that among
those with any 12-month DSM-IV anxiety disorder, 13.02% had an alcohol use
disorder. Panic disorder (PD) with and without agoraphobia was associated with
the highest 21-month alcohol use disorder prevalence rates (18.81% and 15.29%,
respectively). Broken down by whether or not participants met criteria for alcohol
abuse or dependence, 4.96% of individuals with an anxiety disorder diagnosis also
met criteria for alcohol abuse in the past year and 8.06% for alcohol dependence
in the past year. In examining the self-reported temporal ordering of anxiety and
alcohol use disorders within the National Comorbidity Study, Kessler et al. (1997)
found that 21.8% of men and 49.7% of women with alcohol dependence reported
that their alcohol dependence was secondary to an anxiety disorder diagnosis.
Lower rates, especially for men, were found for alcohol abuse (16.6% for men
and 39.7% for women). In a review of epidemiologic surveys, family studies,
and field studies, Kushner, Sher, and Beitman (1990) found that the relationship
between alcohol problems and anxiety appeared to be variable among the anxiety
disorders. Specifically, in agoraphobia and social anxiety disorder (SAD), alcohol
problems were linked to attempts at self-medication of anxiety symptoms, whereas
PD and generalized anxiety disorder (GAD) were found to more commonly occur
following pathological alcohol consumption. Further, simple phobia was not found
to be related to alcohol in any meaningful way.
Whereas the relationship between alcohol use and anxiety disorders is welldocumented (Grant et al., 2004; Kessler et al., 1997; Morris, Stewart, & Ham, 2005),
fewer studies have examined prevalence rates of illicit drug use among individuals with anxiety disorders. However, of the studies that have been conducted, all
have found significant relationships between the presence of an anxiety disorder
and illicit drug use. For example, Merikangas et al. (1998) analyzed data from six
international epidemiological study sites (Germany, Mexico, Netherlands, Ontario,
and two sites in the United States). They found that, across all sites, approximately
24.9% of individuals with any lifetime anxiety disorder diagnosis also exhibited
lifetime drug use (e.g., cannabis, opioids, stimulants, sedatives, or inhalants, but
not alcohol), 35.8% exhibited lifetime drug problems (met at least one DSM-IIIR abuse criteria for any drug), and 45.8% met criteria for lifetime DSM-III-R
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drug dependence. Lopez, Turner, and Saavedra (2005) collected data from 1,747
individuals from the Southeastern United States and examined drug dependence
among individuals with pure anxiety disorder diagnoses (i.e., the occurrence of one
or more anxiety disorders that is not accompanied by any additional psychiatric disorder) or an anxiety disorder that was comorbid with some other psychiatric disorder
(depression, dysthymia, conduct disorder, or attention deficit/hyperactivity disorder). Of the 4.9% with a pure anxiety disorder diagnosis, 13.9% also exhibited drug
dependence. Further, more men (20.8%) than women (10.9%) with a pure anxiety
disorder diagnosis also met criteria for drug dependence. Among the 10.2% with a
comorbid anxiety disorder, 29.2% met criteria for drug dependence. Again, more
men (33.3%) than women (26.9%) with a comorbid anxiety disorder diagnosis also
met criteria for drug dependence.
In regard to the relationship between specific anxiety disorders and the use of
illicit substances, posttraumatic stress disorder (PTSD) has received particular attention (for a review, see Chilcoat & Menard, 2003). Data from the ECA found that
compared to men and women without a diagnosis of PTSD, men with PTSD were
5 times more likely to also exhibit a drug use disorder and women with PTSD
were 1.4 times as likely to exhibit a drug use disorder (overall odds ratio of 2.2;
Helzer, Robins, & McEvoy, 1987). In the NCS, Kessler, Sonnega, Bromet, Hughes,
and Nelson (1995) found that compared to men and women without a diagnosis
of PTSD, men with PTSD were approximately 2.97 times as likely and women
4.46 times as likely to exhibit a drug use disorder. Giaconia et al. (1995, 2000) collected data from 384 18-year-olds as part of The Early Adulthood Research Project
(EARP) and found that compared to individuals without a history of traumatic exposure, individuals with a lifetime diagnosis of PTSD were 8.8 times as likely to also
meet criteria for a lifetime drug dependence diagnosis and 14.14 times as likely to
meet criteria for past year drug dependence.
The NESARC provides extensive data on illicit drug use across additional anxiety disorders, including PD, SAD, specific phobia, and GAD. Specifically, data
from the NESARC indicate that criteria for lifetime drug abuse is met among 14.7%
with PD with agoraphobia, 13.2% with PD without agoraphobia, 12.5% with SAD,
11.4% with specific phobia, and 11.9% with GAD. Criteria for lifetime drug dependence is met among 19.5% with PD with agoraphobia, 9.9% with PD without
agoraphobia, 9.8% with SAD, 7.3% with specific phobia, and 11.1% with GAD.
In regard to the specific types of illicit drugs used, highest rates (across all anxiety
disorders examined) were found for comorbid cannabis use disorder. In addition,
individuals with a diagnosis of PD with agoraphobia exhibited the highest lifetime
rates of sedative, tranquilizer, opioid, amphetamine, hallucinogen, cannabis, and
cocaine use disorders, compared to all other anxiety disorders examined (Conway
et al., 2006).
Recommendations from Assessment through Treatment
These aforementioned results highlight the need for all individuals in treatment for
anxiety to be fully assessed for the presence or absence of a SUD and conversely,
individuals receiving substance abuse treatment should be assessed for a range of
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psychiatric disorders, including anxiety disorders. This is especially important given
that comorbidity has been found to have a negative impact on the course, treatment
outcome, and prognosis of both disorders (e.g., Brown, Stout, & Mueller 1999;
Charney, Palacios-Boix, Negrete, Dobkin, & Gill, 2005; Hien, Nunes, Levin, &
Fraser, 2000; Ouimette, Ahrens, Moos, & Finney, 1998; Ouimette, Moos, & Finney,
2003). Unfortunately, research on and treatment for patients with co-occurring disorders in substance abuse treatment have been slowly evolving (Hunter et al., 2005),
and specific guidelines for assessing and treating the co-occurrence of anxiety and
SUDs are only recently becoming more available, with much of these guidelines
lacking empirical support (Watkins, Hunter, Burnam, Pincus, & Nicholson, 2005).
Nevertheless, there are a few key recommendations that can be developed based on
theory and the available empirical literature from assessment through treatment.
Assessment Issues
Given the complex issues related to the treatment of the comorbidity between anxiety disorders and SUDs, it is especially important to accurately diagnose each
disorder and develop an understanding of the complex interplay across disorders.
Accurate diagnosis and differentiation between substance-induced states and primary affective illnesses is one of the more difficult tasks in assessing patients with
co-occurring mood symptoms and substance use. However, it is also extremely
important, as early and accurate diagnosis is likely to improve treatment outcomes
(Myrick, Culver, Swavely, & Peters, 2004). Key issues to address include (a) the
temporal and functional relationship between anxiety and SUDs, (b) specificity
across disorder categories, and (c) selection of assessment measures.
Temporal and Functional Relationship Between Anxiety
Disorders and SUDs
At times, the complex and bi-directional relationships between anxiety disorders
and SUDs can lead to diagnostic uncertainty. It can be extremely difficult to differentiate between substance-induced states and primary psychiatric diagnoses. The
majority of the studies on the comorbidity of SUDs and anxiety disorders are
cross-sectional in nature, and therefore, it is impossible to determine the temporal
progression of the disorders from these studies. In regard to the specific relationship
between anxiety and SUDs, three temporal paths are possible. First, the use of specific drugs may increase the risk for the onset of an anxiety disorder. It is thought
that chronic and excessive use of some substances may unmask a genetic predisposition to psychiatric illness (Rabinowitz et al., 1998; Volkow, 2006; Zammit,
Allebeck, Andreasson, Lundberg, & Lewis, 2002). Second, illicit drug use may
follow the development of an anxiety disorder diagnosis, consistent with a selfmedication model of illicit drug use (e.g., Preisig, Fenton, Stevens, & Merikangas,
2001; Quitkin, Rifkin, Kaplan, & Klein, 1972; Swendsen et al., 1998, 2000). Thus,
the anxiety disorder precedes the SUD, and substances have been used as a coping
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mechanism for the anxiety symptoms. In some individuals there is likely to be
a cyclic interaction: depressants, such as alcohol and opiates, may be used in an
attempt to decrease anxiety, but anxiety may increase during withdrawal states leading to an exacerbation of the anxiety disorder and making relapse to substance use
more likely. Finally, there may be an underlying third factor that increases the risk
for both anxiety disorders and drug use; that is, there may be a common underlying
mechanism for the comorbid development of these disorders (Goodwin et al., 2002).
To further complicate the clinical picture, it is also clear that intoxication and
withdrawal from substances of abuse can mimic symptoms of anxiety disorders.
For example, alcohol withdrawal may result in symptoms of sweating, tachycardia, and anxiety (APA, 2004), all of which may be viewed or interpreted as panic
attack-related symptoms. While the best way to differentiate substance-induced
temporary symptoms from psychiatric problems is through observation during a
period of abstinence, the duration of abstinence necessary for accurate diagnosis
is controversial. Some have suggested postponing the diagnosis of anxiety disorders for 1 month following treatment entry (Schuckit, 1996). This would potentially
decrease the number of false-positive diagnoses, but there are drawbacks associated with waiting a month to diagnosis the anxiety disorder; if a person does have
an anxiety disorder, the symptoms of anxiety may be contributing to immediate
impairment and may be impeding treatment progress. A family history of the particular anxiety disorder, the onset of anxiety symptoms before the onset of substance
abuse and dependence, and sustained anxiety symptoms during prolonged periods
of abstinence all suggest a primary anxiety disorder (Myrick & Brady, 2003). In
addition, primary anxiety disorders may become more severe after cessation of substance use (as the substance use may have been masking or medicating some of the
symptoms of the anxiety disorder), whereas substance-induced anxiety symptoms
will slowly remit after cessation of substance use (Brown & Schuckit, 1988; Thevos,
Roberts, Thomas, & Randall 2000).
Specificity Across Disorder Categories
Given that research on the links between anxiety disorders and SUDs is only
recently emerging, it is often difficult to move beyond more general impressions.
However, when attempting to create a clear clinical picture of symptoms some
special considerations should be taken into account.
Generalized Anxiety Disorder: The “free-floating” anxiety characteristic of GAD
has considerable overlap with stimulant intoxication and withdrawal from alcohol, sedative/hypnotics, and opiates. Although many substance-abusing individuals
report anxiety symptoms consistent with GAD, they may not meet diagnostic
criteria for GAD because of difficulty determining the etiology of these symptoms.
Panic Disorder: Many substances of abuse (cocaine/marijuana/other stimulants)
may actually induce panic attacks or PD during periods of acute intoxication
(Aronson & Craig, 1986; Moran, 1986) or withdrawal. Several reports have noted
that cocaine can precipitate panic attacks in individuals without previous PD
(Aronson & Craig, 1986; Louie, Lannon, & Ketter, 1989; Rosen & Kosten, 1992).
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Finally, panic symptoms can be misinterpreted as withdrawal symptoms, which may
be especially relevant for those using substances with a more severe withdrawal
profile such as opiates or alcohol.
Social Anxiety Disorder: A protracted period of abstinence may not be needed
to make a diagnosis of SAD, as the fear of interaction in social situations is not
a specific feature of substance use or withdrawal. The social fears that occur only
during periods of intoxication with marijuana or stimulants, however, should not be
considered sufficient to meet diagnostic criteria for SAD, and a reduction in social
fears during periods of chronic substance use also should not be taken to imply
remission of social anxiety.
Obsessive Compulsive Disorder (OCD): Diagnosing OCD in substance abusers
is somewhat less problematic than other anxiety disorders because substance use
withdrawal and OCD have fewer overlapping features and the characteristic symptoms of OCD are distinctive, although some of the rituals associated with cocaine
use may appear related to compulsive symptoms of OCD. In addition, individuals
with OCD may find relief in the rituals associated with substance use and therefore
not display other compulsive symptoms characteristic of OCD (e.g., hand washing,
ordering, counting). There may be some link between substance use and OCD. In a
study conducted by Crum and Anthony (1993), subjects actively using cocaine and
also marijuana were found to be at increased risk for OCD.
PTSD: It is likely that substance use (in particular, cocaine use) and repeated
withdrawal (in particular alcohol, sedative hypnotic, and opiate withdrawal) will
exacerbate symptoms of PTSD. Withdrawal from opiates, benzodiazepines, and
ethanol is associated with central noradrenergic activation, elevation of vital signs,
and subjective states similar to those seen during exacerbations of PTSD symptoms.
As such, conditioned withdrawal symptoms may exacerbate PTSD symptoms, leading to self-medication as individuals attempt to alleviate symptoms (Brady, 2001;
Kosten & Krystal, 1988). For example, cocaine use is associated with paranoia,
hypervigilance, sleep disturbance, and autonomic arousal, all of which may increase
the severity of hyperarousal symptoms of PTSD (Brady, 2001). Given these issues,
it is crucial to understand that although current research and theory rests more so
at a more general picture of anxiety disorders and SUDs, assessment always should
carefully consider unique issues specific to specific SUDs and anxiety disorders.
Further, given more recent attention to these questions, a close eye on new research
is of utmost importance.
Selection of Assessment Measures
Because of the high rate of co-occurrence of anxiety and SUDs, screening patients
presenting at either substance use or mental health treatment settings is critical.
As mentioned above, this is especially important considering that early diagnosis and treatment can improve treatment outcomes. Brief screening tools for
SUDs that have been found useful in mental health settings include the Alcohol
Use Disorders Identification Test (AUDIT; Bohn, Babor, & Kranzler, 1995), the
Michigan Alcohol Screening Test (MAST; Teitelbaum & Carey, 2000), and the
Drug Abuse Screening Test (DAST; Cocco & Carey, 1998; Maisto, Carey, Carey,
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Gordon, & Gleason, 2000). The Symptom Checklist (SCL-90; Derogatis, 1994),
Anxiety Disorders Interview Schedule (ADIS-IV˜L; Di Nardo, Brown, & Barlow,
1994), and Structured Clinical Interview for DSM-IV (SCID; First, Spitzer, Gibbon,
& Williams, 1997) are widely used instruments for psychiatric screening and diagnoses and can be useful for diagnosis when both anxiety disorders and SUDs are
present. The Addiction Severity Inventory is a semi-structured interview designed to
address seven potential problem areas in substance-abusing patients: medical status,
employment and support, drug use, alcohol use, legal status, family/social status,
and psychiatric status (McLellan, Luborsky, O’Brien, & Woody, 1980; Leonhard,
Mulvey, Gastfriend, & Shwartz, 2000).
Despite the value of these measures, there has been wide critique. For example,
the MAST is not designed specifically to measure complex co-morbid psychiatric
states and only includes one question on treatment in a psychiatric hospital or the
psychiatric ward of a general hospital due to drinking problems. Moreover, the
reason for hospitalization is not obtained. The MAST is really not designed to
measure complex psychiatric states. Further, research on the SCID’s differentiation
of substance-induced and primary psychiatric diagnoses in patients with substance
abuse has found little cross-sectional or predictive validity (Kadden, Kranzler, &
Rounsaville, 1995; Kranzler, Kadden, Babor, Tennen, & Rounsaville, 1996); similar
concerns are evident for the ADIS, despite its specific utility for assessing anxiety
disorders. The Addiction Severity Inventory may be useful to obtain information
about consequences of substance use when an anxiety disorder diagnosis is made
using another instrument or to suggest potential need for further anxiety screening,
but the lack of depth in its assessment of anxiety limits its utility for the purposes
at hand here. In line with these problems, the Psychiatric Research Interview for
Substance and Mental Disorders (PRISM) (Hasin et al., 1996; 2006) was developed to address the lack of a diagnostic interview that is suitable for diagnosing the
comorbidity of substance use and psychiatric disorders.
There are three important characteristics of the PRISM that are specific to comorbidity. First the PRISM adds specific rating guidelines throughout the interview,
including frequency and duration requirements for symptoms, explicit exclusion
criteria, and decision rules for frequent sources of uncertainty such as temporal
relationship of psychiatric symptoms and substance use. The PRISM differentiates between substance-induced symptoms, primary symptoms, and symptoms that
are “expected effects” of intoxication and withdrawal. Second, the PRISM positions the alcohol and drug sections near the beginning of the interview, before the
mental disorder sections, so that the history of alcohol and drug use is available at
the time of beginning the assessment of mental disorders. Third, the PRISM adds
more structured alcohol and drug histories to provide a context for assessing comorbid psychiatric disorders. In sum, the PRISM does an excellent job of establishing
chronological relationships between the psychiatric symptom and substance use for
the purpose of diagnostic clarity and treatment planning.
In addition to using measures such as the PRISM which provide excellent information for determining differential diagnosis and temporal specificity, one also may
use a functional analytic approach (Haynes & O’Brien, 1990). In this case, two
useful questions to begin with are the following: (1) to what extent is the function of
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substance use related specifically back to anxiety? and (2) to what extent do anxiety
symptoms tie directly back to substance use? One benefit of this approach is that it is
based on current functional relationships and therefore may proceed without a clear
understanding of temporal sequencing which simply may not be available or may no
longer be relevant as the synergistic effects of the two conditions may lead to a different presentation of each as time progresses. Using a functional analytic approach
clearly aids in identifying the problem behavior both in terms of anxiety and substance use. Beginning with substance use resulting from anxiety, this might include
an examination of the antecedents that precede substance use. In addressing triggers
as well as thoughts and feelings preceding substance use, it can be determined to
what extent substance use is being used to address anxiety-related issues.
One caveat is that the pattern of substance use can become so automatic that it
may be difficult to establish the role of anxiety because avoidance has become so
proficient (resulting in the complete avoidance of anxiety symptoms). In this case,
it may be useful to assess what might happen if substance use as a means of avoidance was not a viable option in a time when the person wanted to use, examining
the resulting exacerbation of anxiety symptoms across the domains of thoughts,
feelings, and behavior. Additionally, it is important to consider that the function of
substance abuse in the context of an anxiety disorder may change over time; that
is, an individual may initially begin to use substances in an attempt to alleviate or
escape anxiety disorder-related symptoms (i.e., self-medication or avoidant function). However, as substance dependence develops, the individual’s substance use
may no longer be in response to anxiety-related symptoms but instead to substance
withdrawal symptoms and other psychopathology such as depression resulting from
the substance use consequences. In this case, basing treatment purely on the chronological order of development of the disorders could be misleading based on the
current inter-relationship of the disorders. Consequently, in doing a functional analysis of the patient’s substance use, it is important to examine the past and current
antecedents of the individual’s substance use behavior in order to determine current
function and its relationship to changes in that function over time.
Moving to a focus on substance use as the factor underlying anxiety, a similar approach is taken with a few specifics regarding pharmacological effects to be
considered. For example, one may examine the extent to which anxiety symptoms
change in response to acute drug administration. Do the symptoms increase as might
be the case with a substance that results in CNS arousal such as cocaine or does
it decrease as might be the case with a drug associated with a dampening effect
such as heroin? Further, do the anxiety symptoms increase in response to more
short-term abstinence with a drug such as heroin or alcohol with a fairly severe
withdrawal profile? Finally, do the anxiety symptoms improve or worsen as more
long-term abstinence is achieved? In asking such questions, a functional analysis
will help identify feedback loops that may provide particularly valuable information for understanding the complex interplay between SUDs and anxiety disorders,
often with some specific understanding of how this might differ across particular
SUDs and anxiety disorders.
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Treatment
Once the co-existing anxiety disorder and SUD are identified, several issues must
be considered in terms of implementing the most effective treatment strategy. In this
section, we discuss issues to be considered when utilizing state-of-the-art treatments
for anxiety disorders and SUDs, with specific attention to the role of (a) willingness
to change, (b) combining stand-alone treatments for anxiety disorders and SUDs,
and (c) the emergence of specialized integrative treatments. Finally, we close with
two hypothetical illustrative case studies.
Willingness to Change
In considering how one might address comorbid SUD for those with an anxiety
disorder, it is crucial to first determine the client’s willingness to make changes
in their SUD. Motivation has been found to predict both dropout and engagement
in community-based treatment of substance abuse (De Leon, Hawke, Jainchill, &
Melnick, 2000; De Leon & Jainchill, 1986; Simpson, Joe, & Rowan-Szal, 1997)
across treatment settings (Joe, Simpson, & Broome, 1998). One theory that attempts
to explain the relationship between an individual’s intent to change and their subsequent behavior is Prochaska and DiClemente’s (1982, 1983) transtheoretical model
of change (TTM). In this model, behavior change is conceptualized as a process
that unfolds over time and involves progression through a series of five stages
of change: precontemplation, contemplation, preparation, action, and maintenance.
They argue that at each stage of change, different processes of change optimally
produce progress. Thus, matching change processes to the respective stages requires
that the therapeutic relationship be matched to the client’s stage of change.
According to Prochaska and DiClemente (1983), individuals in the precontemplation stage are the most resistant to change and are characterized as processing less
information about their problems, engaging in less personal evaluation, and experiencing fewer emotional reactions to their substance use. Individuals who are aware
of their problem and weigh the positive and negative consequences of their actions
are in the contemplation stage. Individuals in the preparation stage have made a
decision to take action within the next month, while individuals in the action stage
are currently taking steps such as changing their behavior, environment, or experiences. Finally, individuals in the maintenance stage have established their recovery
and are learning and engaging in behaviors that will prevent relapse.
Information regarding stage of change is important because if level of motivation
is identified prior to treatment, an opportunity is provided to (1) select a treatment
that is most in line with an individual’s current level of motivation or (2) target motivation level prior to treatment if more advanced treatment approaches are utilized.
This work has largely been applied to SUDs and is likely most relevant for SUDs
here as well, yet value certainly could be gained from its application to anxiety
disorders especially when comorbid with SUDs. Of course one may not consider
anxiety symptoms such as bodily arousal to be under the control of the individuals in the same way as drinking or injection drug use. However, motivation and
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the stages of change can be easily linked to other symptoms such as avoidance as
well as willingness to engage in treatment components such as exposure. We now
consider potential recommendations across the stages for treating comorbid anxiety
disorders and SUDs, again focused primarily on SUDs but with attention to anxiety
disorders specifically as relevant.
Precontemplation and Contemplation. For individuals for whom their motivation to change a SUD falls in these two stages, it may be useful to focus treatment
more directly on anxiety, with the large part of the substance use related components focused on brief motivational strategies. As anxiety treatment is initiated, it
may be useful to tie aspects of how sobriety might be especially useful for anxietyrelated gains, especially for drugs which may exacerbate anxiety symptoms such as
cocaine. Similarly, for individuals more motivated to address their SUD with less
willingness to address anxiety problems, treatment might be targeted more toward
SUDs at the onset. At this point it would be useful to address the factors underlying
the resistance to anxiety treatment. Three fairly obvious possibilities in this regard
are a lack of knowledge of what anxiety is and how it relates to one’s substance use,
stigma regarding other aspects of mental illness beyond SUDs, and/or an unwillingness to engage in typical anxiety disorders treatment such as exposure. Indeed, an
understanding of the factors underlying an inability to commit to anxiety treatment
could be thoughtfully addressed over the course of several weeks at the onset of
SUD treatment including psychoeducation focused on what anxiety disorders are,
how they may impact one’s ability to get and stay sober, and how treating the anxiety
disorder at the same time might actually facilitate sobriety.
Preparation and Action. If the individual is in preparation or action for both
conditions, a more integrated treatment may be useful given the clear identification
of the problems associated with both disorders as well as a commitment to treatment
for both. Indeed, preparation and action indicate that the individual has identified
the problem (and may very well have identified how substance use affects anxiety,
and vice versa). If the individual is in the preparation or action stage for only one
disorder and the other disorder is in the precontemplation or contemplation stages,
recommendations from the previous section should be considered.
Maintenance. If one condition is in the maintenance stage, treatment for the other
condition is less likely to be impaired. However, it is also true that if one condition
is in maintenance, treatment may focus so exclusively on the other condition that
some threats to the condition in maintenance may become evident: for example, a
client with SAD who has essentially covered up the anxiety disorder through chronic
substance use. In this case, assessment might miss the SAD, but upon successful
alcohol treatment, these symptoms may return. If the client and therapist are not
vigilant about the SAD and how the addiction treatment might affect it, improvement in one condition could actually increase the likelihood of relapse in the other.
Alternatively, consider a client that has struggled to overcome an addiction to opiates including heroin and pain medication. Over time the client may develop PTSD
due to a traumatic event and seek treatment. At this point they may not relapse back
to substance use but might feel tempted to do so if the first few sessions of exposure therapy are extremely upsetting. Thus one could say that exposure, although
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certainly appropriate for the PTSD symptoms, might actually increase craving for
opiates. If the therapist is not aware of this substance use issue it might not even be
addressed, with the client given social reinforcement for completing assignments,
despite an undetected increase in opiate use. As such, awareness of problems associated with substances and anxiety, even if these problems are in remission, may
be necessary on the part of both the therapist and client to prevent a relapse of this
condition as their other condition begins to improve.
Issues to Consider in Combining Stand-Alone Treatments for Anxiety
Disorders and SUDs
Beyond motivation, there are a number of factors to take into account for the treatment of comorbid anxiety and SUDs when using standard treatments. In doing so
we consider factors that are specific to both treating only one disorder at a time and
treating both disorders simultaneously, as well as collateral benefits of treating one
disorder in the prognosis of the other disorder.
Issues with treating one disorder at a time. When treating disorders sequentially,
treatment of one disorder could be impaired by the symptoms/consequences of a
second untreated disorder. For example, in the treatment of PTSD, acute intoxication, withdrawal symptoms, and other short-term consequences of substance use
may interfere with exposure. Alternatively, if PTSD is left untreated until substance
use issues can be addressed, symptoms of PTSD (e.g., sleep disturbance, intrusive
thoughts, hyperarousal) may increase risk for relapse back to substance use (stemming from a desire to escape, avoid, or somehow alleviate these symptoms). Also
relevant to untreated anxiety, many traditional substance use treatments including
Narcotics Anonymous and Alcoholics Anonymous heavily utilize group formats
(Myrick & Brady, 1996) which may be difficult to engage in due to anxiety symptoms across a variety of disorders such as impaired concentration, agitation, and
fear of evaluation. Further, these clients may be unduly judged by the staff as not
invested in treatment due to their avoidance of group activities.
Issues with treating both disorders simultaneously. When treating both disorders
together, two factors should be considered. The first factor is the extent to which
symptoms from one disorder worsen as a result of treatment for the other disorder.
This may include typical anxiety treatments such as exposure producing a greater
desire for substances due to initial elevations in anxiety associated with exposure
before exposure begins to have its positive effects on anxiety over time. For example, a patient receiving behavior therapy for SAD who also is struggling with alcohol
use may experience an increase in alcohol cravings as a result of engaging in staged
exposure exercises in-session and homework exercises involving social contact outside of session. To the extent that an individual has used alcohol (or some other
substance) to cope with anxiety-related symptoms, a patient instructed to take part
in in vivo exposure exercises in and outside of session may begin to experience
increased cravings as a result of being placed in an anxiety-provoking situation
where all other avoidance efforts are prevented. In this case, particular attention in
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treatment may need to be placed on helping the patient understand the function of
substance use and increase awareness of situations that may evoke substance cravings. Further, combining strategies for coping with cravings with those for anxiety
may assist the patient in fully engaging in exposure exercises. In addition to cases
in which actual treatment components may place improvement in a second disorder
at risk, there are risks of positive changes associated with treatment for one disorder
affecting improvement of the second disorder. Keeping with the SAD and alcohol
example, if sobriety is achieved early, the removal of that coping strategy may lead
to a strong spike in anxiety symptoms if the alcohol was serving a self-medication
role. Again, attention in session to the functional relationship of the disorders cannot
be stressed enough.
The second factor is the extent to which treatment for one disorder actually is
contraindicated for the treatment of the other disorder. This is most likely going
to become an issue in the case of psychopharmacological interventions for anxiety
disorders. For example, it would be problematic to prescribe benzodiazepines for
a patient with PD who previously used substances to reduce anxiety-related symptoms, as there is an increased risk for abuse and dependence on the medication.
Another problem may arise when a patient’s substance withdrawal symptoms are
so severe that certain anxiety-focused treatment approaches may pose a health risk.
For example, a patient experiencing intense physiological withdrawal symptoms
(e.g., increased heart rate, shortness of breath) may have their well-being put at risk
by engaging in an intense exposure exercise (e.g., flooding). Of course, this speaks
to the previously discussed importance of assessing the current state of a patient’s
withdrawal symptoms before progressing with anxiety-focused treatment, and in
some cases, detoxification may first be required.
Collateral benefits of treating one disorder in the prognosis of the other disorder. In addition to risks, however, it should be noted that some strengths exist in
treating this comorbidity, as treatment for one disorder may have benefits for the
other disorder. For example, it is possible that existing empirically supported substance abuse treatments (e.g., relapse prevention) may include active ingredients
(e.g., stress reduction coping skills, discussion of negative affect situations) that
contribute to the reduction of anxiety symptoms. In addition, learning strategies
to self-regulate anxiety symptoms in anxiety disorder-focused treatment may help
patients to break out of the mindset of using substances to fight subjective states and
obtain alternative coping strategies (Myrick & Brady, 2003).
Specialized Integrative Treatments
Moving beyond the combination of treatments, recent efforts have begun to move
toward more explicitly integrative efforts. As Watkins et al. (2005) point out, there
are unified treatment programs with cross-trained staff, co-location of mental health
and substance abuse services, and integration of services at a broader system level
through interorganizational linkages and referrals. In addition to integration at the
infrastructure level, several specialized integrative treatments have been developed
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to simultaneously address issues relevant to both anxiety disorders and SUDs in one
comprehensive treatment approach. Although the use of these approaches requires
additional training to staff and have been developed for specific disorders, they provide an extra level of support and guidance in addressing the interplay and functional
similarities across the conditions to provide a more comprehensive and targeted
treatment approach.
Seeking Safety. Given the high rates of comorbidity between anxiety disorders
and SUDs, specialized treatments designed to specifically target this comorbidity
are beginning to be developed. Of those treatments that are available, the majority are focused on the comorbidity between PTSD and SUDs. Najavits, Weiss, and
Liese, (1996) developed Seeking Safety to specifically target comorbid PTSD and
SUDs. Seeking Safety is a 24-session cognitive behavioral group therapy protocol treatment that teaches individuals with this comorbid symptom presentation a
variety of cognitive, behavioral, and interpersonal skills particularly applicable to
individuals with both PTSD and substance use difficulties, all of which are designed
with the idea that safety is the top priority in recovery from each disorder (Najavits
et al.); that is, coping skills are focused on maintaining abstinence, reducing selfdestructive and high-risk behavior, and establishing support. Seeking Safety has been
found to be effective, with patients exhibiting significant reductions in substance
use behavior, trauma-related symptoms, suicide risk, suicidal thoughts, depression,
and thoughts about substance use, and improvements in social adjustment, family
functioning, and problem solving (e.g., Hien, Cohen, Miele, Litt, & Capstick, 2004;
Najavits et al.; Zlotnick, Najavits, Rohsenow, & Johnson, 2003).
Concurrent Treatment of PTSD and Cocaine Dependence. Another treatment
specifically designed for individuals with comorbid PTSD and SUDs is Back,
Dansky, Carroll, Foa, and Brady’s (2001) Concurrent Treatment of PTSD and
Cocaine Dependence (CTPCD). This treatment consists of 16 individual 90-min
sessions. The treatment was designed by integrating previously validated cognitive
behavioral treatments for substance dependence (Carroll, 1998) and PTSD (Foa &
Rothbaum, 1998; Foa, Rothbaum, Riggs, & Murdock, 1991). CTPCD involves psychoeducation on the link between PTSD and cocaine dependence, coping skills
training, relapse prevention skills, and cognitive restructuring. Further, patients
undergo in-vivo and imaginal exposure in order to address their PTSD symptoms.
In an initial examination of CTPCD, Brady, Dansky, Back, Foa, and Carroll (2001)
found that individuals who completed treatment evidenced significant reductions in
depressive symptoms, PTSD symptoms, and cocaine use severity.
Anxiety Sensitivity Treatment for Heroin Users. Targeting anxiety sensitivity (an
underlying vulnerability factor that may increase the risk for both anxiety disorders
and drug use), as opposed to any specific disorder within a residential drug treatment
setting, Tull, Schulzinger, Schmidt, Zvolensky, and Lejuez (2007) recently developed a behavioral treatment (the Anxiety Sensitivity Treatment for Heroin Users;
AST-H) meant to be used in conjunction with standard substance abuse treatment.
This treatment was designed to have specific relevance for heightened heroin users
with heightened anxiety sensitivity. Previous research (Lejuez, Paulson, Daughters,
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E.K. Reynolds et al.
Bornovalova, & Zvolensky, 2006) has demonstrated that heightened anxiety sensitivity may increase risk for substance use treatment drop-out among heroin users.
In particular, a tendency to fear and unwillingness to have anxiety-related sensations may prompt individuals to attempt to avoid these sensations through the use of
heroin. Therefore, we developed a six-session adjunctive treatment where individuals engage in interceptive exposure exercises in order to facilitate acceptance of,
and tolerance for, aversive internal sensations, with the goal of preventing the use
of heroin for self-medication of these sensations. This treatment is currently under
development; however, initial pilot evidence suggests reductions in drug craving for
heroin and a significant reduction in anxiety sensitivity and panic symptom severity. In an initial examination of this treatment’s effectiveness, the AST-H was found
to result in reductions in anxiety sensitivity, heroin cravings, avoidance behavior,
and emotion dysregulation (Tull et al., 2007). Improvements were maintained when
measured over 1 month post-treatment. Current efforts are underway to replicate
this finding within a randomized controlled trial.
On a final note, other treatments are available that may be beneficial for comorbid
anxiety and SUDs that were not designed to specifically target this comorbidity.
For example, Acceptance and Commitment Therapy (ACT) has been found to be
successful in treating both anxiety disorders (e.g., Twohig, Hayes, & Masuda, 2006)
and SUDs (Heffner, Georg, Parker, Hernandez, & Sperry, 2003), as well as the cooccurrence of anxiety and substance use (Batten & Hayes, 2005). In addition, the
utility of Dialectical Behavior Therapy (DBT) in the treatment of substance use
(Rosenthal, Lynch, & Linehan, 2005) and anxiety disorders (Gratz, Tull, & Wagner,
2005) has also recently been suggested.
Case Illustrations
Client #1: Presenting problem of Obsessive Compulsive Disorder. Helen was a
28-year-old woman who presented to a psychology clinic with both obsessions and
compulsions that had begun about 1 year ago and had become worse over the past
3 months to the point of severe life impairment. She also reported that she had
currently begun to use alcohol on a daily basis as a maladaptive attempt to manage these symptoms; she reported no previous history of substance use problems.
The ADIS was used to take advantage of its strength in assessing anxiety disorders
and the decision was made not to use a more elaborate assessment to determine
the link between the substance use and OCD such as a functional analysis or the
PRISM because there was little question about the temporal sequencing and function of the alcohol use. The therapist considered beginning treatment focused on
only one condition to limit the burdens associated with treatment, but also had concerns about her ability to engage in exposure if she continued regular alcohol use,
as well as the continued functional value of her substance use if her OCD went
untreated. Because no integrative treatment was available and data indicate no contraindications of treating these conditions simultaneously once withdrawal has been
overcome, exposure with response prevention was planned including a component
for relapse prevention. However, prior to beginning either treatment component, it
Resolving Treatment Complications Associated with Comorbid Anxiety
285
was necessary to determine if detoxification was necessary. Because her likelihood
of severe withdrawal symptoms needing medical attention was low, given her consumption level and dependence profile, it was decided that a plan for immediate
sobriety (including an emergency plan if more severe withdrawal symptoms were
experienced) would be implemented in the initial session following assessment. The
extent to which she was able to abstain by the session, treatment would be set to
focus on exposure with response prevention for OCD supplemented with more secondary attention to relapse prevention (given its clear functional link to her OCD
symptoms). This emphasis would shift if a slip occurred, when high-risk situations
were encountered, or if exposure treatment for anxiety increased her urge to drink
alcohol. As expected, withdrawal symptoms were minimal and within a few weeks
exposure showed some effectiveness in treating her OCD, with a corresponding
reduction in alcohol cravings. Helen initially was somewhat unwilling to continue
to plan out strategies for high-risk alcohol situations once she was able to achieve
sobriety, yet a discussion of how the interaction between alcohol use and OCD
symptoms was sufficient to keep her invested in this aspect of treatment.
Client #2: Presenting problem of heroin dependence. Mark was a 43-year-old
daily heroin user who was court-ordered to a residential drug treatment facility after
being arrested for possession of heroin with intent to distribute. Initial assessment
with the PRISM indicated that he met diagnostic criteria for heroin dependence and
PD. Follow-up screening with the Anxiety Sensitivity Index also confirmed heightened anxiety sensitivity. Of note, when queried about anxiety and panic specifically,
Mark indicated that he was not really sure what was meant by anxiety and that he
has never heard of the phrase “panic attack” before. However, in providing further
details on what anxiety and panic attacks are comprised of, he reported “nerves”
being a problem for him and that he has experienced episodes like the described
panic attack. When going through his drug history he also noted a long history of
substance use starting in his childhood and that his longest period of abstinence was
3 months about 2 years ago. He also reported “nerves” being a problem for him
from childhood. He cited problems with withdrawal symptoms as the key issue in
returning to heroin use after 3 months of being sober. Further querying indicated that
what he considered to be withdrawal symptoms, long after the typical 1–2 weeks for
acute withdrawal, were actually panic symptoms. Given that he already was slotted
to receive relapse prevention and other treatment targeting his heroin at the residential treatment center, the decision was made to undertake the Anxiety Sensitivity
Treatment for Heroin Users (AST-H) to provide a more comprehensive and integrative approach to address his comorbidity. Given his unfamiliarity with anxiety,
treatment began with extensive psychoeducation. Mark initially was skeptical about
any treatment other than those targeted directly at his heroin use. However, following psychoeducation about the nature of anxiety, he was relieved to learn that
the bodily symptoms he continued to experience in abstinence were actually harmless and not continued heroin withdrawal. The psychoeducation made him more
willing to approach and experience anxiety as part of the recovery process and to
limit the functional need for heroin use. Further, the psychoeducation and exposure
exercises reduced the frequency, severity, and believability of negative cognitions
286
E.K. Reynolds et al.
(e.g., beliefs about the harmfulness of anxiety symptoms) linked to his anxiety. He
showed some hesitance about exposure immediately into treatment as his anxiety
symptoms worsened through his initial abstinence from heroin. Because he was
in a residential treatment where the risk for heroin relapse was minimal, a more
aggressive exposure regimen was established after a discussion of how any anxietyrelated gains actually would support his heroin abstinence attempt. Within a few
weeks, Mark had remained abstinent and reported a reduced frequency of panic
attacks and a sense of alternative strategies for coping with panic attacks when they
did occur.
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Resolving Treatment Complications Associated
with Comorbid Eating Disorders
Carolyn Black Becker, Claudia Zayfert, and Elizabeth M. Pratt
Introduction
Eating disorders (EDs) represent an interesting challenge for the anxiety clinician.
ED treatment often is viewed as a distinct specialty; thus, many anxiety clinicians have minimal background in the treatment of EDs. In addition, EDs often
are difficult to treat even with extensive experience, and the substantial medical
comorbidity and high mortality rate associated with them can make ED patients
anxiety-provoking and ethically challenging for providers. Finally, individuals with
EDs often are reluctant to disclose or change their ED behaviors. In this chapter we
will (a) summarize findings on the co-occurrence of EDs in anxiety patients; (b) discuss how to assess for EDs in anxiety patients; (c) review empirically supported and
promising treatments for EDs; (d) describe a case formulation approach for treating
anxiety patients with comorbid EDs; (e) provide illustrative case examples using
this approach; and (f) explore the issue of ordering of treatments for this population.
Likelihood of Encountering Anxiety Patients
with Co-occurring EDs
Research examining the co-occurrence of EDs and anxiety disorders suggests that
anxiety clinicians will encounter patients, particularly female patients, with comorbid EDs. Researchers typically examine ED and anxiety comorbidity either by
assessing the frequency of EDs in samples diagnosed with anxiety disorders or
by assessing the presence of anxiety disorders in ED populations. Although the
former method likely is of greater interest to readers of this book, the majority of
studies adopt the latter approach. Thus, we briefly review the literature from both
perspectives and then highlight the implications for anxiety clinicians.
C.B. Becker (B)
Trinity University, San Antonio, TX, USA
e-mail: cbecker@trinity.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_16,
C Springer Science+Business Media, LLC 2010
291
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A recent review by Godart, Flament, Perdereau, and Jeammet (2002) found that
prevalence rates of at least one anxiety disorder among ED participants ranged
from 23% to 75%. As noted by Godart et al. substantial methodological variation
makes this literature challenging to interpret. For example, studies vary markedly
in population (e.g., inpatient, outpatient, community), types of EDs included (e.g.,
anorexia nervosa [AN], bulimia nervosa [BN], current, lifetime), range of anxiety
disorders included, and diagnostic criteria and assessment instrument used. Despite
this, several relatively consistent findings emerge. First, OCD is the anxiety disorder
most consistently associated with EDs (Kaye et al., 2004; Wonderlich & Mitchell,
1997), particularly AN. Lifetime rates of OCD among AN patients range from
10% to 66% (Lilenfeld, 2004). Among BN patients, rates range from 3% to 73%
(Bulik, 1995).
Social phobia is the next most commonly identified anxiety disorder in ED populations, although the frequent exclusion of PTSD from most studies is a problem
(Kaye et al., 2004). Estimates of the lifetime occurrence of social phobia range from
17% to 59% for patients with AN or BN (Lilenfeld, 2004). Fortunately, Kaye et al.,
in one of the largest studies to date, included lifetime assessment of the full-range
of anxiety disorders, which were assessed with the Structured Clinical Interview for
DSM-IV. Among the 672 participants, each of whom met lifetime criteria for AN
and/or BN, 20% met criteria for social phobia. GAD, panic disorder, PTSD, and
specific phobia were diagnosed in 10%, 11%, 13%, and 15% of this non-clinical
sample, respectively. Notably, the rate of PTSD in this study was somewhat lower
than in other studies. For example, in another large population-based study, Dansky,
Brewerton, Kilpatrick, and O’Neil (1997) found current and lifetime PTSD rates of
21% and 37%, respectively, among women diagnosed with BN. Similarly, StriegelMoore, Garvin, Dohm, and Rosenheck (1999) found that 25% of female VA patients
diagnosed with an ED also met criteria for PTSD. It should be noted, however, that
Schwalberg, Barlow, Alger, and Howard (1992) found a lifetime PTSD rate of 10%
in a clinical BN sample, a rate consistent with that found by Kaye et al.
Of greater interest to anxiety clinicians is ED prevalence in anxiety populations,
particularly clinical samples. As noted above, fewer researchers have investigated
this, and most studies target OCD populations. These studies indicate that between
11% and 42% of female OCD patients meet criteria for an ED at some point during
their lives. Most studies, however, do not assess eating disorder not otherwise specified (EDNOS), the most common ED encountered in clinical practice (Fairburn
& Bohn, 2005). EDNOS consists of atypical, clinically significant EDs that do not
meet the specific diagnostic criteria of AN or BN (e.g., a patient who purges five
times per week but does not meet binge criteria for BN or weight criteria for AN).
EDNOS is frequently as severe as AN and BN and should not be viewed as a less
significant disorder (Fairburn & Bohn, 2005). In sum, available data may underestimate the actual co-occurrence of clinically significant EDs with OCD. Finally, a
recent factor analytic study of OCD found that comorbid EDs were associated with
a symptom dimension that is dominated by contamination obsessions and cleaning
compulsions (Hasler et al., 2005).
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Few studies have examined the presence of EDs in other anxiety populations.
Brewerton, Lydiard, Ballenger, and Herzog (1993) calculated that approximately
20% of female social phobia participants in a study by Van Ameringen, Mancini,
Styan, and Donnison (1991) met criteria for AN or BN. In a study of adolescent mixed-gender PTSD inpatients, researchers found that 25% met criteria for
an ED (Lipschitz, Winegar, Hartnick, Foote, & Southwick, 1999). Similarly, Pratt,
Brief, and Orsillo (2005) found that 14% of female veterans with PTSD met criteria for a current ED (i.e., AN, BN, or binge eating disorder [BED]), and 19% for a
past ED.
To our knowledge only one study investigated ED comorbidity across a range of
anxiety disorders. Becker, DeViva, & Zayfert (2004) examined the rate of EDs in a
sample of female patients presenting to an anxiety clinic. EDs (including EDNOS)
were diagnosed using a validated self-report measure. Between 10% and 12% of
patients who met criteria for panic disorder, OCD, or GAD appeared to have an
ED, and 20% and 16% of social phobia and PTSD patients, respectively, met ED
criteria. Because this was a highly comorbid sample (i.e., many patients met criteria
for multiple anxiety disorders), Becker et al. used hierarchical multiple-regression
analyses to investigate the unique contribution of specific anxiety disorders to eating
pathology. Both PTSD and social phobia accounted for significant unique variance
in eating pathology.
The combined estimated prevalence of AN and BN among young females is
between 1.5% and 4% (American Psychiatric Association, 1994). Thus, available
data suggest that EDs may be substantially more prevalent in anxiety populations
than in the general population. We concur with other researchers (e.g., Brewerton
et al., 1993) who argue that anxiety clinicians should be vigilant for comorbid EDs,
particularly in female patients. Results from Becker et al. also raise the concern that
EDs may go undetected in some anxiety clinics. More specifically, as is common
in many anxiety clinics, Becker et al. relied on the Anxiety Disorders Interview
Schedule (ADIS-IV; Brown, DiNardo, & Barlow, 1994) as the primary diagnostic
instrument. The ADIS is arguably the best structured interview for the assessment
of anxiety disorders, and it also assesses many common comorbid Axis I disorders,
such as somatoform, mood, and substance disorders. Notably, however, the ADIS
does not include assessment of EDs. Because Becker et al. used a self-report instrument to assess EDs, they investigated how many ED cases were missed when the
ADIS was used as the primary diagnostic instrument. Results indicated that interviewers missed 80% of probable ED cases, suggesting that clinicians who rely on
the leading anxiety disorders interview may miss eating pathology because patients
do not necessarily spontaneously volunteer information about eating when it is not
assessed.
In summary, research indicates substantial co-occurrence of EDs and anxiety disorders, and female anxiety patients presenting appear to exhibit substantial
ED comorbidity. Given the potential medical complications and elevated risk for
mortality associated with EDs (Powers & Bannon, 2004), it is imperative that
anxiety clinicians do not assume that they will adequately detect comorbid EDs
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C.B. Becker et al.
if they are not explicitly screening for such disorders. Although anxiety clinicians should remain alert for the presence of EDs in all their patients, clinicians
should be particularly vigilant when treating women with OCD, social phobia,
and PTSD.
Assessment of EDs in Anxiety Patients
Depending on the time constraints, setting, and clinician preference, a variety of
assessment approaches may be used to detect EDs in anxiety populations. One possible strategy that appeals to some clinicians involves simply having patients fill out
a valid self-report questionnaire to ascertain their degree of ED symptomatology.
There are several such assessments that have been widely used in the ED field. They
include the Eating Attitudes Test (EAT; Garner, Olmsted, Bohr, & Garfinkel, 1982),
Bulimia Test-Revised (BULIT-R; Thelen, Farmer, Wonderlich, & Smith, 1991), The
Bulimic Investigatory Test, Edinburgh (BITE, Henderson & Freeman, 1987), and
the SCOFF (Luck et al., 2002). A recent review (Peterson & Mitchell, 2005) of
these instruments, however, highlighted some of the shortcomings of these measures
including absence of screening for specific ED diagnostic criteria (for EAT, BULITR, BITE, and SCOFF), lack of adequate sensitivity and specificity (for the EAT), a
high false-positive rate (for the EAT), and/or lack of validation in US samples (for
the SCOFF).
Two other questionnaires have been developed that demonstrate an advantage over the measures described above in that they directly assess DSM-IV
(American Psychiatric Association, 1994) ED symptoms. The first, the Eating
Disorder Examination-Questionnaire (EDE-Q; Fairburn & Beglin, 1994), is the
self-report version of the Eating Disorders Examination (EDE; Fairburn & Cooper,
1993). The EDE is a semi-structured interview considered to be the “gold standard”
in the assessment of EDs (Garner, 1995). The EDE-Q is a 36-item measure that
assesses both behavioral and attitudinal features of EDs over the past 28 days. Items
are rated on a seven-point scale in terms of frequency or intensity. In addition to
generating a variety of subscale and total scale scores, responses to the specific
diagnostic questions can be used to determine ED case status and a “skip-out”
condition can be used to reduce patient burden (Becker et al., 2004). The second
questionnaire is the Eating Disorder Diagnostic Scale (Stice, Fisher, & Martinez,
2004; Stice, Telch, & Rizvi, 2000) which contains 22 items assessing the DSM-IV
diagnostic criteria for AN, BN, and BED. Responses can be used to generate DSMIV diagnoses or standardized and summed to create a total ED composite score.
Although it is well known that questionnaires are not the ideal method for assessing
EDs, they do offer clinicians a method for screening ED symptomatology and may
be appropriate in some clinical settings. Information obtained via self-report should
be followed up with a clinical interview.
In terms of structured clinical interviews, the Eating Disorder Examination
(Fairburn & Cooper, 1993) is the most comprehensive ED-specific interview and
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Fig. 1 Screening questions for detecting possible eating disorders (Adapted from Fairburn &
Cooper, 1993)
296
Fig. 1 (continued)
C.B. Becker et al.
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can be used to obtain a thorough assessment of ED pathology. Although the EDE is
a very useful tool for in-depth assessment and highly recommended, most anxiety
clinicians likely will find it burdensome to administer on a regular basis. Another
clinical alternative is to have a repertoire of questions that can be added to a standard anxiety interview, such as the ADIS. Clinically, we find it useful to rely on
the wording developed for the EDE. In Fig. 1, we highlight some questions drawn
from the EDE that can be used to screen for ED pathology. It is important to
note that assessment of overeating can be challenging because overeating patterns
vary wildly. Some ED patients may eat small amounts of food (e.g., one cookie)
and report strong feelings of loss of control, whereas others consume very large
amounts of food during out-of-control eating episodes. Patients also may experience strong feelings of shame when discussing overeating or purging behaviors.
Thus, it is important to appear non-judgmental when discussing these behaviors and
to be very comfortable discussing behaviors such as vomiting and the consumption
of large amounts of food. We encourage clinicians to read through the directions for
the EDE, which can conveniently be located in the same book (Fairburn & Wilson,
1993) that contains a copy of the CBT manual for BN, another important resource
discussed below.
Because many patients with EDs display no overt signs of an ED, we encourage
anxiety clinicians to add screening questions to their regular clinical interview, particularly when working with female patients. We also recognize, however, that many
ED patients are evasive about their behaviors, and it can be helpful to be aware of
some classic signs of EDs (see Mitchell, 1995 and Goldbloom & Kennedy, 1995
for further discussion; also see case examples below), while recognizing that a lack
of these signs does not mean the patient is ED free. For instance, although many
ED patients are normal weight, one obvious indicator of a possible ED is weight.
A significantly underweight or overweight patient may suffer from AN or BED,
respectively. Individuals with AN often deny having a problem with eating and may
instead argue that they are naturally thin. Another helpful sign in such cases is the
presence of lanugo, which is fine body hair that may accompany low weight. Also,
AN patients may report significant problems with feeling cold or wear very heavy
clothing to keep warm. Other clinical indicators of patients who purge regularly
include puffiness in the cheeks, which is a result of enlarged salivary glands, and
significant problems with dental enamel erosion (often detected first by a dentist).
Although abrasions on the fingers, resulting from stimulating the gag reflex during vomiting, are a commonly mentioned ED sign in the literature, in our clinical
experience few patients present with this sign, either because they use an implement
such as a toothbrush or are simply able to vomit on demand. In athletes or patients
who exercise extensively, stress fractures, repeated injuries, and prolonged recovery
periods may indicate the presence of an ED (see the case of Emily below for further discussion). Dizziness also may accompany EDs. Anxiety clinicians typically
assess caffeine use because caffeine may increase anxiety; this also is important
with ED patients. Individuals with EDs often use caffeine to increase energy and as
a diuretic.
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In addition to administering any of the measures listed above, clinicians must
assess the patient’s current height and weight (either by self-report or by weighing
at the clinic). This is important not only for the diagnosis of AN but also to get a
sense of whether the patient’s body mass index (BMI) falls within the underweight,
normal, or overweight ranges. Although self-report height and weight are not ideal,
research has shown that self-report weights are reasonably accurate (Stunkard &
Albaum, 1981).
Finally, any ED patient should have a complete medical examination, preferably conducted by a physician who is experienced in treating ED patients, although
these physicians can be hard to find. This typically includes a general medical exam,
blood tests to detect any electrolyte abnormalities, and assessment of the various
physical consequences of the ED (e.g., bradycardia, low bone mass). This information is important in guiding decisions about when to address the ED. Although
it is beyond the scope of this chapter to review all of the medical complications
associated with EDs (e.g., cardiac, endocrine, gastrointestinal, and/or renal complications), clinicians should bear in mind that EDs can affect all organ systems and
lead to permanent changes if not death. Many anxiety clinicians may not have adequate familiarity with health risks associated with EDs and the critical importance
of multi-disciplinary care for ED patients. Mental health clinicians should always
involve a medical practitioner when treating a patient with an ED. We refer clinicians to Powers & Bannon (2004) for a more comprehensive review of medical
comorbidity associated with EDs.
Overview of Empirically Supported and Promising
Treatments for EDs
As is the case with anxiety disorders, varying amounts of empirical support exist
for specific ED treatments. For example, whereas CBT for BN (CBT-BN) is supported by extensive research (Wilson, 2005), treatment for AN has garnered less
support, in large part due to a shortage in the number of controlled trials evaluating
specific interventions. Complicating the picture is the fact that EDNOS is excluded
from most trials. As noted above, EDNOS is more prevalent in clinical practice than
AN and BN; it also has much in common with these disorders (Fairburn & Bohn,
2005). Because CBT-BN has been extensively researched and includes many of the
techniques commonly employed in ED treatment, we first discuss CBT-BN and the
model that underpins it. We then briefly discuss a new intervention, CBT-Enhanced
(CBT-E) and its associated model because this model builds on the CBT-BN model
and is very useful in developing case formulations for comorbid anxiety and ED
patients. Also, preliminary reports of an ongoing trial of CBT-E have been quite
promising (Fairburn, 2004). Next, we highlight some cognitive-behavioral strategies that may be of particular use for anxiety clinicians who encounter patients
with comorbid EDs, and discuss motivational issues associated with comorbid
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EDs. Finally, we briefly review the research supporting several other treatments
for EDs.
CBT-BN and CBT-E
According to recent meta-analyses (Whittal, Agras, & Gould, 1999) and reviews
(Wilson, 2005), the treatment for BN with the most empirical support is manualbased CBT-BN (Fairburn, Marcus, & Wilson, 1993). In fact, after conducting one of
the most comprehensive reviews of the literature, the National Institute for Clinical
Excellence (NICE), an independent organization charged with developing evidencebased guidelines on healthcare in the United Kingdom, recently recommended that
CBT be the first-line treatment for adults with BN (Wilson, 2005)
CBT-BN is based on a cognitive model of BN (Fairburn, Marcus, et al., 1993),
which proposes that over-concern with shape and weight drives extreme and rigid
dietary restriction, which in turn leads to binge eating. Binge eating results secondary to inadequate caloric intake, and to inevitable violation of strict eating
rules (e.g., “now that I’ve blown it by eating this cookie, I might as well binge”).
Compensatory behaviors, such as vomiting, start as attempts to counteract episodes
of overeating, but soon lead to an increase in overeating, in large part because cognitive restraint is reduced when individuals believe they can “get rid of” excess
calories. Moreover, some compensatory behaviors, such as vomiting, are easier to
initiate when one has consumed a large amount of food (i.e., it often is easier to
vomit a gallon of ice cream than two spoonfuls). Binge eating also increases overconcern with shape and weight and fears of gaining weight. Thus, once the disorder
has started, it becomes self-perpetuating.
CBT-BN typically consists of 15–20 sessions over approximately 5 months with
the initial phase of treatment focused on helping patients institute a regular eating pattern of consistent meals and snacks, learn about the consequences of their
behaviors (e.g., extreme dieting, vomiting, and laxative and diuretic misuse), and
employ alternatives to binging and purging when in high-risk situations (Fairburn,
Marcus, et al., 1993). In the subsequent phases of treatment, patients are encouraged
to resume consumption of forbidden foods. They also learn to decrease their weight
and shape concerns (core ED cognitions), and prevent relapse of future episodes of
their ED. Between 40% and 50% of treatment completers cease binge eating and
purging (Fairburn et al., 1995). The CBT-BN manual is extremely helpful for any
clinician wanting to gain knowledge about the treatment of EDs. As noted above,
it is conveniently published in the same book as the EDE (Fairburn & Wilson,
1993).
Despite its efficacy, manual-based CBT does not help all patients with BN. In an
effort to maximize treatment outcomes for patients receiving CBT-BN and to better
treat the full range of EDs, including EDNOS, Fairburn, Cooper, and Shafran (2003)
built on the model described above and proposed a new transdiagnostic model of
the maintenance of all EDs that includes four additional maintaining processes that
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affect the core psychopathology of EDs. These include clinical perfectionism, core
low self-esteem, mood intolerance, and interpersonal difficulties. The transdiagnostic model offers greater flexibility in creating a case formulation for complicated
patients, and highlights many factors (e.g., perfectionism, high achievement standards, mood intolerance/avoidance) that are relevant in conceptualizing anxiety
disorders. A more prominent role also is given to the well-known observation that
many ED patients use binge eating and or purging behaviors to regulate mood
(including anxiety).
In addition to describing a new model of EDs, Fairburn et al. (2003) described a
new transdiagnostic treatment for EDs. Importantly, this treatment can be used with
all forms of clinical EDs that can be managed on an outpatient basis. A patient’s
specific ED diagnosis is not as important as the idiographic model of maintaining psychopathological features and processes. The four stages of treatment include
an intensive initial stage of twice-weekly sessions for 4 weeks which focuses on
engagement of the patient, education about EDs, creation of a personalized formulation of their ED, and early behavioral change (Fairburn et al.). Stage two,
which lasts 1–3 sessions, includes a review of progress, identification of any barriers to change, and revision of the formulation to include the most relevant of the
four additional maintaining factors described above. In the third and most lengthy
stage, the revised formulation guides the interventions such that a focus remains
on the patient’s ED pathology along with the additional processes that have been
identified. Fairburn et al. provide treatment “modules” to be used in each case. As
with the CBT-BN manual, we find the article describing the transdiagnostic model
and treatment (Fairburn et al.; see also Fairburn, 2008) to be very useful in both
conceptualizing and treating comorbid anxiety disorder and ED patients.
Commonly Used CBT Strategies for Treating EDs and General
Treatment Issues
Both CBT-BN and CBT-E share many features, not surprisingly given that CBT-E
was designed to build upon the success of CBT-BN. More specifically, both treatments are anchored by the traditional CBT reliance on self-monitoring. Patients
in ED treatment self-monitor all episodes of food consumption (including exactly
what was eaten) and all compensatory behaviors (e.g., vomiting, laxative use, excessive exercise), along with circumstances that surround the episodes (time, location,
other related factors). Many ED patients find self-monitoring quite aversive; thus, it
is imperative that clinicians educate themselves about how to encourage, respond to,
and reinforce self-monitoring in ED patients. More specifically, ED patients need a
very clear rationale for self-monitoring along with an explanation of how the monitoring will be used to help them. When they complete assigned monitoring, they
need to be reinforced and shaped so that the monitoring continues and becomes
optimally useful. In addition, it is critical to avoid appearing judgmental about the
quantity or types of foods consumed. ED diets can be quite unusual and patients
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are very sensitive to perceived judgment (see CBT-BN manual for more detail about
assigning self-monitoring).
In our experience, getting ED patients to regularly and reliably self-monitor is
somewhat more challenging than getting anxiety patients to self-monitor. Thus,
although it can be tempting to simply assign all patients with comorbid EDs
self-monitoring of their eating even when the primary disorder being treated is the
anxiety disorder, we recommend caution in adopting this approach. If clinicians
do not have a clear clinical plan to use the monitoring then patients often rapidly
find self-monitoring unrewarding and they may be more reluctant to complete similar assignments in the future. We, thus, recommend using detailed self-monitoring
of eating in the following circumstances. First, and obviously, self-monitoring will
be implemented if the clinician decides to start CBT-BN or CBT-E. Second, in
some cases it may make sense to briefly use self-monitoring to better assess current patterns of eating. Finally, at times, self-monitoring of eating can be used to
“keep an eye” on the ED while completing treatment of the anxiety disorder. If selfmonitoring is to be used in this third situation, the clinician should keep two factors
in mind. First, if the primary objective is simply to track the frequency of binge eating and purging, many patients find it easier simply to keep a tally of these behaviors
as opposed to completing detailed food monitoring. Second, if the patient is going
to be asked to complete detailed food records, then some portion of each session
should be spent carefully reviewing and using these records so that the patient is
reinforced for completing this task.
Other common strategies employed in CBT include psychoeducation (e.g., about
dietary restriction, purging behaviors), weekly weighing (e.g., to teach patients to
view weight as useful data and to reduce over- or under-weighing), stimulus control strategies (e.g., to facilitate consumption of regular meals and to decrease binge
eating), cognitive restructuring (e.g., to address maladaptive cognitions about the
importance of weight and shape), and relapse prevention (e.g., to identify situations
in which the patient might be at risk to restrict, overeat, or purge). It is beyond
the scope of this chapter to review the ways in which each of these techniques are
used to treat EDs; we refer readers to the original materials described above for
additional important detail. It is important to note, however, that ED patients are
frequently less motivated for treatment than anxiety disorder patients and that standard CBT techniques for increasing motivation may be useful in this population.
More specifically, many ED patients view their ED as a solution, not a problem,
and this may be particularly the case for individuals with EDs who present for treatment for another disorder, such as an anxiety disorder. In fact, as demonstrated in
the case studies described below, many anxiety patients with a comorbid ED may
come to treatment never intending to discuss their ED with their anxiety therapist.
Thus, in addition to assessing EDs, anxiety clinicians need to be prepared to address
motivational issues with respect to the ED, even if the plan is to refer patients for
specialty ED treatment. Although not a part of the formal CBT-BN manual, we find
decision analysis a very useful CBT strategy for increasing motivation for ED treatment. Decision analysis (Janis & Mann, 1977) is a strategy developed to enhance
motivation in substance abusers, and it can be helpful in increasing motivation for
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ED treatment. In decision analysis, patients explore both the positive and negative
consequences of continuing their behaviors and stopping their behaviors, both in
the short and long term. We also refer clinicians to Vitousek, Watson and Wilson
(1998) for an excellent discussion of other strategies for increasing motivation
for ED treatment.
Other ED Treatments with Empirical Support
Due to the dearth of controlled trials for the treatment of AN (attributable to the
low incidence of AN), there is no current treatment of choice for this potentially
lethal disorder. Several treatments appear promising, however, including manualized family-based treatment (FBT) for adolescents (Lock, Le Grange, & Agras,
2001) and CBT-E (Fairburn et al., 2003; Fairburn, 2008). FBT, also known as the
Maudsley Approach, has garnered some empirical support and further trials are currently underway (le Grange & Lock, 2005; Wilson, 2005). Although there is debate
about the strength of the current evidence for FBT (Fairburn, 2005), it remains the
case that FBT is commonly recommended and utilized with this population (le
Grange & Lock, 2005). As noted above, CBT-E (Fairburn et al.; Fairburn, 2008)
targets all EDs. For example, it includes a focus on several clinical features distinctive to AN, including fear of weight gain and perfectionism. Final results from the
ongoing trial of this treatment are eagerly anticipated by the ED community.
It is important to note that the medical issues associated with AN (e.g., refeeding
syndrome) raise a number of ethical concerns for ED novice providers. In general,
we recommend referring severely underweight patients for ED specialty care. At
minimum, care of such patients requires supervision by an ED specialist and collaborative nutritional and medical care. As noted by Vitousek et al. (1998), ED
treatment generally requires clinicians to obtain extensive knowledge about a wide
range of topics including, but not limited to, nutrition, effects of dietary restriction,
exercise, factors contributing to weight including metabolic factors, and recent diet
fads so as to help patients disentangle myth from fact. We recognize that many anxiety clinicians may not want to devote significant time to obtaining this knowledge;
thus, a good network of ED specialists for referral can be one of the most important
tools in working with comorbid anxiety and ED patients. The Academy of Eating
Disorders (www.aedweb.org) can be a useful source for finding ED providers.
The treatment for BED (the only well-categorized EDNOS to date) with the
most empirical support is CBT-BED (Wilson, 2005). However, in contrast to CBTBN, CBT-BED has not been shown to be superior to other forms of psychosocial
treatments (Wilson & Fairburn, 2002). Interestingly, CBT and interpersonal psychotherapy (IPT) for BED have shown almost equivalent outcomes in both the shortand long-term (Wilfley et al., 2002; Wilfley et al., 1993). In addition, dialectical
behavior therapy (DBT) has been used successfully to treat BED (Telch, Agras, &
Linehan, 2000). Research on the treatment of BED is less extensive than that of BN
(Wilson, 2005) and several projects are underway in an effort to add to this area of
knowledge.
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Using the Case Formulation Approach to Guide Treatment
Planning for Anxiety Patients with Comorbid EDs
No empirically tested treatment manual is available to address any combination
of comorbid anxiety and EDs or the complicating life problems of these patients.
Therefore, treatment planning for such patients can be exceedingly challenging
for clinicians who want to deliver evidence-based treatment. We have found the
evidence-based case formulation approach described by Persons and her colleagues
(Persons, 2005; Persons & Tompkins, 2007) to be a powerful method for addressing
comorbid presentations and resolving complications and obstacles as they emerge in
treatment (see Zayfert & Becker, 2007) for more specific discussion. This approach
helps clinicians organize an array of clinical information in a theoretically coherent manner, resulting in a case formulation that serves as a guide for systematic
selection and ordering of interventions.
When using the evidence-based case formulation approach, the clinician starts by
identifying predisposing, precipitating, and maintaining factors. Next, the clinician
generates hypotheses about the interrelationships among the patient’s multiple problems. To the degree possible, hypotheses are based on evidence-based nomothetic
models of specific disorders and associated problems, so as to reduce clinical judgment errors (Wilson, 1996). By considering a range of evidence-based nomothetic
models within a hypothesis-testing approach to the individual case, the clinician
can, in effect, apply a scientific method to the treatment of complicated patients,
maximizing the likelihood of a positive outcome. Based on the hypotheses, the clinician then selects treatment strategies, drawing as much as possible from treatments
with substantial empirical support. Finally, the clinician assesses response on a regular, ongoing basis to determine if the patient is responding as predicted by the
hypotheses. If the patient is not responding as predicted, the clinician revisits the
hypotheses.
Persons & Tompkins (2007) outline seven steps for constructing a case formulation (see Fig. 2). Following these steps, the clinician aims to construct a formulation
that is evidence-based, has clinical utility, and is reasonably parsimonious.
OCD Case Example
Case Description
Emily, a 17-year-old student, was referred by her high school counselor for treatment of OCD. Emily reported an extensive history of contamination obsessions,
washing and checking compulsions, and avoidance behaviors. Emily feared being
contaminated by “AIDS” and cancer, and she recently had been unable to handle
her textbooks for fear that someone with AIDS or cancer might have previously
handled the books. Emily reported that her contamination fears dated back to childhood, when she engaged in elaborate washing rituals when she thought she had been
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given “cooties” by another child. Emily tried to make her thoughts “go away” but
was unable to banish them. She currently engaged in extensive showering and handwashing rituals; the skin on her hands and arms were noticeably red and chapped. In
addition, Emily also reported “sterilizing” her food to prevent it from contaminating
her. This compulsion began at age 15 when she learned of an Escherichia coli outbreak and became highly concerned that food could contaminate her. Emily reported
that she only ate foods cooked at very high temperatures for significant periods of
time to insure that the food was clean. Emily realized that her concern was irrational in that she was willing to feed her younger sister, who she loved very much,
food that had not been sterilized. At intake, Emily reported that her food intake was
“somewhat limited” by her contamination fears, but stated that it was more important to overcome some of her other contamination fears first because they impaired
her academically.
Emily was a healthy looking, thin young woman (i.e., BMI of 18.5) who enjoyed
being on the varsity cross-country team. She noted that she had played soccer as a
child, but had given it up secondary to feeling contaminated by her contact with the
other players on the field. She also reported significant difficulty showering in public
places, and had special showering rituals to wash off the germs from the showers in
athletic facilities.
Noting Emily’s thin appearance, her participation in weight-oriented sport, and
some evasiveness about her actual diet, Emily’s therapist probed further into Emily’s
eating. Emily stated that her eating was the “least of my worries” but ultimately
began to disclose further. She noted that after she began sanitizing food, she also
started to reduce the number of foods that she ate because some foods were harder
to sanitize. For example, she eliminated dairy foods from her diet because sanitizing
Steps in Constructing a Case Formulation (Persons & Tompkins, 2007)
1.
Obtain a comprehensive Problems List
2.
Assign a five-axis DSM diagnosis
3.
Select an anchoring diagnosis
4.
Select a nomothetic formulation of the anchoring diagnosis to use as a template
for the hypothesized psychological mechanisms part of the formulation
5.
Individualize the template so that the formulation accounts for the details of the
case at hand and for all of the problems on the Problem List and their relationships
6.
Propose hypotheses about the origins of the psychological mechanisms
7.
Describe the precipitants of the current episode of illness or symptom
exacerbation
Fig. 2 Steps in constructing a case formulation (Persons & Tompkins, 2007)
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burned these foods to the point that they were unappetizing. Emily also reported that
after developing the food obsession she lost weight, which pleased her from both an
appearance perspective and because of positive feedback from her coach that her
running was improving due to her weight loss. At intake, Emily limited her diet to
two kinds of canned, low-fat soup (chicken noodle and tomato) that she boiled for a
minimum of 45 min to sanitize. When asked why the soup had to be low fat, Emily
reluctantly admitted that she also was concerned about gaining weight. Further
questioning revealed that Emily avoided some foods due to contamination issues,
though she avoided other foods due to weight and shape concerns. Questioning also
revealed extensive misuse of diuretics and the consumption of large amounts of
(highly boiled) coffee for energy and diuretic properties. Emily described her weight
as one of the most important things in how she judged herself, even though she felt
superficial for considering it important. Her menstrual cycle was highly irregular.
Case Formulation
1. Problem List:
• Contamination obsessions
• Checking and cleaning (including sterilizing) rituals which interfere with
studying
• Avoidance (of particular foods and of touching objects she believes contaminated) interfering with ability to function (e.g., academically)
• Over-concern with weight and shape
• Malnutrition secondary to inadequate intake: related to both obsessions and
over-concern with weight and shape
• Repeated problems with stress fractures during running; possibly related to
osteoporosis and irregular menses
• Possible electrolyte imbalance and cardiac abnormalities
• Misuse of diuretics (including caffeine)
• Episodes of dizziness, which are interpreted to indicate possible contraction
of disease or contamination by inadequately sterilized food
• Overtraining: related to weight/shape concerns and perfectionist standards
about needing to be the best runner on the team
2. Diagnoses:
• Axis I: OCD, EDNOS1
• Axis II: None
• Axis III: Malnutrition, R/O osteoporosis, R/O electrolyte imbalance, R/O
cardiac abnormalities
1 Although
underweight, Emily did not meet the weight criteria for AN. She also did not meet
criteria for BN because she did not engage in binge eating.
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• Axis IV: Interpersonal problems with teachers secondary to attending classes
poorly prepared
• Axis V: 50
3. Anchoring Diagnosis: OCD
4. Relevant Nomothetic Formulations
• Cognitive-behavioral models of OCD (see Steketee & Barlow, 2002)
• Transdiagnostic CBT model of EDs (Fairburn et al., 2003; Fairburn, 2008)
5. Individualize the Template –
Biological/Somatic factors: Weight loss, dizziness, and weakness due to malnutrition
Behavioral factors: Avoidance: Excessive washing rituals, sterilizing foods,
avoiding touching “contaminated objects,” avoiding particular foods
Cognitive factors: “Food can be dangerous – it can make me sick.” “I need to
be very careful about what I eat or else I will get sick or fat.” I’m only worthwhile when I’m thin. “Being thin is the most important thing in life.” “Being thin
makes me a better athlete.”
6. Working Hypotheses –
The therapist hypothesized that, as a result of both biological and psychological vulnerabilities, Emily viewed her obsessions as dangerous thoughts to be
avoided, and also overestimated the likelihood of danger from contamination.
In response, she attempted to suppress the thoughts, which led to them occurring more frequently. In addition, she attempted to neutralize her thoughts by
engaging in cleaning and checking rituals and by avoiding stimuli that triggered
the thoughts in the first place. Cleaning and checking initially reduced Emily’s
anxiety; thus, these behaviors became negatively reinforced and increased.
The therapist further hypothesized that a variety of life factors led Emily to
become over-concerned with weight and shape as a means of improving how she
felt about herself. These factors included a father who teased Emily if she gained
weight, learning to overvalue the importance of achieving (i.e., perfectionism),
and core low self-esteem. When Emily lost weight, many people reinforced her
weight loss, including her coach and her father, who both actively praised her
for becoming thinner. Emily reported that, for the first time, these two important people regularly told her she was doing well. Emily also reported that she
enjoyed the weight loss because she looked better (i.e., was closer to both the
thin-ideal standard of female beauty and the cross-country runner’s thin-ideal
standard of appearance). In order to maintain and even increase her weight loss,
Emily engaged in more drastic restriction. She began using diuretics after her
boyfriend, who wrestled, mentioned using them to make weight. Diuretic misuse
can result in hypokalemia (low serum potassium). Thus, the therapist hypothesized that Emily’s dizzy spells might be related to both general malnutrition
and hypokalemia, which put Emily at risk for cardiac problems. Low protein
intake also raised risk of cardiac abnormalities. Emily’s dizzy spells served to
increase her anxiety in that she interpreted dizziness as a sign of illness, due
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either to contamination from touching an object or inadequate sterilizing of food.
The therapist also hypothesized that the female athlete triad (Nattiv, Agostini,
& Yeager, 1994), which consists of disordered eating, irregular or cessation of
menses, and osteoporosis, was a potential problem for Emily. The female athlete
triad recognizes that many female athletes (even those without clinical EDs) do
not consume diets adequate to maintain regular menses given the excess calorie expenditure associated with competitive sports. Regular menses are needed
for bone health; Emily’s stress fractures suggested that she might be experiencing early (i.e., osteopenia), or not so early, stages of osteoporosis. Because most
people cannot build bone mass after age 25, determining Emily’s bone status was
important.
Finally, the therapist hypothesized that Emily’s reluctance to discuss her eating indicated that, like many individuals with EDs, Emily was not motivated
to address her ED. Thus, as long as medical issues were addressed, Emily
might respond better to an approach that first targeted her OCD. After Emily
experienced progress in this area, and after she and her therapist had built a
more solid therapeutic alliance, Emily might be more willing to tackle her ED
behavior.
7. Precipitants of current episode: E. coli outbreak triggered food sanitizing;
weight loss triggered further dieting and diuretic use.
Treatment Plan
After reviewing the case formulation hypotheses, Emily and her therapist agreed to
start relatively straightforward exposure and response prevention (ERP) for Emily’s
OCD because Emily was motivated for OCD treatment and it appeared that she
could make progress faster in this area. Emily and her therapist also agreed that it
would be difficult to proceed with ED treatment as long as she felt compelled to sanitize her food. In contrast, the ED would not necessarily interfere with exposure to
unsanitized foods, as long as they were relatively low calorie. Because of the medical concerns associated with Emily’s ED, the therapist made treatment contingent
upon Emily meeting with a physician; explaining her nutritional status, diuretic use,
and exercise level; having a complete physical (including cardiac) assessment; having her electrolyte levels checked; arranging for a bone scan; and agreeing to allow
contact between physician and therapist. Emily also agreed that she would take supplements (e.g., potassium and/or calcium) if recommended by her physician. The
therapist explained that exposure could be used to help Emily consume the supplements if contamination fears arose, as predicted by Emily. In addition, Emily
agreed to decrease caffeine use (in consultation with the physician), which often
exceeded a pot of coffee per day and likely exacerbated her anxiety, and to attempt
to decrease diuretic use. Finally, Emily agreed to emphasize nutritious foods on
her exposure hierarchy. For example, Emily had no calorie concerns about adding
spinach, bananas, or skim milk to her diet, but had contamination fears about these
foods. After 15 sessions of twice-weekly ERP with ongoing assessment, Emily and
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her therapist would review her progress and reassess her ED. At that time, if indicated, Emily would either start CBT for her ED or begin decision analysis aimed at
increasing her motivation to engage in ED treatment. ERP consisted of exposure to
a variety of objects (e.g., books, tables at school, unsanitized food) and prevention
of compulsions (e.g., washing after contact with books, extensive showering). With
regard to food exposure, Emily agreed to bring a designated unsanitized food to
therapy, and she and the therapist would eat the food together, with Emily attending
to her anxiety for the remainder of the session. Emily then continued with home
practice of exposure.
Social Phobia Case Example
Case Description
Patricia was a 24-year-old female who sought treatment for social anxiety. Patricia,
an only child, had “always been shy.” She reported having just a few friends in high
school, although she developed a more active social life in college, primarily by
drinking alcohol to reduce her anxiety. Patricia recently started graduate school in
a new city and was intent on making friends at student social gatherings. Her busy
schedule motivated her to drink less, and as a result, she found her anxiety elevated
at social events.
Patricia’s anxiety also increased abruptly after she was asked to deliver a 5-min
presentation to her class summarizing a homework assignment. She recalled that
she froze, her heart pounded, her hands shook, her face flushed, and her mind “went
blank.” “Nothing came out of my mouth – everyone stared at me and I looked like
a complete idiot.” When she finally spoke, her voice was shaking but she delivered
her presentation reading from her prepared notes. She spent the remainder of the day
“obsessing” about her performance and anticipating negative reactions from peers.
In the coming weeks her anxiety increased as she realized that her graduate classes
would require more frequent class presentations. Overtime, she became preoccupied with wondering when the next presentation would be and she became more
uncomfortable with raising her hand to speak in class. In addition, she became more
self-conscious at social gatherings, fearing that her peers would ask her about what
happened in class. Increasingly, she began to dread social gatherings expecting that
she would “make a fool of herself again” and she often made excuses to avoid them,
or else endured them by “keeping a low profile.” Her ever-present dread of speaking
in class caused her to avoid classes and her concern about her academic performance
led her to seek treatment.
Unbeknownst to her therapist, Patricia also had suffered from an ED intermittently since age 15. Patricia did not disclose this at intake because she did not see it
as part of the problem that was interfering with daily life. On the contrary, Patricia
thought the behavior was helpful to her in maintaining her weight; moreover, it
reduced her anxiety because she could reassure herself at social situations that she
was one of the thinnest women in the room.
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At intake, the therapist focused on Patricia’s social anxiety, its effects on her life,
and how she was coping; her eating habits were not discussed. Several weeks into
treatment, however, Patricia alluded to discomfort eating with others in restaurants.
When the therapist probed further Patricia acknowledged that this was not solely
due to concerns about others watching, but also because the food choices were “fattening.” Patricia was concerned both that the foods would cause weight gain and that
others would think her gluttonous for eating such foods. At this point, the therapist
began to suspect an ED and decided that further assessment and a more comprehensive case formulation would be helpful. Upon further probing, Patricia confessed
that she “sometimes” vomited after large meals or after “gorging” while she was
home studying. She had begun purging in high school. She had vomited less frequently in college and noted that living in the dorm made it hard to conceal. Instead,
she restricted her intake to a limited range of low-calorie foods. With the increased
stress of graduate school, the escalating social anxiety, lower alcohol consumption,
and living alone, she began binging more when highly stressed. Within a few weeks
she became very concerned about her weight, which had increased slightly, and
increased the frequency of her vomiting from occasional to several times per week.
She also started vomiting after fairly moderate meals. In addition, Patricia began
to look forward to evenings alone when she could binge to escape the stress of the
day knowing that she would have the release of vomiting afterward. Despite her
efforts, Patricia was slowly gaining weight due to the increasing binges and this led
to increased self-consciousness in pubic and increasing avoidance of social gatherings. In addition, her fears of weight gain led her to further limit her food intake
during the day as she ruminated about the effects of her previous night’s binging
and anticipated an upcoming social event.
1. Problem List:
•
•
•
•
•
•
•
•
•
•
Fear of public speaking
Anxiety and avoidance of social gatherings
Avoidance of classes and declining academic performance
Social isolation
Binge eating
Weight gain
Vomiting after binges and forbidden foods
Excessive concern with shape and weight
Food restriction (including low protein intake)
Possible electrolyte imbalance and cardiac abnormalities
2. Diagnoses:
• Axis I: Social phobia, BN
• Axis II: None
• Axis III: R/O electrolyte imbalance; R/O cardiac abnormalities; R/O
osteoporosis
• Axis IV: None
• Axis V: 50
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3. Anchoring Diagnosis: Social phobia
4. Relevant Nomothetic Formulations:
• Cognitive-behavioral model of social phobia (Hofmann & Scepkowski,
2006).
• Cognitive-behavioral model of Bulimia Nervosa (Fairburn, Marcus
et al., 1993)
• Transdiagnostic CBT model of EDs (Fairburn et al., 2003; Fairburn, 2008)
5. Individualize the Template:
Biological/Somatic factors: Blushing, heart pounding, shaking when speaking
to others. Also, evening fatigue from high anxiety, and hunger/lightheadedness
from food restriction.
Behavioral factors: Avoidance: public speaking, social gatherings, eating in
restaurants, daytime food consumption. Safety behaviors: wearing loose clothing
to conceal weight gain.
Cognitive factors: “I’ll never measure up.” “People will think I’m an idiot.” “If
they knew about my vomiting they would be disgusted and not talk to me.”
“They’ll see how fat I am and think I’m disgusting.” “I’ll never make friends
here.” “I don’t fit in.”
6. Working Hypotheses. The nomothetic model of social anxiety proposes that
social anxiety is maintained by an interaction of cognitive (high standards for
social performance, low perceived ability to meet standards, and high perceived
social costs of not meeting standards; negative self-perception, low perceived
emotional control) and behavioral factors (increased self-focused attention,
avoidance and/or safety behaviors in social situations). The therapist hypothesized that the social phobia was the core disorder and that the same factors
(e.g., perfectionism, avoidant coping) that helped to maintain the social phobia
also maintained the ED, along with the self-perpetuating cycle of restriction,
binge eating, and purging. The therapist presumed that the ED also contributed
to maintenance of her social anxiety but that this influence was less powerful.
Patricia’s therapist hypothesized that Patricia had set very high standards for her
performance in social situations. After the speaking incident, Patricia believed
that she was incapable of performing to her standards for public speaking. This
led to increased self-focused attention as she scanned her body and behavior for
indications that she might perform poorly by displaying her anxiety while speaking either to a group or in a social interaction. The more she attended to herself,
the more anxious she became about signs of anxiety she detected, which further
increased her anxiety. Her growing anxious apprehension in anticipation of possible public speaking tasks or other social situations then led to elevated levels
of arousal. Without her old coping strategy (alcohol), Patricia resorted to binging
as a means of reducing anxiety. Although binging resulted in short-term anxiety
reduction by distracting her from social fears, it triggered anxiety about weight
gain, which resulted in increased vomiting. Purging reinforced Patricia’s use of
binging to cope with anxiety. Binging also, however, resulted in slight weight
gain. Moreover, it led to an increase in negative self-perceptions due to weight
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gain and strengthened her perception of herself as being unable to meet her high
social standards. Patricia also began to feel ashamed of her binge/vomit behavior which she believed was “disgusting” and fears of rejection by others if they
found out compounded her anxious apprehension of social encounters. Her therapist hypothesized that her weight gain and her reliance on binge/purge behaviors
to cope with her social anxiety, together, were increasing her avoidance. Her
avoidance of public speaking and social gatherings was, in turn, interfering with
habituation of her fears of these situations and preventing her from testing the
validity of her beliefs about her social performance.
7. Precipitants of current episodes: Starting graduate school, decreasing alcohol
use, living alone, the “speaking incident,” weight gain.
Treatment Plan
Patricia was not motivated to address her ED, in part because it was her only strategy for coping with her anxiety as well as the overall stress of graduate school. She
remarked to her therapist on several occasions how stressed she felt during the day
and the remarkable relief she felt when she came home knowing that the comfort
of food awaited her. At the same time, she felt consumed by her preoccupation and
dread of public speaking and wanted to rid her mind of her “obsession” with this
fear so that she could focus on her studies. Her therapist hypothesized that it would
be difficult to reduce her binging while her anxiety levels were high. Likewise, if
her social anxiety were diminished it would result in less reliance on binging as a
distraction and escape from her anxiety. Thus, the initial treatment plan focused primarily on direct treatment of social anxiety using an exposure-based protocol while
monitoring her binge–purge behaviors. Patricia agreed to keep daily records of her
binging and vomiting. She also agreed to meet with a physician to assess her medical
status. The therapist anticipated that teaching Patricia to consume regular daytime
meals (rather than restricting daytime food intake) would decrease her propensity
to binge, but to ensure that the strategy would succeed, she decided to postpone
implementing it, and more complete self-monitoring of food intake, until later in
treatment – approximately 8 weeks into the social anxiety component of treatment.
At this point she expected that Patricia’s overall anxiety might be reduced to the
point that adding this intervention (regular meals per CBT-BN) might result in a
decrease in binge frequency before directly addressing her purging behaviors and
over-valuing of the thin-ideal.
Ordering of Treatment: Factors to Consider
Several approaches can be taken to address comorbid conditions. First, treatment
can be administered sequentially (i.e., treat one disorder, then reassess and treat
the second disorder). This is often the most parsimonious course of action. One
other advantage to this approach is that treatment may be closer to that employed
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in clinical trials thus increasing the likelihood that research results will generalize
to the individual case. In addition, emerging anxiety disorder research indicates that
targeting one disorder (e.g., panic disorder) may bring about reductions in comorbid anxiety conditions (e.g., GAD; Tsao, Mystkowski, & Zucker, 2005). Also, as
noted by Wilson (1998), research suggests that effective treatment of BN with CBT
results in generalized improvement in depression and self-esteem (Fairburn, Jones,
Peveler, Hope, & O′ Connor, 1993). Thus, it is possible that effective treatment of
one disorder may lead to improvement in the comorbid condition, and that a single
intervention is sufficient.
One challenge in using a sequential approach – either with the hope that the
comorbid disorder will resolve or with the plan to address the second disorder at a
later date – is deciding which disorder to address at the outset. In addition, given
the relative paucity of research clearly demonstrating whether treating an anxiety
disorder leads to a reduction in ED symptoms, clinical decisions about which disorder to target first must be made on the basis of the case formulation. Although each
patient is unique, we use the following rules of thumb when considering a sequential
approach. First, in our experience, compared to EDs anxiety disorders are usually
somewhat easier to treat. Thus, rapid improvement may be more readily obtained by
focused anxiety disorder treatment, which may strengthen the therapist’s credibility
in the eyes of the patient. A second advantage of targeting the anxiety disorder first
is that patients are often less ambivalent about receiving treatment for their anxiety disorder, particularly if they are presenting to an anxiety clinic or therapist. In
addition, because ED treatment increases anxiety, patients with comorbid EDs and
anxiety disorders sometimes find the increase in anxiety difficult to tolerate, thus
stalling progress during ED treatment. Finally, the ED may function as a coping or
avoidance strategy, particularly for patients with a comorbid diagnosis of PTSD. ED
behaviors commonly have an anxiety-reducing function – binging, purging, and/or
preoccupation with food and weight/shape can serve to distract from anxiety and
anxiety-provoking stimuli. Thus many patients understandably are reluctant to give
up their ED. In such cases, it may be difficult to resolve the ED without resolving at
least some of the need for the coping strategy.
Some factors, however, may point to addressing the ED first. For example, if the
anxiety disorder is not severe and/or the patient admits that the ED is a problem,
it may make sense to begin with ED treatment. A sizeable number of patients with
BN respond to CBT-BN, and Axis I comorbidity has not been a solid predictor of
outcome in clinical trials (Wilson, 2005). Also, at times, the medical implications
of the ED may necessitate immediate intervention.
In many cases, a true sequential approach may not be feasible, as highlighted
by the cases described above. In such cases another option is what we refer to as a
simultaneous monitoring approach (Zayfert & Becker, 2007). In this approach, the
patient and clinician agree to predominantly target one disorder while simultaneously monitoring the other disorder. Often the “monitoring” may also include some
low-level intervention. For example, in Patricia’s case, the therapist planned to start
with social phobia treatment while monitoring binge eating and vomiting. She then
planned to introduce food monitoring and a regular pattern of eating (i.e., a schedule of three meals and two snacks per day) once some reduction of overall anxiety
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had been achieved from the social anxiety treatment. The therapist expected that
the lower anxiety level would potentiate the effect of this intervention and result in
reduced binge frequency.
In yet other cases, a completely blended (simultaneous) approach may be warranted. In our experience, these cases often present to ED clinics because of the
severity of the ED. They also, however, may present to trauma treatment programs. Thus, clinicians who treat PTSD may encounter such cases. Unfortunately,
it is beyond the scope of this chapter to fully detail a simultaneous approach. We
refer readers to Zayfert and Becker (2007) for more detailed discussion of the
simultaneous treatment of PTSD and comorbid conditions, such as EDs.
Conclusion
EDs can present a challenge for anxiety disorder clinicians. Although they co-occur
with anxiety disorders more often than many clinicians realize, anxiety patients
rarely disclose ED symptoms to clinicians from whom they are seeking anxiety treatment. Such patients often are highly distressed by their anxiety and less
motivated to address their ED. They may see troublesome eating as a legitimate
and normal (and not unhealthy) weight management strategy and/or as essential to
coping with their anxiety. They may not even recognize anything unusual. Yet, as
the above cases illustrate, the interactions between EDs and anxiety problems can
be complex and the problems can become mutually maintaining. ED behaviors can
be precipitated by anxiety (such as when Patricia used binging to cope with high
anxiety or when Emily’s food avoidance took on a weight-loss function in addition
to neutralizing her contamination obsessions). They can also precipitate anxiety (as
when Emily interpreted dizziness due to electrolyte imbalance as a sign of illness
and thus increased her food sanitizing and avoidance, and when Patricia’s binging and purging exacerbated her social anxiety because she feared others would
notice her weight gain or discover her vomiting). EDs also present a challenge for
anxiety clinicians because many clinicians well-versed in anxiety disorders do not
have specialized training in evidenced-based treatment for EDs. Nonetheless, clinicians can manage these co-occurring problems by first being prepared to detect
them, and secondly incorporating them into the evidence-based case formulation.
Formulating hypotheses about how the ED may reinforce the anxiety disorder and
vice versa is often essential to treatment success. Often the formulation will lead to
a treatment plan that begins with anxiety treatment and aims to build motivation to
eventually address the ED, either with the anxiety clinician, or accepting a referral
to a specialized ED treatment provider.
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Resolving Treatment Complications Associated
with Comorbid Medical Conditions
Joseph Greer, Jessica Graham, and Steven Safren
Introduction
Anxiety disorders, the most prevalent psychiatric morbidity diagnosed within the
United States (Kessler, Berglund, et al., 2005; Kessler, Chiu, Demler, Merikangas,
& Walters, 2005), frequently co-occur with serious medical conditions. Indeed,
recent epidemiological studies confirm that individuals with anxiety disorders are at
substantially greater risk for experiencing comorbid medical illnesses, such as cancer, cardiac, and respiratory diseases, even when adjusting for patient demographic
characteristics, depression, and substance use disorders (Honda & Goodwin, 2004;
Sareen, Cox, Clara, & Asmundson, 2005; Sareen et al., 2006). Not surprisingly,
individuals with anxiety and medical conditions are more likely to report functional
disability and poorer quality of life, compared to patients without anxiety (Kessler,
Ormel, Demler, & Stang, 2003; Sareen et al., 2006; Sherbourne, Wells, Meredith,
Jackson, & Camp, 1996; Stein et al., 2005). Moreover, the comorbidity between
anxiety and various physical disorders substantially increases mean total annual
medical costs, with a notable incremental expense of $7,378 for patients with acute
myocardial infarction (Marciniak et al., 2005).
Despite the emergence of several large-scale studies examining the strong
association between anxiety disorders and medical illness, the exact nature and
direction of this complex relationship remains unclear. As Sareen et al. (2006)
note, one potential explanation is that medical illness leads to an increase in symptoms of anxiety by provoking the stress response, particularly when the physical
condition is life threatening and involves invasive medical procedures. Beyond
simply triggering autonomic arousal, medical illness can also cause anxiety symptoms directly through physiological mechanisms, such as dyspnea associated with
pulmonary embolus or tachycardia in hyperthyroidism. Conversely, anxiety may
potentially lead to the development or exacerbation of certain medical conditions
through chronic activation of the hypothalamic-pituitary axis and related changes
in immune function (Sareen et al., 2006). Moreover, treatment adherence and
other health behaviors, genetics, and socio-environmental circumstances play salient
J. Greer (B)
Department of Psychology, Bronfman Science Center, Williams College, Williamstown, MA, USA
e-mail: joseph.greer@williams.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_17,
C Springer Science+Business Media, LLC 2010
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roles in the association between anxiety and physical illness. For example, anxious patients with coronary artery disease are more likely to continue smoking
than non-anxious patients (Benninghoven et al., 2006). Further complicating the
assessment of anxiety within the context of medical conditions, some physical
illnesses (e.g., cancer) involve toxic medical treatments, which may lead to symptoms that are often mistaken as anxiety. Close collaboration between the medical
team and mental health clinician is essential for accurate diagnosis and management of anxiety, given the multiplicity of etiologies and overlap in disease
presentation.
Complications are likely to arise not only in the assessment but also in the treatment of anxiety comorbid with medical conditions. Although cognitive-behavioral
therapy (CBT) is an effective first-line treatment for anxiety disorders (Otto, Smits,
& Reese, 2004), it has been tested primarily in medically healthy populations and
focuses on the elimination of unrealistic fears as well as behavioral avoidance and
other maladaptive coping. By restructuring distortions in perceptions, particularly
the overestimation of negative outcomes, and by confronting feared stimuli through
exposure-based therapies, CBT helps individuals to challenge catastrophic thoughts
and to extinguish their anxiety (Barlow, 2002). In contrast, individuals with medical
conditions, who frequently experience disease-related symptoms and treatment side
effects, report realistic concerns about pain, functional disability, and in some cases,
even death. Within this context, traditional CBT for restructuring fears about mortality or symptoms of disease progression is less useful, depending on the patient’s
prognosis. Cognitive restructuring plus exposure may not be sufficient to reduce
symptoms of anxious preoccupation and worry in patients who are physically ill
and coping with medical symptoms, tests, procedures, and an uncertain future.
In addition, medical patients often report an escalation of anxiety when experiencing somatic concerns like fatigue, pain, or nausea, which are functionally
limiting and at times difficult to interpret. This anxiety, in turn, through the
physiologic changes associated with the stress response (e.g., muscle tension,
rapid respirations, digestive slowing), can heighten the severity of disease and
treatment-related symptoms, perpetuating the cycle and causing further disability. Comprehensive cognitive-behavioral approaches to the management of anxiety
comorbid with physical disease must therefore address both psychological and medical illness concerns. Figure 1 depicts a treatment approach for evaluating and
managing the maladaptive worry and functional limitations associated with medical
illnesses (partially adapted from Moorey & Greer, 2002).
To highlight methods for resolving treatment complications for anxiety comorbid with medical conditions, we discuss three disease states that have a welldocumented association with anxiety disorders. Although anxiety is related to
numerous other medical conditions, we have chosen to narrow our focus to these
three illnesses in order to illustrate a comprehensive approach for adapting standard
cognitive-behavioral techniques in resolving treatment complications. Specifically,
we review the literature on the symptoms, epidemiology, correlates, and psychological treatment of anxiety associated with cancer, coronary heart disease, and
asthma. Many of the challenges and recommendations for treating anxiety comorbid with medical illness naturally can be applied across various diseases, though we
Anxiety and Comorbid Medical Conditions
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Fig. 1 Algorithm for addressing illness-related worry
have decided to highlight methods for adapting cognitive-behavioral therapy when
discussing each of the specific conditions throughout the chapter.
Anxiety Comorbid with Cancer
Cancer, or malignant neoplasm, is characterized by unregulated cell growth, resulting from chromosomal mutation. Malignancy can develop in nearly every cell type
of the body, and these cancer cells may invade organs locally or spread to distant
sites via the blood stream or lymphatic system. More than 1.4 million Americans
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received a new cancer diagnosis in 2008, the most of which were prostate, breast,
and lung (American Cancer Society, 2008). Cancer is responsible for one in every
four deaths in the United States, making it the second leading cause of mortality
behind cardiovascular disease (Kung, Hoyert, Xu, & Murphy, 2008) Yet, ongoing
advances in screening procedures and improvements in medical treatment regimens
have led to significant increases in cancer survival over the last two decades, with
approximately 10.8 million Americans living with cancer today (National Cancer
Institute, 2007; Ries et al., 2008).
A generation ago, the diagnosis of cancer carried with it the stigma of poor prognosis and expectation for an early and painful death. Today, while some people
still experience rapid decline, particularly those with certain types of lung or pancreatic cancers, many more individuals are either cured of their disease or receive
ongoing treatment (American Cancer Society, 2008). As cancer care continues to
evolve, allowing for longer survival and transforming cancer into a chronic medical condition, even for those with advance-stage malignancy, many individuals will
experience concomitant anxiety that is debilitating and at times exacerbating of the
disease-related symptoms and treatment side effects.
Approximately 10–25% of individuals with cancer have a diagnosable anxiety
disorder (Stark & House, 2000). In some cases, this anxiety reflects an exacerbation
of a premorbid sub-clinical or clinical condition, while in others, anxiety symptoms
emerge in response to stressors from the cancer diagnosis and treatment. Indeed,
the experience of anxiety is a natural reaction to news of a life-threatening diagnosis and abates for many patients with cancer as the prognosis and treatment plan
are clarified. Thus, differentiating persistent, maladaptive anxiety symptoms from
more transient, self-limited distress is often challenging. Although as many as 40%
of individuals with cancer screen positive for psychological distress (Fulton, 1998;
Zabora, Brintzenhofeszoc, Curbow, Hooker, & Piantadosi, 2001), Stark et al. (2002)
found that approximately 18% qualify for an ICD-9 anxiety disorder. Such variation
in prevalence may be due to differences not only in the methods and timing of
anxiety assessment but also in the types and stages of cancers sampled as well as
medical treatment factors.
While some degree of anxiety is protective and useful, ideally facilitating effective coping behaviors, the acute cognitive and behavioral changes associated with
the stress response may become maladaptive, particularly among individuals with
medical illness. Common features of dysfunctional anxiety among individuals with
cancer include intrusive negative thoughts (Devine, Parker, Fouladi, & Cohen,
2003), excessive worry (Nordin, Glimelius, Pahlman, & Sjoden, 1996), and deficient
coping (Wasteson, Nordin, Hoffman, Glimelius, & Sjoden, 2002). Patients experiencing such symptoms report disruptions in concentration, decision-making, sleep,
and social/occupational functioning (Stark & House, 2000). This impairing anxiety
is also associated with ineffective behavioral responses, such as decreased medical
adherence, reassurance seeking, longer hospital stays, social withdrawal, and other
avoidance behaviors (Prieto et al., 2002; Ristvedt & Trinkaus, 2005; Shapiro, 1987;
Stark et al., 2004; Thomas, Glynne-Jones, Chait, & Marks, 1997; Weinmann et al.,
2005). For example, patients with specific phobias such as claustrophobia or needle
Anxiety and Comorbid Medical Conditions
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phobias may compromise their cancer care by avoiding necessary medical procedures and scans. Recent findings from our own work (Greer, Pirl, Park, Lynch, &
Temel, 2008) in patients with advanced non-small-cell lung cancer revealed that
heightened anxiety symptoms within 2 months of diagnosis predicted poorer treatment adherence, including more chemotherapy dose reductions and dose delays,
compared to those with less anxiety.
Cancer-Related Symptoms, Treatment Side Effects,
and Quality of Life
In addition to precipitating maladaptive changes in thought and behavior, anxiety
symptoms aggravate the expected somatic symptoms and treatment side effects
seen in patients undergoing cancer care. Fatigue, insomnia, and pain are among the
most common complaints in patients with cancer diagnoses. Anxiety may intensify
the experience of these symptoms, given that it strongly relates to patients’ perception of cancer-related pain (Theobald, 2004; Thielking, 2003; Velikova, Selby,
Snaith, & Kirby, 1995; Zimmerman, Story, Gaston-Johansson, & Rowles, 1996)
as well as fatigue and insomnia (Barnes & Bruera, 2002; Fossa, Dahl, & Loge,
2003; Redeker, Lev, & Ruggiero, 2000; Stark et al., 2002). Additionally, compared
to non-anxious patients, individuals with cancer and comorbid anxiety report more
complications with chemotherapeutic treatments, including side effects of medications, such as tamoxifen (Cameron, Leventhal, & Love, 1998), worse nausea and
vomiting (Andrykowski, 1990; Chin, Kucuk, Peterson, & Ezdinli, 1992; Watson,
Meyer, Thomson, & Osofsky, 1998), and poorer response to anti-emetic drugs
(Fujii et al., 2001). The relationships among anxiety, disease, and treatment-related
symptoms are complex and, as Theobald (2004) notes, each may contribute to the
maintenance of the other, resulting in significant impairments in quality of life.
Cancer patients with higher levels of anxiety also report having poorer quality of
life than less anxious individuals. In one investigation of women receiving treatment
for breast cancer, for example, higher levels of anxiety at the start of treatment were
negatively correlated with quality of life at initiation of chemo-radiotherapy and
1 year later (Schreier & Williams, 2004). The authors advocated further research
into interventions targeting anxiety symptoms at the onset of treatment. Similarly,
Stark et al. (2002) reported that, in a sample of 178 oncology patients with diverse
primary tumor sites, anxiety disorders measured by screening questionnaires and
diagnostic interviews were present in 18% of participants and associated with poorer
quality of life, especially insomnia. Two other studies confirm that impaired quality
of life for cancer patients correlates strongly with anxiety and that cancer-related
symptoms such as global health status, fatigue, pain, and illness severity do not
explain observed quality-of-life deficits (Redeker et al., 2000; Smith, Gomm, &
Dickens, 2003).
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Psychological Interventions for Anxiety Comorbid with Cancer
Psychosocial interventions to treat patients with cancer ranged in format (e.g., group
versus individual), technique (e.g., supportive versus psychoeducational), target
population (e.g., patient versus provider), and method of delivery (e.g., face-toface versus telephone versus web-based) (Andersen, 2002; Fawzy, Fawzy, Arndt, &
Pasnau, 1995). Given the large number of studies in this area, several investigators
have conducted meta-analyses of the literature to discern the benefit of psychosocial
interventions for a variety of mental health and cancer outcomes, including anxiety, quality of life, and survival (Chow, Tsao, & Harth, 2004; Devine & Westlake,
1995; Meyer & Mark, 1995; Newell, Sanson-Fisher, & Savolainen, 2002; Sheard &
Maguire, 1999). Employing rigorous methodology to evaluate the efficacy of psychological therapies for cancer, Newell et al. (2002) found 1 “good-quality” trial
and 24 “fair-quality” trials that evaluated interventions aimed at reducing oncology patients’ anxiety. Of these, only 11 included cognitive-behavioral therapy,
with 3 demonstrating statistically significant results. The authors therefore recommended that CBT for anxiety among cancer patients warrants further exploration
since published investigations to date have yielded inconsistent findings due to poor
methodological quality (e.g., inadequate specification of randomization strategy,
poor monitoring or protocol adherence), small sample sizes, and short-term followup periods. However, a more recent meta-analysis of randomized controlled trials
of cognitive-behavioral therapy revealed a large effect size (ES = 1.99) for decreasing anxiety among cancer survivors (Osborn, Demoncada, & Feuerstein, 2006).
Whereas these results provide some encouraging evidence for the utility of CBT
to alleviate anxiety in medically complex patients, further high-quality trials testing
the efficacy of CBT tailored to the needs of patients with cancer may help overcome
the limitations of previous research.
Complications in Treating Anxiety Comorbid with Cancer
The difficulties of treating anxiety comorbid with cancer often begin with the referral for psychosocial services and the challenges in scheduling sessions (Curry,
Cossich, Matthews, Beresford, & McLachlan, 2002). Upon receiving a cancer
diagnosis, patients need to attend numerous medical appointments for diagnostic procedures, treatment planning, surgery, and chemo-radiotherapy. As a result
of anti-cancer treatment, patients may experience functional limitations and side
effects such as nausea, pain, and severe fatigue, frequently lasting for days. These
symptoms not only interfere with quality of life but also result in family role disruptions, work absenteeism, and considerable financial cost (Fortner et al., 2003;
Hassett, O’Malley, Pakes, Newhouse, & Earle, 2006; Kim, 2007). Scheduling psychotherapy appointments in addition to those for primary cancer care may at times
feel overly burdensome to patients.
In addition to barriers to providing care, clinicians may struggle with the
differential diagnosis of patients’ somatic symptoms (Ryan et al., 2005). For
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example, while some patients present with complaints of feeling anxious and
worried, others simply describe problems with dyspnea, nausea, palpitations, or
difficulty concentrating. These somatic complaints may indicate a primary anxiety
disorder but also could be due to serious medical complications related to the
disease process (e.g., acute shortness of breath from pulmonary embolus), medical
treatment (e.g., nausea from chemotherapy), or medication side effects (e.g.,
agitation and restlessness from use of corticosteroids and phenothiazines; Massie
& Greenberg, 2005). Of course complicating the diagnostic considerations further
is that the associations between patients’ anxiety and illness-related symptoms are
likely bidirectional and complex in nature.
After considering the medical reasons for anxiety symptoms, clinicians must then
discern a treatment plan and the optimal approach for adapting empirically based
psychotherapies to address the individual needs of the cancer patient. Given that
researchers have predominantly tested and validated cognitive-behavioral therapy
for anxiety disorders in relatively homogenous samples, often excluding patients
with multiple conditions, the application of these techniques to patients with comorbidities poses another challenge to the mental health clinician (Ruscio & Holohan,
2006). In the case of cancer, of primary concern is how to help anxious patients
cope with fears about an uncertain future, whether due to disease progression, cancer recurrence, or imminent death; that is, what methods should be employed when
trying to intervene and challenge maladaptive thoughts that are based on realistic
concerns? How does the mental health clinician within the oncology setting help
to reduce anxiety and life stress when a patient’s functioning is compromised and
triggers of disease worries (e.g., pain) are chronic and recurrent? In response to
these issues, investigators have begun to publish clinical guides that address the tailoring of cognitive-behavioral therapy for individuals coping with various chronic
illnesses, including cancer (Sperry, 2006; Taylor, 2006; White, 2001).
Resolving Treatment Complications for Anxiety Comorbid
with Cancer
To minimize barriers for patients with cancer to access care, mental health professionals would ideally be integrated into the ambulatory cancer center setting.
While this is generally not the case at present (Greenberg, 2004), clinicians who
are co-located at a tertiary care hospital may schedule psychotherapy sessions in
tandem with the patient’s existing medical appointments in order to decrease the burden of multiple hospital visits. When not located on-site, however, clinicians would
want to consider the patient’s current medical treatment regimen and determine
the appropriate timing for scheduling outpatient psychotherapy sessions. For example, patients who experience extreme fatigue secondary to chemotherapy should
schedule their counseling sessions only after sufficient time has passed following
infusions.
To address assessment issues regarding anxiety comorbid with cancer, clinicians
need to stay abreast of the most common organic etiological factors, such as those
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discussed earlier, which potentially underlie patients’ anxiety symptoms. However,
oncologic care will continue to evolve at a rapid pace, and multidisciplinary teambased approaches, encouraging regular communication among medical and mental
health colleagues, facilitate effective diagnosis and targeted treatment of anxiety
comorbid with cancer. Such models are being tested with notable benefits for
patients in the ambulatory oncology settings (Bruera et al., 2001; Graves et al.,
2007; Strasser et al., 2004). Recognizing the importance of identifying and alleviating psychological distress associated with cancer, the National Comprehensive
Cancer Network, a non-profit alliance of leading cancer centers worldwide, has
recommended routine screening for psychological distress and developed specific
guidelines for the evaluation and treatment of anxiety in this patient population
(National Comprehensive Cancer Network, 2006).
As detailed in the treatment algorithm at the beginning of the chapter, the
therapist and patient must evaluate disease-related worries in order to establish which are realistic when providing cognitive-behavioral therapy. Standard
cognitive-restructuring practices are applicable to those thoughts that represent
likely distortions. For example, during a follow-up medical visit, a patient treated
for breast cancer could receive encouraging news about her health and prognosis but
misinterpret the oncologist’s nonverbal cues (e.g., poor eye contact, not smiling) and
make negative predictions about her risk of cancer recurrence. The role of the therapist in this case would be to identify these thoughts as forms of “mind-reading” and
“catastrophizing” while working with the patient to develop more rational responses
by considering disconfirming evidence, such as the positive results from recent scans
and alternate explanations for the oncologist’s behavior.
Of course, however, many cancer-related fears will be valid and rooted in reality,
based on the patient’s experiences and on available data from imaging procedures and feedback from the oncology team. For example, soon after diagnosis,
most patients with lung cancer report major concerns about the illness, prognosis, and effects on family (Hill, Amir, Muers, Connolly, & Round, 2003); many
of these worries represent realistic risks given the high mortality rates due to lung
cancer (Surveillance, Epidemiology, & End Results Program, 2006). Under such
circumstances, mental health clinicians should not challenge such thoughts as cognitive distortions, even though they may cause maladaptive responses including
disturbances in concentration, sleep, and well-being (Taylor, 2006; White, 2001).
Rather, as per the guidelines of the aforementioned treatment algorithm, a more
effective approach would include helping patients discern how and when to apply
problem versus emotion-focused coping strategies to their realistic worries. More
specifically, Moorey and Greer (2002) suggest that clinicians utilize a decision tree
to determine the extent to which patients are able to take some action in resolving
their concerns. If action is possible or needed, such as seeking further medical consultation, clinicians may then employ problem-solving skills, developing a list of
possible solutions, evaluating the pros and cons for each, choosing the best option,
and creating a step-by-step action plan to address the worry (Nezu, Nezu, Friedman,
Faddis, & Houts, 1998).
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325
However, there will be times when patients correctly note that no action can
be taken to resolve their worry, as in the case of a patient with advanced pancreatic malignancy who is anxious about poor prognosis. In such moments, clinicians
may encourage patients to tolerate their fears, drawing on alternate interventions
aimed at coping with the emotional distress such as engaging in pleasurable activities, mindfulness meditation, distraction, and self-soothing techniques (Moorey &
Greer, 2002; Taylor, 2006). Rather than focusing on the maladaptive thought, a
patient may find solace by directing attention toward an enjoyable hobby, listening
to music, preparing a favorite meal, or receiving a massage. Of growing interest among researchers is the benefit of mindfulness-based meditation for relieving
stress and worry among cancer patients (Smith, Richardson, Hoffman, & Pilkington,
2005). Mindfulness meditation involves raising conscious awareness by intentionally bringing attention to internal and external experiences in the present moment
and observing thoughts, feelings, and physical sensations in a non-judgmental manner (Kabat-Zinn, 1994). For patients who are at risk of having catastrophic thoughts
related to unfavorable prognosis, recurrent pain symptoms, and functional disability,
mindfulness may be a useful method for regulating attention, enhancing focus on the
present moment, habituating to the experience of negative affect and unpleasant sensations, and increasing acceptance of current physical status (Hamilton, Kitzman, &
Guyotte, 2006).
Anxiety Comorbid with Coronary Heart Disease
Coronary heart disease, also known as coronary artery disease or atherosclerotic
heart disease, is the leading cause of death for men and women in the United States
despite impressive advances in cardiac risk reduction, development of high-tech
interventions in cardiac care, and increasing knowledge about the benefits of drug
treatment after heart attack. Sixteen million Americans have coronary heart disease, causing as many as 450,000 deaths annually in recent years. In 2008, the
estimated cost of coronary heart disease was $156.4 billion, which included not
only direct medical expenses but also indirect costs, such as lost wages and productivity (American Heart Association, 2008). The symptoms of coronary heart disease
result from the narrowing of the coronary arteries, which supply blood to the heart.
Also called atherosclerosis, the narrowing and hardening of the coronary arteries
develops over time from the accumulation and calcification of cholesterol plaques
on the inner wall of the blood vessels. Eventually, this progressive narrowing may
reduce the flow of blood and oxygen to the heart (called ischemia) either chronically or acutely, causing serious cardiac conditions including angina, arrhythmia,
heart attack, and potentially heart failure (Selwyn & Braunwald, 2005).
Few data exist regarding the prevalence of anxiety disorders in patients with
coronary heart disease. Based on the extant literature, panic disorder ranged from
10% to 50% in studies of cardiology outpatients and individuals with diagnosed
coronary artery disease (Fleet, Lavoie, & Beitman, 2000). Using the Structured
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Clinical Interview for the DSM-IV to assess for psychiatric diagnoses, Bankier,
Januzzi, and Littman (2004) reported high rates of posttraumatic disorder (29%)
and current generalized anxiety disorder (24%) in a sample of 100 stable outpatients with coronary heart disease. However, these results provide no indication as
to whether the anxiety disorders preceded coronary heart disease (CHD) diagnosis
or were the result of experiencing a significant medical stressor, such as myocardial
infarction.
Anxiety as Risk Factor for Coronary Heart Disease
In addition to poor health behaviors (e.g., smoking), investigators have identified
anxiety, depression, anger, hostility, personality traits (e.g., Type A & D behavior
patterns), and chronic life stressors, such as social isolation and low socioeconomic
status, as key risk factors for coronary heart disease (Januzzi, Stern, Pasternak, &
DeSanctis, 2000; Kop, 1999; Kubzansky, Davidson, & Rozanski, 2005; Rozanski,
Blumenthal, Davidson, Saab, & Kubzansky, 2005; Smith & Ruiz, 2002). Although
studies have been limited and somewhat mixed due to methodological weaknesses
(Rozanski et al., 2005), early investigations revealed associations between coronary heart disease, especially sudden cardiac death, and anxiety symptoms such as
panic disorder (Coryell, Noyes, & House, 1986), phobic anxiety (Haines, Imeson,
& Meade, 1987; Kawachi et al., 1994), and worry (Kubzansky et al., 1997). More
recently, researchers have questioned the utility of studying psychological attributes
in isolation (Suls & Bunde, 2005) and begun to explore the covariation and shared
contributions of multiple affective states, such as anxiety, depression, and anger,
given that the combination appears to account for greater variability in the incidence
of coronary heart disease (Boyle, Michalek, & Suarez, 2006; Kubzansky, Cole,
Kawachi, Vokonas, & Sparrow, 2006). Interestingly, even when adjusting for the
general distress from the overlap of negative emotions, aspects of anxiety still independently predict the development of non-fatal myocardial infarction (Kubzansky
et al., 2006).
Anxiety symptoms increase risk for coronary heart disease primarily through
two pathways: unhealthy lifestyle behaviors and direct biological mechanisms.
The worldwide INTERHEART study of 52 counties showed that greater than
90% of the risk for acute myocardial infarction is due to modifiable factors, with
smoking and elevated cholesterol accounting for two-thirds of the risk (Yusuf
et al., 2004). Although the results from this large-scale investigation demonstrated
that psychosocial variables exert independent effects on the likelihood of first
myocardial infarction (Rosengren et al., 2004), anxiety may simultaneously play
an indirect role, via the development and maintenance of other primary cardiac
risks, such as smoking (Benninghoven et al., 2006; McKenna & Higgins, 1997)
and obesity (Simon et al., 2006). Moreover, researchers have begun to explore the
degree to which anxiety and mental stress relate to the development of atherosclerosis and risk for cardiovascular events through a myriad of physiological processes
(Rozanski et al., 2005) including impairment in myocardial perfusion (Fleet et al.,
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327
2005), thrombosis (von Kaenel et al., 2005), ventricular arrhythmias (Watkins et al.,
2006), and decreased heart-rate variability (Lavoie et al., 2004).
Persistent Effects of Anxiety and Quality of Life in Patients
with Coronary Heart Disease
Anxiety not only precedes the diagnosis of coronary heart disease but also occurs
subsequent to major cardiac morbidity such as heart attack, causing worse psychological effects among young patients (Lavie & Milani, 2006). Such anxiety
symptoms are common following myocardial infarction (Lane, Carroll, Ring,
Beevers, & Lip, 2002) and confer greater risk for recurrent cardiac events as well
as increased utilization of healthcare services (Benninghoven et al., 2006; Strik,
Denollet, Lousberg, & Honig, 2003). Moser and Dracup (1996) observed that anxious patients were almost five times more likely to have ischemic and arrhythmic
complications after acute myocardial infarction compared to patients with less anxiety. Moreover, cardiac treatment providers fail to detect clinically significant anxiety
symptoms in at least 50% of distressed patients (Huffman et al., 2006), underscoring
the need for enhanced screening procedures both before and after the occurrence of
major heart-related events.
In addition to changes in anxiety levels, patient-reported quality of life frequently
worsens after myocardial infarction or cardiac revascularization procedures, particularly among women (Westin, Carlsson, Erhardt, Cantor-Graae, & McNeil, 1999).
Several prospective studies have shown that anxiety symptoms significantly predict
decrements in health-related quality of life and physical functioning not only in the
first 12 months after a major cardiac event (Dickens et al., 2006; Hofer, Doering,
Rumpold, Oldridge, & Benzer, 2006; Sullivan, LaCroix, Baum, Grothaus, & Katon,
1997) but up to 5 years later as well (Sullivan, LaCroix, Spertus, & Hecht, 2000).
Moreover, the persistent negative effects on health-related quality of life and functional status in coronary artery disease are more strongly linked to anxiety and
depression than to biomedical factors, such as the number of diseased coronary
vessels (Hofer et al., 2005; Sullivan et al., 1997) or type of medical intervention
(e.g., percutaneous angioplasty versus coronary artery bypass grafting; Hofer et al.,
2006). One potential explanation for this strong association with anxiety is that cardiac events significantly threaten and disturb patients’ attainment of higher-order
life goals (Boersma, Maes, & Joekes, 2005), and thus is an important target of
psychological treatment in this patient population.
Psychological Interventions for Anxiety Comorbid with Coronary
Heart Disease
Non-pharmacological interventions for coronary heart disease include cardiac
rehabilitation programs, which may be comprised of monitored aerobic exercise, stress management, nutrition counseling, and smoking cessation, as well
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as individual and group psychotherapy, and complementary treatments. Although
accumulating evidence demonstrates worse medical outcomes in anxious patients
with coronary heart disease, researchers have not observed reduced mortality
through treatment of psychological conditions (Rees, Bennett, West, Davey, &
Ebrahim, 2004). For example, results of the ENRICHD study, the largest NIHfunded trial to date investigating the utility of empirically supported cognitivebehavioral therapy for depression and social isolation in 2,481 patients with
coronary heart disease, showed that rates of mortality and recurrent myocardial infarction were no better in patients receiving CBT versus usual care,
despite modest improvements in depression and social support (Berkman et al.,
2003). Of note, the ENRICHD study investigators did not address lifestyle
behaviors or medical treatment adherence as part of their psychosocial intervention.
The Cochrane Collaboration published a review of psychological interventions for coronary heart disease (Rees et al., 2004) and identified 36 randomized
controlled trials that measured clinical events, modifiable risk factors, and/or psychological outcomes. Only 9 of the 36 trials had interventions that targeted anxiety
symptoms, which overall yielded a small but statistically significant effect size
(weighted mean difference = –0.17) for anxiety reduction. Most of these trials
included complex stress management interventions with a variety of cognitivebehavioral techniques, such as relaxation training. Although psychological treatment studies for anxiety and depression in patients with coronary heart disease have
yet to reveal significant benefit in reducing disease-related morbidity or mortality,
the poor quality and heterogeneity of research trials to date limit firm conclusions regarding biomedical outcomes (Rees et al., 2004). Moreover, given the
additive impact of anxiety and physical illness on patient’s quality of life, mental health clinicians who encounter cardiac patients with psychiatric comorbidities
must endeavor to provide and tailor the most efficacious psychological treatments
available.
Complications in Treating Anxiety Comorbid with Coronary
Heart Disease
Given the overlap between cardiac and anxiety symptoms, a common challenge
for many clinicians and their patients with coronary heart disease is differentiating chest pain and shortness of breath due to cardiac ischemia from symptoms
of panic or other anxiety disorders. For example, Fleet et al. (1998) found that in
a sample of patients with a history of coronary artery disease presenting to the
emergency department with non-cardiac chest pain, 34% met criteria for panic disorder. Further complicating this diagnostic challenge are gastrointestinal disorders,
such as gastroesophageal reflux disease, another common cause of chest pain in
this patient population that may result from treatment with anti-anginal medications
(Ros et al., 1997).
Anxiety and Comorbid Medical Conditions
329
Treatment complications arise for many patients with coronary heart disease after
acute myocardial infarction, when they may experience greater somatic monitoring and heightened anxiety associated with symptoms of chest pain, tachycardia,
and arrhythmias. This somatic and anxiety sensitivity often leads to avoidance of
physical activity, work, and social withdrawal, which may in turn lower anginal
thresholds. Standard cognitive-behavioral therapy for panic disorder includes interoceptive exposure treatment in which patients generate and experience feared anxiety
symptoms, such as heart palpitations, so that they may habituate to the internal
physical sensations and decatastrophize their meaning (Barlow, 2002). However,
in the case of coronary heart disease, the warning signs for major cardiac events
(i.e., chest tightness, palpitations, diaphoresis, nausea, and shortness of breath)
are essentially identical to those of panic and other anxiety disorders. Therefore,
exposure-based therapy in this context, while potentially still beneficial for anxiety reduction, must be modified to account for the genuine risks of acute cardiac
ischemia.
Although most individuals with coronary heart disease will be able to resume
normal functioning relatively soon after an acute myocardial infarction, some will
experience Class III or IV angina, characterized as chest discomfort causing marked
limitation in physical activity (Selwyn & Braunwald, 2005). In addition, fatigue, or
exhaustion, is a common complaint in patients with coronary heart disease (Appels,
2004), which is compounded by use of cardiac medications (Kop, Appels, Mendes
de Leon, & Bar, 1996). These functional limitations and side effects may heighten
anxiety and reduce quality of life by interfering with patients’ abilities to work and
achieve their life goals. Anxiety treatment, therefore, must incorporate strategies for
adjusting to and managing such disability.
Resolving Treatment Complications for Anxiety Comorbid
with Coronary Heart Disease
As discussed previously with respect to cancer, challenges of differential diagnosis again raise the importance of collaborative care when treating patients with
serious chronic medical conditions, such as cancer and coronary heart disease.
Communicating with the medical team is essential for the mental health clinician to have an informed understanding of the patient’s risk factors, current status,
disease course, and prognosis, especially when developing psychotherapy goals
and treatment strategies. The biological data, which may be gathered directly
from consultation with the cardiologist and from scans and other laboratory tests
results, are salient factors when assessing the cognitive, affective, and behavioral
targets of care (Belar & Deardorff, 1995). Although western medicine continues to
dichotomize patients’ symptoms as either medical or psychological in nature, mental health clinicians treating patients with physical illness have perhaps a greater
responsibility to bridge these reductionistic approaches in order to develop a com-
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prehensive biopsychosocial conceptualization (Engel, 1977) of the relationships
and interactions among the patient’s psychological disorder, disease, and environment (Belar & Deardorff, 1995). Such models are helpful not only in assessment
but for patient education as well. For example, in the case of CHD, clinicians
might validate the challenges and burden of managing symptomatic disease, while
simultaneously encouraging patients to appreciate the complex ways in which
anxiety and stress are both caused by and worsen pain, fatigue, and disability,
at times leading to maladaptive coping behaviors, such as avoidance of physical
activity.
A primary behavioral target for anxiety treatment in coronary heart disease
includes helping patients to generate, experience, and habituate to the somatic
sensations of the stress response, which may be achieved through interoceptive
exposure and physical activity. As noted, interoceptive exposure, such as conducting an overbreathing exercise or inducing palpitations, often raises alarm
for the patient and mental health clinician about stressing the heart given that
these symptoms mimic the physical signs of coronary ischemia. However, for
a patient with stable heart disease, a clinician may consider employing interoceptive exposure after consultation and clearance with the patient’s medical care
providers. Additionally, exposure-based therapy could be integrated into structured cardiac rehabilitation programs, which incorporate supervised and graded
physical exercises. In such programs, patients are initially encouraged to experience and tolerate unpleasant physical sensations as they exercise at or near
their anginal threshold, with the reassurance of continuous electrographic and
blood pressure monitoring by a cardiology nurse specialist or exercise physiologist. Over time, patients withdraw monitoring and supervision as they gain
confidence in their ability to manage somatic symptoms of the stress response
and physically exert themselves safely. In a sample of 588 consecutive patients
with coronary artery disease, Lavie and Milani (1997) observed that cardiac
rehabilitation with exercise training significantly reduced anxiety symptoms by
40%.
For those individuals who are unable to return to relatively normal physical
and role functioning due to impairment from coronary artery disease or its medical treatment, illness management strategies may aid in anxiety reduction (White,
2001). Several validated behavioral techniques derived from the chronic pain literature, such as activity planning and pacing, may assist patients in adjusting their
expectations for performance while remaining engaged in social, recreational, and
even occupational pursuits (Keefe, Abernethy, & Campbell, 2005). Specifically, for
individuals disabled by severe fatigue and recurrent chest pain, clinicians can help
guide prioritization and scheduling of daily tasks by alternating physically stressful and less demanding activities, thus enabling the patient to achieve an optimal
balance between physical exertion and rest. For many individuals with coronary
artery disease, particularly after myocardial infarction, the tendency may be to
avoid any physical stress for fear of subsequent heart attack, leading to greater
deconditioning. Also, family, friends, and coworkers may inadvertently contribute
Anxiety and Comorbid Medical Conditions
331
to maladaptive illness behavior by being solicitous in taking over responsibilities
for the patient. While this avoidance may help to reduce patients’ anxiety in the
short term, it ultimately reinforces their fear of recurrent cardiac events and perpetuates the cycle of increasing disability. Activity pacing and other adaptive illness
management techniques, such as energy conservation strategies, may benefit individuals with chronic physical limitations to reduce symptom burden, overcome
their fears, and work toward desired life goals (Caudill, 2001; Turk & Gatchel,
2002).
Anxiety Comorbid with Asthma
Asthma, a chronic respiratory disease which affects approximately 20 million
Americans, is a lung disorder characterized by obstruction of airflow. The underlying causes for airflow obstruction are bronchoconstriction, a narrowing of the
small airways through contraction of the muscular walls of the bronchioles, and
inflammation, which results in swelling of the mucous membranes and an increase
in mucous secretion into the airway lumen. Although airway inflammation and bronchoconstriction are normal reactions of the immune system in response to serious
infection, the reasons for airway hyperactivity and disproportionate inflammatory
response seen in asthmatic patients, even in the absence of infection, remain unclear.
Researchers have identified multiple stimuli that incite asthma, including allergens,
pharmacologic effects, air pollution, occupational factors, respiratory infections,
and perhaps emotional stress (McFadden, 2005). The incidence of asthma appears to
be increasing in both the developing and developed world (Eder, Ege, & von Mutius,
2006). The annual economic costs to our nation related to asthma are substantial,
with 14.7 billion dollars in direct healthcare costs, much of which is accounted for
by prescription drug expenditures. Indirect costs including productivity losses add
another $5 billion (American Lung Association, 2009).
Anxiety disorders, especially panic symptoms, are common among individuals with asthma, with previous research confirming high rates of comorbidity in
community and clinical samples (Goodwin, Jacobi, & Thefeld, 2003; Goodwin,
Olfson et al., 2003; Heaney, Conway, Kelly, & Gamble, 2005; Katon, Richardson,
Lozano, & McCauley, 2004). For example, in a large-scale epidemiological study of
4,181 adults in Germany, 21% of individuals with severe asthma met criteria for a
current DSM-IV anxiety disorder, compared to 8.7% of participants without asthma
(Goodwin, Jacobi, et al., 2003). Accumulating evidence further suggests that respiratory disease such as asthma significantly increases the likelihood of experiencing
panic attacks (Goodwin & Pine, 2002), and there appears to be a bidirectional, dose–
response relationship between asthma symptoms and likelihood of having anxiety
disorder (Goodwin, Jacobi, et al., 2003; Hasler et al., 2005). These associations
are pronounced among smokers and women (Hasler et al., 2005; Tovt-Korshynska,
Dew, Chopey, Spivak, & Lemko, 2001).
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J. Greer et al.
Hypotheses for Comorbidity Between Asthma and Anxiety
Disorders
Various theories have emerged in the last decade to explain the pathophysiological, environmental, cognitive, and behavioral mechanisms linking asthma to anxiety,
and most notably, panic disorder (Katon et al., 2004). Correlational and experimental investigations of biological factors indicate that adult patients suffering from
asthma with panic disorder or self-reported anxiety are more likely to perceive worse
asthma symptoms such as breathlessness; yet, despite this association, researchers
have failed to demonstrate that anxiety relates to pulmonary function indices, including peak-flow variability (Janson, Bjornsson, Hetta, & Boman, 1994), vulnerability
to a 35% CO2 challenge (van Beek et al., 2003), bronchial responsiveness to histamine (PC20 ; Van Peski-Oosterbaan, Spinhoven, Van der Does, Willems, & Sterk,
1996), or forced expiratory volume in one second (FEV1 ; Rimington, Davies, Lowe,
& Pearson, 2001). At the same time, other data suggest that psychosocial variables, and in particular depression, may play a role in pulmonary function (Ritz &
Steptoe, 2000; Schmaling, McKnight, & Afari, 2002). Further research is necessary
to elucidate these complex relationships and biological pathways.
In their 21-year prospective study, Goodwin, Fergusson, and Horwood (2004)
reported that adolescents and young adults with asthma are at increased risk having
panic attacks and other anxiety disorders; however, these associations do not remain
statistically significant after controlling for confounding factors. According to the
authors, asthma and such psychiatric morbidity may not necessarily share a direct
causal relationship but rather may be connected through other common factors that
need further exploration.
Environmental variables that may influence the development of both asthma and
anxiety disorders include low socioeconomic status, urban residence, parental smoking, and stressful life events (Creer, Bender, & Lucas, 2002; Goodwin, 2003). For
example, in a study of individuals of diverse socioeconomic status, Rumbak, Kelso,
Arheart, and Self (1993) observed that 51% of indigent, asthmatic patients noted
that their acute asthma attacks were frequently triggered by anxiety compared to
only 19% of patients who were privately insured and not indigent. Similarly, asthmatic patients with less education report greater anxiety symptoms versus those
with more years of school attendance (Centanni et al., 2000). Finally, investigators
have found a greater prevalence of respiratory disorders in first-degree relatives of
individuals with panic, though whether this finding indicates a genetic diathesis or
environmental influence remains unclear (van Beek, Schruers, & Griez, 2005).
Previous research also indicates that cognitive attributions, or catastrophic
thoughts, are a potential salient mediator in the bidirectional relationship between
asthma and anxiety. Ley (1987; 1989) discussed the role that fear of dyspnea and of
related somatic symptoms caused by hyperventilation play in the etiology of panic
disorder. Considering that the primary symptoms of asthma include unpredictable
constriction of the airway and breathlessness, cognitive perceptions of this physiological experience would intuitively predict the likelihood of developing an anxiety
Anxiety and Comorbid Medical Conditions
333
disorder. Indeed, investigators have found that asthmatic patients with greater fear of
bodily sensations (as measured by the Anxiety Sensitivity Index) were more likely
to qualify for panic disorder (Carr, Lehrer, Rausch, & Hochron, 1994). Catastrophic
cognitions also significantly predict illness-specific and generalized panic fear
among individuals with asthma, even when controlling for pulmonary function
variables (Carr, Lehrer, & Hochron, 1995). Tests of histamine-induced bronchoconstriction show that anxious patients perceive worse symptoms of breathlessness
(Spinhoven, van Peski-Oosterbaan, Van der Does, Willems, & Sterk, 1997) and
greater discomfort of breathing, increasing the need for use of bronchodilators independent of actual bronchial closing (Nouwen, Freeston, Cournoyer, Deschesnes, &
Boulet, 1994). In sum, these findings underscore the need to target oversensitivities
to pulmonary sensations with cognitive restructuring and/or modified interoceptive
exposure (see below) as part of treatment of anxiety secondary to asthma.
Healthy lifestyle behaviors, such as compliance with taking inhaled medications,
monitoring respiratory symptoms, and attending medical appointments regularly,
are essential to maintaining effective asthma control. Whereas some researchers
have found that anxiety is associated with poor compliance and asthma management (Cluley & Cochrane, 2001; Lavoie et al., 2005; Smith et al., 2005), others
have failed to demonstrate such relationships (Bosley, Fosbury, & Cochrane, 1995;
Lavoie et al., 2006). Comprehensive understanding of self-care behaviors is another
indicator that predicts good asthma control. However, patients with anxiety are
less knowledgeable about self-management practices for acute respiratory episodes
(Kolbe, Vamos, Fergusson, Elkind, & Garrett, 1996). Noncompliance with treatment regimens and anxiety disorders compromise a variety of asthma outcomes.
More specifically, asthmatic individuals with panic disorder and related anxiety
symptoms are more likely to visit the emergency department, to be admitted to
the hospital and have longer stays, and to receive prescriptions for oral corticosteroids, which may cause side effects, exacerbating the physiological stress response
(Adams, Boath, Homan, Campbell, & Ruffin, 2001; Carr, 1998; Dahlen & Janson,
2002; Kolbe, Fergusson, Vamos, & Garrett, 2002). Adapting anxiety treatment to
include cognitive-behavioral strategies for improving adherence to disease management protocols may not only reduce psychological distress but also enhance asthma
control.
Effect of Anxiety on Quality of Life Related to Asthma
As in the case of cancer and coronary artery disease, adults with asthma report
poorer quality of life, which corresponds to frequent mental distress (Strine, Ford,
Balluz, Chapman, & Mokdad, 2004), higher dosage of inhaled corticosteroids
(Bonala et al., 2003), increased visits to primary care physicians (Feldman, Lehrer,
Borson, Hallstrand, & Siddique, 2005), as well as limited ability to work and perceived lack of control over health (Adams et al., 2004). Using the PRIME-MD
to diagnose DSM-IV disorders in 504 consecutive patients from an asthma clinic,
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Lavoie et al. (2006) found that patients with anxiety disorders are more likely to
report greater bronchodilator use and worse asthma-related quality of life across
four domains: activity limitation, asthma symptoms, emotional distress, and management of environmental triggers. One potential explanation for these relationships
is that individuals with asthma fear situations that may trigger symptoms of asthma
and panic, potentially initiating a cycle of avoidance behaviors that lead to greater
social isolation, distress, and functional limitations. Therefore, cognitive-behavioral
interventions designed to alleviate anxiety for this patient population may be augmented by addressing phobic avoidance and various domains of asthma-related
quality of life (Deshmukh, Toelle, Usherwood, O’Grady, & Jenkins, 2007).
Psychological Interventions for Anxiety Comorbid with Asthma
Psychological interventions for asthma generally include psychotherapy, patient
education programs, and self-management interventions (Bender & Creer, 2002).
Only one randomized controlled trial to date has tested a cognitive-behavioral therapy intervention within a sample of patients with coexisting asthma and panic
disorder (Ross, Davis, & MacDonald, 2005), demonstrating notable acute treatment
effects for both conditions but only long-term reduction in anxiety outcomes. A
Cochrane review (Yorke, Fleming, & Shuldham, 2006) of psychological interventions for adults with asthma identified 15 randomized controlled trials, 9 of which
incorporated a variety of relaxation techniques and 3 of which utilized cognitivebehavioral therapy. Overall, the usefulness of these treatments for anxiety symptoms
and control of asthma remains inconclusive due to the methodological weaknesses
and lack of consistency in outcome measures and types of interventions. Cognitivebehavioral therapy, however, did significantly improve quality of life in the patient
population. These findings draw attention to the marked gap in high-quality efficacy
studies aimed at comorbid anxiety and asthma.
Treatment Complications for Anxiety Comorbid with Asthma
The process of diagnosing anxiety disorders is understandably challenging for clinicians working with asthmatic patients and may lead to inadequate treatment for
either or both conditions. Given that the symptoms of panic disorder in particular
mimic many medical conditions, including asthma, patients with this psychological condition are likely to undergo multiple diagnostic tests and utilize healthcare
services (Roy-Byrne, Craske, & Stein, 2006). When the anxiety and respiratory
condition are comorbid, accurate detection becomes even more problematic, yet
essential for appropriate treatment planning.
Considering the paucity of data on the use of cognitive-behavioral therapy for
anxiety associated with asthma, mental health clinicians have no clear guidelines
Anxiety and Comorbid Medical Conditions
335
and must discern how best to adapt standard CBT treatments for patients with respiratory conditions. Recognizing this deficit in the treatment literature, authors have
questioned the utility of empirically validated panic control therapy and interoceptive exposure for patients with asthma (Deshmukh et al., 2007; Feldman, Giardino,
& Lehrer, 2000). More specifically, as in the case of coronary heart disease, the
optimal method for desensitizing a patient systematically to anxiety-provoking triggers, which often include internal somatic sensations that may aggravate the medical
condition, remains unclear (Carr, 1998; Deshmukh et al., 2007).
A third complication in the management of anxiety comorbid with asthma is
the lack of attention to medical adherence issues in traditional cognitive-behavioral
treatment protocols. Many chronic illnesses, such as asthma, diabetes, and HIV,
require lifelong management of medications, diagnostic testing, and follow-up care.
Moreover, as noted earlier, poor adherence to medical regimens is often related to
psychological morbidity that negatively impacts asthma outcomes. Therefore, mental health clinicians play a pivotal role in the multidisciplinary team for helping
patients identify and address obstacles to maintaining good compliance and other
salient health behaviors, for the dual purpose of reducing anxiety symptoms and
improving asthma control, which interact and influence one another (Bender &
Creer, 2002).
Resolving Treatment Complications for Anxiety Comorbid
with Asthma
To aid in the diagnosis of anxiety comorbid with asthma, researchers have identified a number of indicators to consider during evaluation. First, the most reliable
method for discriminating anxiety symptoms from asthma include pulmonary function tests, such as measures of peak flow and FEV1 (Feldman et al., 2000). In
addition, as is true with any other psychiatric disorder, conducting a comprehensive
assessment of the situational triggers and the presence of a family history of anxiety
may clarify diagnosis. Beyond these standard techniques, the types and clusters of
symptoms associated with each condition may also assist in the differential diagnosis. For example, panic attacks typically have rapid onset and reach their peak within
10 minutes while this is generally not the case for asthma. Furthermore, in a study
comparing asthmatic patients to a cohort-matched group of individuals with panic
disorder, Schmaling and Bell (1997) found that reports of panic-fear and hyperventilation were strongly associated with panic disorder, while airway obstruction
symptoms, such as wheezing, mucous congestion, and coughing, were more predictive of asthma attacks. These three symptoms demonstrated high sensitivity (> 0.90)
and specificity (> 0.70) in distinguishing the patients groups, thereby serving as useful tools for identifying when patients are experiencing one or both types of attacks
(Feldman et al., 2000; Schmaling & Bell, 1997).
Again, as discussed previously with cancer and coronary heart disease, the
approaches for tailoring cognitive-behavioral therapy for anxiety depend on the
336
J. Greer et al.
nature of the medical condition. Rather than emphasizing graded in-vivo or interoceptive exposures that potentially place a patient at risk of an asthma attack,
Deshmukh et al. (2007) suggest that behavioral interventions for anxiety should
address fears of asthma stimuli and related avoidance behaviors through a combination of symptom monitoring, problem-solving techniques, appropriate use of asthma
medications, and development of an asthma action plan for managing attacks. The
authors argue that these behavioral methods will assist patients with differentiating
anxiety from asthma and bolster confidence in the ability to cope effectively with
asthma symptoms and dyspnea, thereby minimizing triggers of panic.
Similarly, Feldman et al. (2000) argue that CBT must be adapted for anxiety
related to asthma and that teaching patients to discriminate between panic and anxiety symptoms, including the ways that hyperventilating and wheezing are different,
is essential for cognitive restructuring and appropriately treating somatic sensations.
Considering the potential risks of bronchoconstriction associated with interoceptive
exposure techniques (e.g., voluntary hyperventilation, production of chest tightness,
and inhaling through a straw), the authors substitute HRV biofeedback, slow breathing exercises, and pursed lips breathing as safe alternatives for treatment. Also,
to improve self-management of asthma and panic attacks, the authors developed
a decision tree in which they use indicators of peak-flow monitoring, the presence of mucous production or coughing, and rapid onset of the attack to guide
decision-making for proceeding with an action plan to resolve the asthma or anxiety
symptoms (Feldman et al., 2000).
Finally, cognitive-behavioral therapy needs to be modified to target compliance
with medical treatments. Simply treating adherence in isolation or anxiety in isolation is not sufficient, as these factors synergistically affect asthma control. Some of
the work of our research team (Safren, Gonzalez, & Soroudi, 2007; Safren et al.,
2004; Safren et al., 2009; Soroudi et al., 2008) integrates adherence interventions
into standard CBT protocols designed to treat psychological conditions comorbid
with medical illness. More specifically, Safren et al. (2004), Safren, Otto, and Worth
(1999) developed a brief guide that includes 11 steps for patient education, motivational enhancement, and behavior change to increase medication adherence among
people with HIV. Incorporating this intervention as part of several randomized studies testing the efficacy of CBT for depression in patients with HIV (and currently
being tested with Type 2 diabetic patients), the authors have demonstrated positive
effects for both adherence with medical treatment and mood symptom reduction
(Safren et al., 2004, 2009). Rigorous cognitive-behavioral therapy trials testing
similar integrated models are needed for anxiety and asthma.
Summary and Conclusions
In this chapter, we demonstrated an approach to the assessment and treatment
of anxiety disorders in medically ill populations. To illustrate these concepts, we
first reviewed relevant literature pertaining to the symptoms, prevalence, correlates,
Anxiety and Comorbid Medical Conditions
337
and outcome studies of anxiety comorbid with cancer, coronary heart disease, and
asthma. Second, we highlighted the types of treatment difficulties mental health
clinicians frequently encounter when providing cognitive-behavioral therapy to
patients who have concomitant anxiety and medical conditions; lastly, we provided
suggestions for resolving those complications. The following is a summary of the
clinical recommendations, which may be applied more broadly to patients coping with a variety of illnesses beyond those presented, such as diabetes, HIV, and
irritable bowel syndrome:
1) Minimize barriers for patients to access psychotherapy by scheduling sessions
either in conjunction with other medical appointments or at the time when
patients are less likely to be disabled by the ill-effects of medical treatments
(e.g., allow sufficient time after chemotherapy infusion).
2) Communicate regularly with medical providers to clarify and confirm patients’
diagnoses and to develop an appropriate treatment plan.
3) Resist mind–body dualism and employ biopsychosocial models of illness when
educating patients about the complex and bidirectional relationships among their
anxiety symptoms, disease, and environment.
4) Adapt cognitive-behavioral therapy by considering with patients the extent to
which their health-related worries and fears reflect realistic concerns and tailor
treatment decisions based on this assessment.
5) Incorporate illness, symptom, and pain management strategies, such as activity
pacing techniques, to enhance physical and role functioning, if needed.
6) Utilize interoceptive exposure-based therapy only when patients have appropriate medical clearance and modify techniques so as not to exacerbate symptoms
of the medical condition.
7) Assess for compliance with medical treatment regimens and integrate cognitivebehavioral strategies for improving medical adherence, when necessary.
While the above recommendations may offer assistance to clinicians working
with this complex patient population, further research is needed to test the efficacy and effectiveness of psychosocial interventions with medically ill patients.
Few methodologically rigorous, published studies exist regarding the psychological treatment of anxiety disorders in patients with chronic medical conditions. The
development of novel therapies that are theoretically driven and empirically based,
targeting the clinical features and concomitant psychosocial sequelae of physical illnesses and their treatments, will ideally enhance a number of disease, psychosocial,
and healthcare-related outcomes for patients.
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Resolving Treatment Complications
in Children and Adolescents
Jamie A. Micco and Jill T. Ehrenreich
Numerous randomized controlled studies have found that cognitive-behavioral therapy (CBT) is efficacious in treating childhood anxiety disorders, including those
evaluating individual or group CBT for children and adolescents with social phobia
(Beidel, Turner, & Morris, 2000; Spence, Donovan, & Brechman-Toussaint, 2000),
specific phobia (Silverman et al., 1999), school refusal (King et al., 1998), panic
disorder (Pincus, Ehrenreich May, Whitton, Mattis & Barlow, 2009), and PTSD
(Cohen, Deblinger, Mannarino, & Steer, 2004), as well as for heterogeneous groups
of children diagnosed with separation anxiety disorder, generalized anxiety disorder,
and/or social anxiety disorder (Kendall, 1994; Kendall et al., 1997).
Kendall’s Coping Cat program (Kendall, 1994), designed for anxious children
ages 9–13, is perhaps the most well-known CBT protocol for childhood anxiety.
Of the children randomized to the individual Coping Cat treatment, 64% no longer
met criteria for their primary anxiety disorder at post-treatment, compared to only
5% of the children in the waitlist control group (Kendall, 1994). In a second randomized controlled trial (Kendall et al., 1997), similar results were obtained, with
53% no longer met criteria for their primary anxiety disorder at post-treatment,
compared to 6% of the children in the waitlist control group. For children continuing to meet criteria for their primary anxiety disorder, the majority experienced
significant improvement in the severity of their disorder. Treatment gains were
largely maintained over long-term follow up (Kendall et al., 1997; Kendall, Safford,
Flannery-Schroeder, & Webb, 2004).
A recent meta-analysis of 20 randomized controlled trials of CBT for children
and adolescents with anxiety disorders found a large pre- to post-treatment effect
size (d= 0.94) when comparing children who received CBT to controls (Ishikawa,
Okajima, Matsuoka, & Sakano, 2007). Further, a review of the longer-term treatment outcomes of CBT for childhood anxiety reported that overall, treatment gains
tend to be maintained for at least one year post-treatment (Compton et al., 2004).
J.T. Ehrenreich (B)
Department of Psychology, University of Miami, Coral Gables, FL, USA
e-mail: jehrenreich@psy.miami.edu
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0_18,
C Springer Science+Business Media, LLC 2010
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However, despite these studies supporting the use of CBT with anxious children,
a sizeable minority of children and adolescents with anxiety disorders fail to respond
adequately to CBT (see Cartwright-Hatton, Roberts, Chitsabesan, Fothergill, &
Harrington, 2004; Velting, Seltzer, & Albano, 2004). Consequently, there is a great
need to increase our understanding of why CBT is not effective for a sub-sample of
anxious children and how treatment can be tailored to meet the needs of these nonresponders.
This chapter will describe the most commonly observed complications that arise
in CBT of childhood anxiety disorders. Specifically, we will review the current
literature examining the degree to which treatment of children with anxiety is
influenced by comorbid disorders, parenting behaviors, parental anxiety, sociodemographic characteristics, and parent–child symptom agreement. We will also
provide evidence-based recommendations for how standard CBT for child anxiety
can be modified to address these potential complicating factors, followed by detailed
case examples drawn from our experience working with children at the Center for
Anxiety and Related Disorders at Boston University and Massachusetts General
Hospital.
Comorbidity
Clinically anxious children and adolescents who present for CBT often meet criteria
for additional disorders, including major depression and dysthymia (Kendall, 1994;
Strauss, Last, Hersen, & Kazdin, 1988), attention-deficit/hyperactivity disorder
(ADHD; Last, Hersen, Kazdin, Orvaschel, & Perrin, 1991), and oppositional-defiant
disorder (ODD; Verduin & Kendall, 2003). Cognitive-behavioral therapists who use
empirically supported treatments for childhood anxiety disorders, such as Kendall’s
(1994) Coping Cat manual, March and Mulle’s (1998) CBT for obsessive compulsive disorder, and Beidel and colleague (2000) treatment for social anxiety disorder,
may find that these treatments need to be adapted to maximize treatment gains
in anxious children with comorbid depressive or externalizing disorders. In this
section, we present data on the prevalence of the most common disorders that cooccur with anxiety in children and adolescents, including depression, ADHD, and
ODD. For each type of comorbidity, we review common patient characteristics and
research showing how comorbidity affects response to CBT. We then describe adaptations that can be made to CBT for anxiety disorders that help to address the needs
of children with comorbid conditions.
Treating Comorbid Anxiety and Depressive Disorders
Prevalence
Depressive disorders are likely to co-occur with anxiety disorders at a rate greater
than chance expectations in children and adolescents (Seligman & Ollendick,
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1998). In a prospective community study of 785 11-year-olds (Anderson, Williams,
McGee, & Silva, 1987), over 15% of the participants who met criteria for an anxiety disorder also met criteria for a depressive disorder. When these children were
followed up at age 15, 13% of the anxiety-disordered adolescents had a comorbid depressive disorder (McGee et al., 1990). Another community study found
much higher rates of comorbid anxiety and depression in adolescents (Kashani &
Orvaschel, 1988). Specifically, 9 out of 13 adolescents (69%) meeting criteria for an
anxiety disorder, from a sample of 150 adolescents, also had an affective disorder.
Studies employing clinical samples have found varying rates of comorbidity
between anxiety and depressive disorders in children. In a sample of children (ages
8–13) with primary depression, 31.5% also met criteria for an anxiety disorder
(Kovacs, Gatsonis, Paulauskas, & Richards, 1989). Meanwhile, two studies of children and adolescents with primary anxiety disorders found that approximately 30%
also have clinical depression (Kendall, 1994; Strauss et al., 1988). However, these
rates were lower in a study conducted by Verduin and Kendall (2003). Of the 199
children (ages 8–13 years) in this study with primary social anxiety disorder, generalized anxiety disorder, or separation anxiety disorder, 4.5% also met criteria for
major depressive disorder, while 8.5% had dysthymic disorder. Similarly, in a study
of group treatment for anxiety disorders in children ages 7–16 years (Rapee, 2003),
only 6.1% also had a mood disorder.
Patient Characteristics and Treatment Response
A number of studies have found that children with comorbid anxiety and depressive disorders tend to be older and more functionally impaired than children with
anxiety disorders or depressive disorders alone (Bernstein, 1991; Brady & Kendall,
1992; Manassis & Hood, 1998; Manassis & Menna, 1999; Masi, Favilla, Mucci,
& Millepiedi, 2000; Strauss et al., 1988). For instance, Strauss et al. (1988) found
that children and adolescents (5–17 years old) with comorbid anxiety and major
depressive disorders had more severe and interfering anxiety symptoms than anxious participants without depression (Strauss et al., 1988). In another study by
this group, anxiety and comorbid depression in school-aged children was associated with decreased popularity with peers (Strauss, Lahey, Frick, Frame, & Hynd,
1988). Research also suggests that depression is more likely to co-occur with generalized anxiety disorder and social anxiety disorder than other anxiety disorders
(Last, Strauss, & Francis, 1987; Manassis & Menna, 1999; Verduin & Kendall,
2003). In a study of 58 children and adolescents with primary generalized anxiety, more than half of the sample had a comorbid depressive disorder (Masi, Mucci,
Favilla, Romano, & Poli, 1999). In addition, Verduin and Kendall (2003) found that
while 17.4% of children with generalized anxiety disorder and 15% with social anxiety disorder also met criteria for either major depression or dysthymia, only 2% of
children with separation anxiety disorder also had a depressive disorder.
Despite the common co-occurrence of anxiety and depression in children and
adolescents, only a few studies have examined the degree to which this comorbidity affects treatment outcome. Berman et al. (2000) found that symptoms of
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depression significantly predicted worse treatment response in anxious children
receiving CBT (Berman et al., 2000). On the other hand, Rapee (2003) found
that among children (ages 7–16) receiving group CBT for primary anxiety, those
with comorbid disorders (including mood and externalizing disorders) had similar levels of post-treatment improvement as those without a comorbid disorder.
However, at 1-year follow-up, the children with comorbid disorders showed a
slight symptomatic increase on parent-report measures whereas the children without comorbidity continued to maintain their treatment gains (Rapee, 2003). This
suggests that anxious children with comorbid disorders may need extra support in
maintaining improvements made in CBT.
Modifications for Treating Children with Comorbid Depression
While children with anxiety and depression both experience negative affect, children with depression also have low levels of positive affect (Watson & Clark, 1984;
Watson & Kendall, 1989). Depressed children with anhedonia and low energy often
avoid activities with peers, which in turn gives them little opportunity to experience positive affect associated with outside activities. In addition, the hopelessness,
low self-efficacy, and low energy associated with childhood depression may affect
willingness and motivation to engage in a structured treatment like CBT. Thus,
anxious children with depression may benefit from the inclusion of behavioral
activation and scheduling of pleasant events early on in the treatment. Therapists
should help these children make a list of activities that are enjoyable and likely
to produce a sense of mastery; then, between sessions, the children engage in at
least one activity from the list each day. As children experience greater positive
affect, they begin to understand that their actions have an influence on their mood,
which may produce a greater willingness to discover new ways to cope with their
anxiety.
In addition, cognitive restructuring should be modified to include cognitions
associated with depression. While anxious children tend to overestimate threat in
situations (Bögels & Zigterman, 2000), children with depression tend to selectively
focus on negative aspects of events (Weems, Berman, Silverman, & Saavedra, 2001)
and endorse thoughts of personal loss and failure (Schniering & Rapee, 2004). As
such, anxious–depressed children benefit from learning ways to challenge their negative self-evaluations about past events in addition to their future-oriented worries.
Hypothesis testing, or gathering evidence for or against specific beliefs, can also
help children generate adaptive self-talk. For instance, a child who declares, “I never
get good grades,” after not doing well on one test would be asked to keep track of all
his grades over the course of the week in order to evaluate the veracity of his belief.
Assuming that he earns a range of grades, his therapist can help him construct a new
coping statement, such as, “I do well in school many times.”
Children with depression (particularly when it is comorbid with social anxiety)
may have social skills deficits that need to be addressed in treatment (Segrin, 2000).
Social skills training, tailored to the child’s specific areas of difficulty (such as maintaining eye contact, starting conversations, etc.), is a key component of CBT for
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child depression (Stark, Sander, Yancy, Bronik, & Hoke, 2000). Children with anxiety and depression also benefit from learning social problem-solving skills that
consist of identifying a problem, generating solutions to the problem, and selecting
the most effective solution. Problem-solving goals include increasing involvement
in pleasurable activities (which addresses the depressive symptoms) and enacting
a coping plan for engaging in anxiety-provoking situations (Kendall, Kortlander,
Chansky, & Brady, 1992).
Case Example
Jake was a 13-year-old boy with a primary diagnosis of generalized social anxiety disorder and a secondary diagnosis of dysthymic disorder. His parents were
divorced, and he lived with his mother and stepfather, although he frequently spent
time with his father as well. By the time that he began CBT at our clinic, Jake was
avoiding nearly all social situations with peers or unfamiliar adults. He engaged in
no extracurricular activities; after school, he walked home and spent the afternoon
and evening playing video games or watching TV by himself. He was failing most
of his classes in eighth grade. He reported that he had felt depressed “for years,”
while his mother described him as “always irritable.”
At the first session of individual CBT, Jake indicated that he did not have much
confidence that treatment could help him. He and his therapist discussed the advantages (“I could feel less unhappy,” “My parents will stop asking me what’s wrong”)
and disadvantages (“It will be hard and it might not work”) of engaging in treatment,
after which Jake decided that, “it’s worth a try, I guess.” The therapist described
how his avoidance of social situations led to a short-term decrease in his anxiety,
but also resulted in a longer-term lack of confidence in his ability to handle social
situations and an increase in depression because he did not have the opportunity to
receive positive social reinforcement. The therapist also addressed Jake’s depression
by teaching him that his choice about how to respond to difficult situations had a big
effect on his mood; thus, he learned that he had some control over his feelings. For
instance, if he got a bad grade on an assignment, he could choose to do nothing (and
feel sad and angry), or he could ask his teacher for extra help and the opportunity
to redo the assignment, which would likely boost his mood and increase his selfefficacy. Jake and the therapist also made a list of activities he most enjoyed, and he
was asked to pick one pleasant activity to do each day.
Jake learned to identify his automatic thoughts and his most common cognitive
errors, including mind reading (assuming others thought he was “dumb”), black
and white thinking (“you’re either popular or a loser”), and mental filter (focusing
on the negative at the expense of the positive). He learned to challenge his anxious and depressed thoughts with coping self-statements. For instance, when he was
fearful he would “say the wrong thing” during a class presentation, he challenged
this thought by reminding himself that, “Everyone makes mistakes sometimes – if
it happens to me, I’ll make the best of it.”
Situational exposures were designed to gradually address Jake’s fear of social
interactions while maximizing the likelihood that he would experience pleasure and
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mastery after completing each exposure. Items on his Fear and Avoidance Hierarchy
(FAH) included asking an acquaintance to the movies, going to brunch with his
family in a crowded restaurant, talking to a new person at lunch, and signing up for a
confidence-building activity (martial arts classes). Jake was taught problem-solving
skills to determine ways in which he could handle himself if social interactions did
not go as planned. In addition, his therapist worked with him to enhance his social
skills in conversations, particularly varying his tone of voice, asking open-ended
questions, and maintaining eye contact. He first practiced these skills in role-plays
with the therapist, then with “confederates” at the clinic, and finally as situational
exposures over the course of the week.
Jake was regularly talking to other boys at school and seeing acquaintances on
the weekends by the time he finished eighth grade. However, he experienced a setback in his anxiety and depression when summer vacation began; without regular
opportunities to talk with peers at school, he engaged in fewer exposures. In addition, he was not involved in a structured activity for the summer, resulting in him
spending a lot of time by himself. Further, he complained that his parents worked
long hours with little time to spend with him. Thus, his therapist strongly encouraged Jake’s parents to enroll him in an extracurricular summer activity and to devote
more time to one-on-one activities with him to promote positive family interactions.
After working on these goals with his parents, Jake again felt less depressed and
more motivated to call friends from school.
At the beginning of ninth grade, a reward system was developed with Jake and
his parents to increase his motivation to complete schoolwork; he could earn points
towards rewards (i.e., paintballing with his friend, a DVD, etc) in exchange for completing homework on time. Jake began to earn As and Bs in his classes, and after two
weeks of the reward plan, he felt that he no longer needed extrinsic rewards to spend
time on his schoolwork. He reported feeling more confident in his academic skills.
By the end of treatment, in the fall of ninth grade, Jake reported few symptoms of
depression. Although he continued to experience anxiety about talking to new peers,
he had made several good friends and regularly saw them outside of school. He felt
more supported by his parents, who set aside time each week to check in with him.
At his termination session, he and his therapist reviewed the skills he had learned
during his treatment as part of his relapse prevention plan.
Treating Comorbid Anxiety and Externalizing Disorders
Prevalence
Epidemiological and clinical studies have found a high level of comorbidity between
anxiety disorders and ADHD and/or ODD in children and adolescents. Bird et al.
(1988) found that in a community sample of 386 children (ages 4–16), 9.3% met
DSM-III criteria for an anxiety disorder and ODD or conduct disorder (CD), while
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approximately 6% had co-occurring anxiety and attention-deficit disorder (Bird
et al., 1988). Among studies using DSM-IV criteria, presence of ADHD in children with anxiety disorders ranged from 0% to 16.7%, and presence of ODD or CD
ranged from 7.9% to 33.3% (Angold, Costello, & Eklani, 1999).
In children presenting for treatment for anxiety disorders, comorbidity with
externalizing disorders is quite high. Verduin and Kendall (2003) found that in
clinically anxious children ages 8–13, 17.6% met criteria for ADHD and 9.5%
met criteria for ODD; there was no significant difference in rate of comorbidity
among diagnoses of social anxiety disorder, separation anxiety disorder, or generalized anxiety disorder, although there was greater comorbidity between anxiety and
externalizing disorders among boys. Comparable rates of comorbidity were found
by Last et al. (1987) in a study of 91 children referred to an anxiety disorders clinic.
They found that 1% and 9% of the children were diagnosed with an anxiety disorder and ADHD or ODD, respectively (Last, Hersen, Kazdin, Finkelstein, & Strauss,
1987). In another study, they found that 13% of 381 children with primary anxiety
disorders also had ADHD (Last et al., 1991).
Patient Characteristics and Treatment Response
By and large, children with comorbid anxiety and externalizing disorders tend to
be younger and more impaired than children with anxiety alone (Anderson et al.,
1987; Bird, Gould and Staghezza, 1993; Manassis & Hood, 1998; McGee et al.,
1990; Strauss, Lease, Last, & Francis, 1988). In a study of children and adolescents with primary DSM-III overanxious disorder, 61% of children aged 5–11 years
were also diagnosed with an externalizing disorder, compared to only 15% of those
between 12- and 19-years old (Strauss et al., 1988). Children with comorbid anxiety
and externalizing disorders tend to have more severe symptomatology, with greater
irritability, mood lability, and frequency of emotional outbursts (Kashani, Deuser, &
Reid, 1991). In addition, mothers’ ratings of conduct problems in clinically anxious
children significantly correlate with level of impairment as measured by the Global
Assessment of Functioning (GAF; Manassis & Hood, 1998).
Several studies have examined the degree to which comorbid externalizing disorders impact CBT outcome for child anxiety. Kendall, Brady, and Verduin (2001)
found that anxious children with pre-treatment externalizing disorders improved to
the same degree after manualized CBT as children without externalizing disorders.
Indeed, 68.4% of children with anxiety alone were free of their principal anxiety disorder diagnosis at post-treatment, compared to 70.6% of children with anxiety plus
ADHD or ODD. In addition, children with pre-treatment comorbid externalizing
disorders also had fewer diagnoses of ADHD and ODD at post-treatment, suggesting that treatment gains generalized beyond anxiety. Notably, however, children who
continued to meet criteria for a comorbid disorder at post-treatment were less likely
to experience remission of their pre-treatment principal anxiety disorder (Kendall
et al., 2001). In a follow-up to this study, Flannery-Schroeder et al. (2004) compared
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19 anxious children with ADHD or ODD/CD to 19 anxious children without this
comorbidity and found that both groups maintained comparable levels of improvement in their principal anxiety disorder 7 years post-treatment, although parents of
the anxiety plus externalizing group of children rated their children as having more
externalizing symptoms than children with anxiety alone (Flannery-Schroeder et al.,
2004).
In contrast, Costin et al. (2002) piloted an eight-session CBT group treatment
for anxiety with five boys (ages 9–12) who also were diagnosed with both ADHD
and ODD. This group included a separate parent group that focused on psychoeducation and strategies for managing child anxiety, although explicit training for
handling oppositional behavior was also included in the parent sessions. At posttreatment, the boys did not experience improvements in self-ratings of anxiety or
parent-ratings of internalizing and externalizing symptoms, suggesting that more
severe comorbidity may interfere with the efficacy of brief CBT for anxiety (Costin
et al., 2002).
Modifications for Treating Comorbid ADHD and ODD
When treating anxious children with comorbid ADHD, we have found that several
modifications to standard CBT are typically required to ensure children’s engagement in treatment. First, children with ADHD may learn CBT skills more effectively
in the context of shorter individual sessions (i.e., dividing one manualized session into two sessions), with brief breaks within sessions. Second, particularly
for children with hyperactive or combined types of ADHD, it may be necessary to implement a behavioral plan within sessions to reinforce on-task behavior
and discourage inappropriate behavior. For example, children can earn stickers for
remaining in their seat for 5- or 10-minute intervals of time; at the end of session,
they can pick a small prize for earning a specified number of stickers. Third, breaking CBT principles and skills down into simple “bullet points,” and writing down
what was learned at the end of each session, can be particularly helpful for inattentive children. Homework assignments may also need to be modified to reduce the
amount of written work children need to produce between sessions. Fourth, when
teaching problem-solving skills to anxious children with ADHD, therapists may
wish to especially focus on problems the children encounter at school as a result of
their inattentiveness and/or hyperactivity. In our experience, children with anxiety
and ADHD tend to be easily overwhelmed by the demands of school and extracurricular activities, to the point that they worry a great deal about their performance in
these areas. When teaching problem-solving skills, these children appear to benefit
from learning how to generate and implement solutions to organizational difficulties
and problems with time management.
For children with comorbid ODD or conduct problems, it is first important to
determine the degree to which their oppositional behavior is triggered by anxiety
or fear, as this will guide the therapist in providing affective education to the child.
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For example, imagine an 8-year-old girl with separation anxiety disorder who hides
in her room and tells her parents she “hates” them as they get ready to take her
to school. During treatment, the girl’s therapist would first teach her to distinguish
between nervous and angry feelings; in later sessions, the girl would then practice
using coping skills for anxiety (i.e., relaxation techniques, deep breathing, positive
self-talk) as soon as she noticed she was having nervous feelings, which could then
“short-circuit” the pathway between anxiety and subsequent angry feelings.
When teaching anxious and oppositional children ways to manage physiological
symptoms of anxiety (i.e., relaxation), the therapist should encourage the application of these skills to times when the children feel angry. Modifications to cognitive
components of the treatment are based on findings that children with ODD tend to
have difficulty identifying social cues and misattribute hostile intent to their peers
or parents (Crick & Dodge, 1994). Consequently, these children will need assistance in challenging their assumptions about others’ intentions, which can be done
in the context of cognitive restructuring. The tendency for children with ODD to
select aggressive solutions to problems (Lochman & Dodge, 1994) should also be
addressed when children learn problem-solving skills or through the addition of a
social skills training module.
The inclusion of parents in the treatment of comorbid anxiety and ODD is essential. In particular, parents benefit from learning how to implement rewards and
consequences at home in order to reinforce both brave and non-aggressive behaviors. The therapist may model a behavioral plan for parents by setting ground rules
for behavior during sessions (i.e., using respectful language) and rewarding children’s adherence to the rules. Selective ignoring skills can be used for both anxious
and oppositional behaviors; in other words, parents may be encouraged to practice diverting their attention away from excessive reassurance-seeking or acting-out
behavior followed by close attention to the child as soon as he/she engages in
appropriate behavior.
Case Example
Daniel, a 9-year-old boy with diagnoses of separation anxiety disorder, specific phobia of vomiting, ADHD (inattentive type), and ODD, was referred for individual
CBT after he had been in supportive therapy for over a year without improvement.
At his diagnostic interview, Daniel’s parents reported that he had been extremely
fearful of vomiting ever since he saw another child in school throw up in his classroom when he was in second grade. He avoided being separated from his parents
(especially his mother) because he was intensely afraid that he would feel sick while
he was by himself and would not know how to handle it. His parents told the interviewer that Daniel had become increasingly irritable and “touchy.” He “constantly”
talked back to his parents when they asked him to complete homework and chores,
and recently he had been screaming and throwing objects when his mother was
about to leave the house. However, his parents noted that he was typically well
behaved in school and had several close friends.
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At his first treatment session, Daniel insisted that his mother stay with him in
the room, after which he put his jacket over his head and refused to remove it. He
answered the therapist’s questions about school and friends with the jacket on his
head, but soon after, he agreed to the therapist’s suggestion that they could play a
game if he took the jacket off. As they played the game, Daniel was able to answer
more specific questions about his fears and worries. During the second session, he
again wanted his mother with him in the room, although this time he was willing for
her to wait in the waiting room after 10 minutes in order to earn a reward from the
clinic’s “treasure box.” To maximize Daniel’s attention and interest in learning CBT
principles of anxiety, the therapist helped Daniel understand the difference between
his thoughts, feelings, and actions when he became nervous or angry by having him
play a quiz-show game that involved putting examples of each component into their
appropriate categories. At the end of psychoeducational sessions, he worked with
the therapist to write down three things he learned during the session, after which
he earned pencils or stickers.
In addition to learning to distinguish between “nervous thoughts” and “calm
thoughts” in response to situations Daniel found to be anxiety provoking, he also
practiced identifying his “angry thoughts,” which often occurred right after he had
an anxious thought. For example, he drew a picture during session that depicted his
mother dropping him off at school; the therapist asked him to include “thought bubbles” over his head in the picture. In the thought bubbles, he wrote his usual nervous
thought (“If Mom leaves, I’m going to get sick”) and angry thought (“It’s stupid I
have to stay here!”), and he and his therapist generated a new coping thought (“I’ve
never gotten sick in school before, so I probably won’t today”). Daniel’s therapist
also taught him a progressive muscle relaxation exercise, which he was encouraged
to use whenever he noticed he was having the nervous or angry thoughts/feelings he
had identified with his therapist.
When it became time to construct a fear and avoidance hierarchy (FAH) of feared
situations and to begin situational and interoceptive exposures, the therapist met
individually with Daniel’s parents to discuss how to best implement exposure practices at home with the help of a reward plan. When Daniel completed an exposure
(particularly at the beginning of this portion of treatment), he could choose from
several rewards, including baseball cards and playing a game with his parents. At
the same time, the therapist also worked with Daniel’s parents to determine how
to apply rewards to appropriate behavior at home. For example, when Daniel was
able to get out of the car at school without yelling at his mother, he earned points
toward something from his reward menu. After Daniel experienced some success
with exposures from his FAH and earning rewards for appropriate behavior, the
therapist introduced consequences for acting-out behavior to the behavioral plan.
For instance, Daniel’s parents removed previously specified privileges (i.e., video
game time, ice cream after dinner) when he called them names or threw objects.
As Daniel reached the top of his FAH and experienced a significant decrease in
his fear of vomiting and being away from his parents, his parents found that they
no longer needed the behavioral plan to manage Daniel’s oppositional behavior.
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Overall, Daniel became more confident in his ability to handle his fears on his own,
and he became more certain that it was not dangerous to feel nervous or sick (with
the help of cognitive restructuring and interoceptive exposure). His parents noticed
that when Daniel began to feel less nervous being by himself at school, he seemed
to have greater “emotional energy” left over at the end of the day to handle minor
frustrations or disappointments at home.
Parenting Behaviors and Parental Anxiety
While comorbid disorders are frequently a challenge in the treatment of primary
anxiety disorders in children and adolescents, parenting behaviors and parental
anxiety may also need to be addressed during CBT in order for treatment to be
maximally effective. Multiple studies demonstrate that a family history of anxiety
symptoms is a significant risk factor for the development of anxiety among offspring (e.g., Beidel & Turner, 1997; Kashani & Orvaschel, 1990; Kendler, Neale,
Kessler, Heath, & Eaves, 1992). These studies reveal that, in general, anxiety disorders proliferate within families. While this indicates that parental anxiety is likely
related to a child’s anxiety through biological mechanisms, the risk conferred genetically seems to be a somewhat generalized one that may be common to many forms
of internalizing psychopathology (Andrews, 1996). However, family studies appear
to support a rather specific linkage between the type of anxiety disorder observed
within families, indicating that environmental factors may interact with biological
mechanisms to influence the specific form of anxiety observed between parents and
their children (Beidel & Turner, 1997; Eley, 1997; Rapee, 2002).
Few environmental factors in the development of anxiety have received as much
research and clinical attention as parenting behavior. Many authors have argued that
the manner in which a parent responds to their child’s emotions and directs their
behavior is central to the likelihood of that child developing anxiety (Rapee, 2002).
Two parenting constructs: overprotection/control and low warmth/high criticism
have dominated the theoretical and empirical parenting literature in terms of demonstrable associations with childhood anxiety. However, other parenting behaviors,
including parental modeling of anxiety and a parent’s engagement in catastrophizing or similar communications that enhance a child’s fear (Barrett, Rapee, Dadds,
& Ryan, 1996; Beidel & Turner, 1998) may also be relevant to child anxiety and its
maintenance over time (Fisak, Negy, & Ehrenreich, 2008).
Some models of anxiety development (Chorpita, Brown, & Barlow, 1998;
Ginsburg & Schlossberg, 2002; Rubin & Mills, 1991) suggest that family-related
biological and environmental risks may interact when high levels of anxiety in
parents interfere with effective parenting, leading to the overuse of strategies that
promote child anxiety symptoms. With these models in mind, in this section we will
explore the existent literature on the role of parenting behaviors in the development
of child anxiety disorders. We will then present some family-based modifications
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to CBT for childhood anxiety that address parental and family factors in treatment.
Following this, a case example demonstrating the interaction of several parental
variables in a child anxiety treatment context will be discussed.
Parenting Behavior and Child Anxiety
Warmth and Control
Studies of both clinical (Hudson & Rapee, 2001; Moore, Whaley, & Sigman, 2004)
and community (Ehrenreich & Gross, 2002; Woodruff-Borden, Morrow, Bourland,
& Cambron, 2002) samples support that at least one caregiver, typically mothers, may exhibit a greater frequency of controlling behavior and lower amounts
of warmth (or a higher degree of criticism) during interactions with their anxious
children. A number of studies have used observational methods to examine these
behaviors across various interaction tasks with the families of anxious children
(see Wood, McLeod, Sigman, Hwang, & Chu, 2003, for a review). For example,
Siqueland, Kendall and Steinberg (1996) analyzed the interrelationships between
maternal control, maternal warmth, and childhood anxiety using both self-report
and observational techniques. Siqueland et al. (1996) observed parents in dyadic
interactions with their child, plus a triadic interaction with both parents and the
child, while discussing a “hot topic,” identified by the parents as a prevalent and
contentious family issue. Across the types of family interaction, parents of children
with anxiety disorders were rated as less granting of psychological autonomy (a
variable related to parental control that specifically examines the degree to which
parents allow their child independent decision-making and action) than parents of
non-anxious children. Although anxious mothers were rated as less granting of psychological autonomy than comparison group mothers, no significant differences in
maternal warmth were found between groups (Siqueland et al., 1996). However, a
replication and extension of these findings by Moore et al. (2004) found that regardless of maternal levels of anxiety, mothers of anxious children were observed to be
both less warm and less granting of autonomy than mothers of non-anxious children.
An interesting twist on such findings may be gleaned from a recent investigation by
Ginsburg, Grover, Cord and Ialongo (2006), in which mothers with an anxiety disorder displayed both overcontrolling behavior and heightened criticism in a highly
structured task, but only heightened criticism in a low-structure task, suggesting that
situational demands may play a role in the use of these anxiety-related parenting
strategies.
Parental behavior that is low in warmth and high in control may interact with
a child’s anxiety through several potential mechanisms. Barlow (2002) has suggested that these parenting behaviors may reinforce anxiety disorder development
by diminishing a child’s own sense of control. For instance, overcontrolling behavior may minimize a child’s sense of control by conveying that the anxious child
is incapable of handling novel or difficult situations, a notion that may be reinforced through the presentation of fewer opportunities for the child to learn how to
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negotiate such situations independently (Hudson & Rapee, 2004). Parenting behaviors that communicate a low degree of warmth and a high degree of criticism may
also indicate to the child that his/her caregiver may not act in a supportive manner
toward him/her when difficult or threatening situations arise (Moore et al., 2004).
Conversely, children with high levels of anxiety, who frequently display distress and
may fail to respond to other more supportive parenting behaviors, may naturally
evoke critical and controlling behaviors from their parents over time (Ehrenreich
& Gross, 2002). Manassis and Bradley (1994), for example, observed that even
non-anxious parents of anxious children may be conditioned to respond to their
children’s distress through overprotective behavior.
Parental Modeling and Communications About Threat
Parenting influences on child anxiety have also been examined in terms of direct
modeling of anxiety and communications about potential threat between parents
and anxious children. Beidel and Turner (1998) suggest that observational learning
between a socially phobic parental model and his/her child may contribute to the
concordance rates observed for this disorder, acting partly through a process they
call information transfer. Information transfer refers to caretakers verbally and nonverbally engaging in communications leading to a child’s fear acquisition and may
be typified by a parent repeatedly avoiding seemingly benign social interactions or
discussing such events as anxiety-provoking in the presence of the child (Beidel
& Turner, 1998). Similarly, the work of Barrett et al. (Barrett et al., 1996; Dadds,
Barrett, & Rapee, 1996) indicates that family communications about the potential
for threat in an anxiety-provoking situation may stimulate or encourage anxious
thoughts in children with anxiety disorders, resulting in the selection of avoidant
behavior more frequently than in families of children without anxiety disorders.
Moore et al. (2004) identifies maternal communications that are catastrophizing,
or that exaggerate the potential for negative consequences, as particularly likely
to occur in parent–child interactions associated with child anxiety, regardless of
whether their parent also exhibits an anxiety disorder.
A theoretical model of anxiety development presented by Craske (1999) suggests that parenting styles characterized by such communications and behavior may
activate trait anxiety in offspring and subsequently reinforce patterns of increasing
anxiety symptoms in children with anxiety over time. Micco and Ehrenreich (2008)
indicate that one factor underlying this type of parenting behavior may be a parent’s belief that his/her child is unable to cope with the demands of fear-evoking
situations, particularly those that are more salient in their fear value to the child. It
follows that a negative interaction cycle may persist between parents and anxious
children in which a parent develops a negative belief about their child’s ability to
adequately handle a feared situation (possibly perpetuated by his/her own anxiety,
where present; Whaley et al., 1999) and conveys this belief to the child through modeling of anxious/avoidant behavior and communication regarding anxious thoughts
about the degree of threat in a given scenario. Since children with anxiety disorders
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appear to mirror the negative coping expectations and heightened threat perception
of their parents (Micco & Ehrenreich, 2008) and are more likely to select an anxious or avoidant solution following discussions about anxiety-provoking scenarios
(Barrett et al., 1996), such avoidant child behavior may perpetuate this cycle by
reconfirming parents’ negative beliefs about a child’s ability to cope with feared
stimuli or events.
Parenting-Based Modifications and Treatment Response
Family factors, such as those cited above, are often implicated as a variable in the
failure of individual CBT to sufficiently benefit some children and adolescents with
anxiety disorders (Ginsburg & Schlossberg, 2002). In response to such concerns,
several investigators have augmented individual CBT formats to allow for a greater
degree of parental involvement. The resulting treatment approach is often referred
to as Family Cognitive Behavior Therapy (FCBT; e.g., Barrett, Dadds, & Rapee,
1996; Cobham, Dadds, & Spence, 1998).
Over the last 10 years, FCBT has been examined using a number of variations
regarding the degree and type of parent involvement incorporated into a relatively
fixed child anxiety CBT format similar to the one first developed by Kendall et al.
(1990). However, evidence for the incremental utility of FCBT over individual CBT
for child anxiety remains scant and inconsistent (Wood, Piacentini, Southam-Gerow,
Chu, & Sigman, 2006). Seven investigations have examined FCBT in comparison to
an individual CBT methodology (Barrett, 1998; Barrett et al., 1996; Cobham et al.,
1998; Mendlowitz et al., 1999; Nauta, Scholing, Emmelkamp, & Minderaa, 2003;
Spence et al., 2000; Wood et al., 2006), all with children presenting for treatment
of generalized anxiety disorder, separation anxiety disorder, or social anxiety disorder. As summarized by Wood et al. (2006), the majority of these studies present
findings supportive of FCBT in comparison to individual treatment, but only across
a minority of treatment outcome measures, with most measures failing to support
significant differences between treatment modalities. Taken together, these results
may indicate that the addition of family components to individual CBT is unlikely
to improve treatment outcomes for anxious children. However, some have also suggested that FCBT skills are best applied with anxious parents of anxious children
and that FCBT usage with non-anxious parents might be unnecessary or mask
positive treatment effects for families with a greater degree of psychopathology
(Cobham et al., 1998). Yet another compelling explanation may be the possibility
of a somewhat poor match between the types of parenting skills utilized in typical
FCBT and common parenting factors observed in the families of anxious children
(Wood et al., 2006).
In most iterations of FCBT, parents are engaged as treatment “coaches” who
are encouraged to serve as models for the effective usage of CBT skills. Parents
often receive psychoeducation about the cognitive-behavioral model of anxiety
and its intervention components, along with anxiety management or parent training skills. However, as observed by Wood et al. (2006), FCBT rarely includes an
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explicit focus on parental intrusiveness, autonomy granting or similar control behaviors developmentally linked to childhood anxiety disorders. To remedy this, these
authors created an FCBT protocol that adds to the original approach used for parent
involvement (e.g., Barrett et al., 1996) through an explicit focus on altering parent
communications that may convey a greater level of intrusiveness or limit the child’s
autonomy inappropriately. During these modified FCBT sessions, which are part
of the Building Confidence program (Wood & McLeod, 2008), the child is seen
alone for the first 15–20 min of the session, after which parents are seen alone for
25–30 min, followed by a 10–15 min family meeting to conclude the session. The
goal of parent-only time in session is to teach parents communication techniques
that will enhance the child’s self-efficacy and aid in the child’s acquisition of new
anxiety management skills. Specific communication skills taught include: (1) how
to give children choices if they appear indecisive in a feared situation (rather than
choosing a solution for them); (2) allowing children to experience distress and learn
new solutions through “trial and error”, as opposed to taking control of the situation
for them; (3) effectively identifying and accepting emotions and emotionally driven
responses, rather than criticizing these; and, (4) facilitating the uptake of new selfhelp skills (Wood et al., 2006). Appropriate responding to anxious child behaviors
using the behavioral reward system and planned ignoring skills set forth by Barrett
et al. (1996) are also included in the parent-oriented component of the Building
Confidence program.
Wood et al. (2006) compared the efficacy of the Building Confidence FCBT
approach to an individual child CBT protocol (Kendall et al., 1990) in a sample
of 40 children (aged 6–13 years) with generalized anxiety disorder, separation anxiety disorder, or social anxiety disorder who were randomly assigned to one of the
two treatment conditions. Similar to previous controlled trials comparing individual
CBT to FCBT, both groups of children improved significantly from pre- to posttreatment on several measures of child anxiety. However, not only did the youth in
the Building Confidence FCBT condition improve to a significantly greater degree
across parent- and independent evaluator-rated child anxiety symptom measures,
including measures of disorder severity, child distress, functional impairment, and
interpersonal/familial relationships, but they did so at a more rapid rate of change
(Wood et al., 2006). These results suggest that the explicit incorporation of relevant
parenting factors associated with child anxiety into treatment of childhood anxiety disorders may significantly enhance treatment outcomes while simultaneously
averting potential deleterious family-related complications in child treatment.
Case Example
Ella, an 8-year-old female diagnosed with separation anxiety disorder and several
sub-clinical specific phobias (water, darkness, planes) presented for treatment along
with her mother, Mrs. A. Ella’s father participated in the initial clinical assessment
process, but was unable to attend subsequent treatment sessions due to his work
schedule. At the start of treatment, Mrs. A reported that Ella was experiencing very
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high levels of fear and worry, along with a strong reluctance to separate prior to
school several mornings per week and at dance classes, play-dates, birthday parties,
and similar activities. The prior summer she reportedly refused to attend summer
camp after one half-day of attendance. Although Mrs. A indicated that she and her
husband rarely went out without Ella and her younger sister, Grace, she reported
being unable to leave Ella with a babysitter on those occasions due to Ella’s distress.
In the initial assessment, Ella only reported some fears of the dark and swimming
in the ocean, and moderate concern about being “taken” from school. In a pretreatment behavioral observation task, during which Ella and her mother played
together briefly followed by a clean-up task, Mrs. A appeared to have difficulty
allowing Ella to play independently and made a relatively high frequency of critical comments with regard to Ella’s play. For instance, when Ella picked up a doll
and attempted to engage in pretend play about her doll running in a race, Mrs. A
responded, “Don’t be silly. Dolls can’t run in races.”
Given the observed interaction patterns between Ella and her mother, along with
Mrs. A’s reported history of generalized anxiety, a treatment plan that maximized
both the teaching of parent anxiety management skills and child CBT components
was selected. At first, Ella and her mother were typically seen together for the
majority of session, with some additional time spent independently with Mrs. A
to teach parenting strategies that might help facilitate the use of child anxiety management skills. The first three sessions, which covered basic emotion identification,
psychoeducation about how thoughts, feelings, and behaviors perpetuate separation anxiety, and a review of anxiety-related physiological sensations and relaxation
skills, proceeded without incident. In parent-alone time, the therapist introduced a
behavioral reward system and discussed how to combine planned ignoring skills
with labeled praise to encourage Ella’s appropriate management of her anxiety
symptoms.
In the interval prior to session 4, Mrs. A called the therapist and indicated that she
was having increasing difficulty managing Ella’s anxiety, particularly in the mornings before school. In fact, Mrs. A had allowed Ella to stay home from school on the
day she called following a particularly intense and lengthy tantrum. Mrs. A stated,
“I just couldn’t talk her into going and she wouldn’t stop crying. . .I started worrying
that if I didn’t give her a break today then I would never get her to school again.”
Over the next two sessions, it was determined that a stronger focus on both parent communication skills when Ella exhibited fear or reluctance to engage in feared
activities and expedited movement toward graduated exposure plans, created in consultation with Ella, were appropriate. Given Ella’s young age, the therapist decided
to forgo cognitive restructuring and concentrated on the creation of an FAH and discussion of the rationale for exposure instead. Ella and her mother selected the least
fear-evoking item from the list (staying at dance class without mom for 10 min)
and a contingency contract was developed to ensure that Ella would receive a tangible reinforcer (an inexpensive bracelet from a local store) following completion
of this activity, since Mrs. A had been inconsistent in the delivery of rewards previously. During parent-only time, the therapist reviewed the rationale for exposure and
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role-played several communication principles for verbal and non-verbal responding
to Ella’s distress. Among these, an emphasis was placed on Mrs. A tolerating her
own distress about Ella experiencing anxiety and allow Ella, wherever possible,
to approach feared situations and negotiate solutions to difficult scenarios, without
Mrs. A’s direct influence.
Sessions 7– 12 largely followed the format of the previous two sessions, with
a review of exposure homework, followed by the selection of increasingly difficult situations from Ella’s FAH and the establishment of a contingency contract to
support reinforcer delivery for successful completion of FAH items. In parent-only
time, it became clear that Mrs. A had difficulty recognizing when it was appropriate to praise and reward her daughter’s increasingly brave behaviors. Therefore,
therapist modeling of positive behavior identification and reinforcer delivery was
provided, along with extensive role-playing of communications that would support
Ella’s independent usage of self-help skills. Over time, tangible reinforcers were
largely minimized in Ella’s treatment plan and replaced by enhanced usage of praise
and other reinforcers, such as time spent playing or eating privately with one of her
parents. By session 12, Ella was no longer consistently avoiding any of the items on
her original FAH and Mrs. A asked to discontinue treatment, owing to difficulties
with the scheduling of future sessions. Following a termination “party” celebrating
Ella’s achievements, a post-treatment assessment was conducted. This assessment
found that while Ella’s avoidance was now minimal, Mrs. A and Ella both felt that
she still experienced sub-clinical fears about separation, particularly when alone at
night or going on school trips independently. According to Mrs. A, if these situations were targeted for exposure, Ella complied with requests to engage in these
situations independently and her fear decreased significantly following separation.
In novel or unexpected fear situations, Mrs. A indicated more difficulty applying
treatment techniques and newly acquired communication skills. Following discussion with Ella’s therapist, Mrs. A opted to seek CBT for her own generalized anxiety,
rather than engaging Ella in further treatment of these concerns. A 6-month followup revealed that neither Ella nor her mother was currently experiencing clinically
significant anxiety symptoms.
Additional Complicating Factors in Child Anxiety Treatment
The research on additional factors impacting the outcome of child and adolescent anxiety disorder treatment is still at an early stage of development. Some
sociodemographic and clinical variables, such as parent–child (dis)agreement about
presenting problems, have been identified that may affect the course of treatment for
childhood anxiety. However, since the research on these potentially complicating
factors in child anxiety treatment is either new or lacks consistent substantiation,
we will only briefly review these here in hopes of further stimulating research on
these topics.
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Sociodemographic Characteristics
Similar to findings observed in community mental health settings (e.g., Gould,
Shaffer, & Kaplan, 1985; Weisz, Weiss, & Langmeyer, 1987), research has supported that children and their families who complete treatment for anxiety disorders
differ very little from those who fail to complete treatment (Kendall & Sugarman,
1997; Pina, Silverman, Weems, Kurtines, & Goldman, 2003). For instance, Pina
et al. (2003) examined characteristics of 137 children or adolescents (aged 6–16) and
their families who were either considered treatment completers or non-completers
following administration of a brief (10–12 session), exposure-based cognitive and
behavioral treatment for either a phobic or anxiety disorder. Treatment completers
(n = 106) were considered those participants who completed the entire 10- or
12-session protocol, while non-completers (n = 31) began the program but discontinued completely at some point prior to protocol completion (average number
of sessions attended = 5). Other than some suggestion that attrition rates may
have been higher among Hispanic/Latino participants in this study, few differences between groups were observed. The authors of this study recommended that
future investigations concentrate less on sociodemographic characteristics of children receiving anxiety treatment and more on stressors and barriers to treatment
attendance, along with therapist, relationship, and context issues or demands that
might discourage attendance in treatment (Pina et al., 2003).
Parent–Child Symptom Agreement
A common problem across domains of child psychopathology treatment is the
degree to which parents and their children disagree about the nature and severity
of the child’s difficulties and the associated need for treatment of such concerns. For
instance, in a study by Yeh and Weisz (2001), 381 clinic-referred children and their
parents were asked to list the child’s primary or target concerns. Of these participants, 63% failed to concur on even a single target problem. Even when grouped
by broad problem category, a third of the parent–child pairs still demonstrated no
overlap in problems identified (Yeh & Weisz, 2001). While these authors speculate that difficulties or conflict about the nature of a child’s difficulties may explain
instances of poor outcome for both internalizing and externalizing treatment samples, a child’s acceptability of and positive engagement in the treatment context
seems to be particularly important to the success of child anxiety treatment (Chu &
Kendall, 2004).
To this end, the resolution of significant parent–child conflicts or differences
about presenting concerns and intervention needs should be prioritized in child
anxiety treatment. Thorough clinical assessment procedures may provide several
opportunities to build consensus across any existent areas of shared concern and, as
appropriate, emphasizing the fit between anxiety treatment components and shared
treatment priorities. While some providers may be tempted to only share clinical
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conceptualizations of child problems with parent alone (a process that may provide
some opportunity to address areas of disagreement and conflict), it is also vital to
identify and validate any significant misgivings or areas of divergence in problem
focus with children and adolescents who voice such concerns directly. In addition,
prioritizing intervention components that fit best with problem areas identified by
both parent and child early in treatment may help build rapport with families and
help facilitate subsequent child and parent engagement in therapy.
Summary and Future Directions
Despite strong support for the efficacy of CBT in treating childhood anxiety disorders, there are some children who fail to benefit from standard CBT approaches.
This chapter identified several complicating factors that may contribute to resistance
to CBT for anxiety disorders and provided practical recommendations for modifying standard CBT to address these factors. First, children presenting with comorbid
anxiety and depressive disorders may be prone to symptomatic relapse following
CBT; as such, the addition of treatment components specifically targeting children’s
depression (including behavioral activation, challenging negative self-evaluation,
social skills training, and positive reinforcement) may be beneficial for this subsample of anxious children. Second, studies of the effects of externalizing disorders
on anxiety disorder treatment have produced mixed results, with some studies showing that this comorbidity has no effect on treatment outcome (Flannery-Schroeder
et al., 2004), and other studies showing that it affects immediate treatment outcome
(Costin et al., 2002) or ability to maintain treatment gains (Rapee, 2003). When
treating children who present with secondary externalizing disorders (most common in younger boys), it may be necessary to include treatment modifications that
specifically target inattention/hyperactivity (i.e., shorter sessions, problem solving)
and aggression (i.e., behavioral contingency plans, learning to differentiate between
anxious and angry feelings).
Family interactions, characterized by parental criticism/lack of warmth and overcontrol (behaviors that may, in turn, be reinforced by children’s anxious behaviors),
are common challenges in CBT for child anxiety, particularly if one or both of
the parents is also anxious. Recent advances have been made in developing CBT
for child anxiety that effectively address parenting characteristics; family CBT that
specifically targets problematic communication patterns, such as overly intrusive
comments and reinforcement of anxious behaviors, has been found to be particularly efficacious (Wood et al., 2006). Therapists treating anxious children should
also work with children and their parents to achieve consensus regarding important treatment targets in order to maximize children’s engagement and motivation in
treatment.
Although recent advances have been made in determining factors that contribute
to treatment resistance, much work remains in identifying how best to individualize
CBT for different sub-populations of anxious children. In particular, future research
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should examine the effect of more severe comorbidity (i.e., co-principal anxiety
and externalizing disorders; Costin et al., 2002) on CBT for anxiety disorders, followed by a controlled evaluation of a modular CBT approach (see Chorpita, Taylor,
Francis, Moffitt, & Austin, 2004) and emotion-focused or “unified” CBT approaches
(e.g., Ehrenreich, Goldstein, Wright, & Barlow, 2009) that include treatment components that address a wider spectrum of co-occurring problems. In addition, while
it has been established that FCBT is efficacious in treating separation anxiety, generalized anxiety, and social anxiety disorder, further research should examine the
inclusion of parents in treatments for other childhood anxiety disorders (such as
panic disorder and OCD). Finally, we have very little information on the degree to
which sociodemographic variables, including race/ethnicity and SES, impact perceptions of and response to CBT; it is imperative that further research determine the
effectiveness of standard CBT for child anxiety in diverse populations and settings.
With greater understanding of the factors underlying treatment complications that
arise in CBT, we will be able to more effectively tailor CBT approaches for use with
specific sub-groups of children with anxiety disorders.
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Index
Note: The letters ‘f’ and ‘t’ following locators refer to figures and tables respectively.
A
ABAB single-subject designs, 197
Abel, J., 185
Abelson, J. L., 209
Abernethy, A. P., 330
Abramowitz, J. S., 26, 68, 127, 133–134, 235
The Academy of eating disorders, 302
Acceptance and commitment therapy (ACT),
25, 160, 284
Acculturative stress, 89–90, 92
ACES, see Anxiety change expectancy scales
(ACES)
Achenbach, G. G., 35
Acosta, F. X., 95
ACT, see Acceptance and commitment therapy
(ACT)
Acute myocardial infarction, 317, 326–327,
329
Acute-phase combined treatments, efficacy of,
68–70
Acute stress disorder (ASD), 3, 68
Adams, H. E., 40
Adams, R. J., 333
Addiction Severity Inventory, 277
Addis, M. E., 61, 112
Addison, L. M., 26
ADDRESSING Framework
psychological assessment, paradigm of, 91
ADHD, see Attention-deficit/hyperactivity
disorder (ADHD)
ADIS, see Anxiety disorders interview
schedule (ADIS)
Adler, D., 72
Adolph, D., 209, 219
Afari, N., 332
Agostini, R., 307
Agras, W. S., 42, 299, 302
Ahles, T. A., 73
Ahrens, C., 274
Akbar, M., 86
Albano, A. M., 263, 348
Albaum, J. M., 298
Albee, G. W., 83
Albert, U., 128
Alcaine, O., 187
Alcohol use disorders identification test
(AUDIT), 276
Alden, L. E., 174–176
Alegria, M., 90
Alger, S. A., 292
Allan, T., 186
Allebeck, P., 274
Allen, L. B., 20, 238
Allmon, D., 260–261
Alm, T., 214
Alpers, G. W., 4, 209–222
Alpert, J. E., 176
Alprazolam, 60, 70, 72
Alvarez-Conrad, J., 151
Amado, D., 176
American Psychiatric Association (APA), 89,
103, 126, 185, 209, 252, 260, 275,
293–294
Amir, N., 26
Amir, Z., 324
AN, see Anorexia nervosa (AN)
Anastasiades, P., 186
Ancis, J. R., 93
Andersen, B., 322
Anderson, C. A., 72
Anderson, E., 148
Anderson, J. C., 349, 353
Anderson, K. C., 77
Anderson, R. A., 133
Andreasson, S., 274
Andrews, B., 156
Andrews, G., 357
Andrus, T., 40
M.W. Otto, S.G. Hofmann (eds.), Avoiding Treatment Failures in the Anxiety
Disorders, Series in Anxiety and Related Disorders, DOI 10.1007/978-1-4419-0612-0,
C Springer Science+Business Media, LLC 2010
371
372
Andrykowski, M. A., 321
Angold, A., 353
Anhedonia, 233, 240, 350
Annas, P., 210
Anorexia nervosa (AN), 12, 292–294, 297, 302
Antaki, C., 59
Anthony, J. C., 276
Antipova, A. V., 103
Antisocial personality disorder, 129
Antony, M. M., 127, 217, 220, 232
Anxiety change expectancy scales (ACES), 55
Anxiety comorbidity
with asthma, 331
anxiety effect on quality of life,
333–334
asthma/anxiety disorders, hypotheses,
332–333
psychological interventions, 334
treatment complications, 334–335
with cancer/malignant neoplasm, 319–321
complications in treating, 322–323
psychological interventions, 322
resolving treatment complications,
323–325
symptoms, side effects, and quality of
life, 321
with coronary heart disease, 325–326
anxiety as risk factor, 326–327
complications in treating, 328–329
persistent effects/quality of life in
patients, 327
psychological interventions, 327–328
resolving treatment complications,
329–331
Anxiety-coping skills, 355
Anxiety-dampening effects, supplements with,
59, 278
Anxiety disorder, children/adolescents
(resolving treatment complication),
254
complications and treatment, 363
parent-child symptom agreement,
364–365
sociodemographic characteristics, 364
depressive disorders (comorbidity), 348
case study, 351–352
patient characteristics, 349–350
prevalence, 348–349
treatment modification, 350–352
treatment response, 349–350
externalizing disorders (comorbidity), 350
case study, 355–357
patient characteristics, 353–354
Index
prevalence, 352–353
treatment modification, 354–355
treatment response, 353–354
FCBT, 360
case study, 361–363
treatment modification, 359–360
treatment response, 360–361
future directions, 365–366
parenting behaviors
vs. child anxiety (warmth and control),
358–359
vs. parental anxiety, 357–358
threat, parental modeling and communication, 359–360
Anxiety disorders interview schedule (ADIS),
170, 211, 277, 284, 293
Anxiety sensitivity, 75, 90, 103, 163, 217,
281–283, 329, 333
index, 285, 333
Anxiety sensitivity treatment for heroin users
(AST-H), 283–285
Anxiety spiral, 189, 190–192
Anxiety treatment outcome, impact of
comorbid depression on
OCD, 235
panic disorder, 233
PTSD, 236
social anxiety disorder, 234
treatment outcome literature, 236
Anxiogenic effects, supplement (herbal)
with, 59
APA, see American Psychiatric Association
(APA)
APD, see Avoidant personality disorder (APD)
Appels, A., 329
Arheart, K. L., 332
Arkowitz, H., 22, 176
Armstrong, H. E., 260–261
Arndt, L. A., 322
Arnkoff, D. B., 56–57
Arnoult, L. H., 72
Arntz, A., 54, 151, 158, 175
Aronson, T. A., 275
ASD, see Acute stress disorder (ASD)
Asmundson, G. J., 317
Assessment issues, through treatment
anxiety disorders/SUDs, temporal/
functional relationship, 272–273
assessment measures, selection of, 276–279
specificity across disorder categories
generalized anxiety disorder, 275
OCD, 276
Index
panic disorder, 275
social anxiety disorder, 276
Assessor-rated anxiety, 186
AST-H, see Anxiety sensitivity treatment for
heroin users (AST-H)
Asthma/anxiety disorders, comorbidity
hypotheses for
asthma, symptoms of, 331, 333
development variables, 332
domains, 334
healthy lifestyle behaviors, 333
pulmonary function, 332
Astin, M. C., 42, 150, 232
Ataque de Nervios, 89
see also Culture-bound syndrome
Atherosclerosis, 325–326
Atherosclerotic heart disease, see Coronary
heart disease (CHD)
Atkinson, D. R., 93
Attention/behavior during extinction, 43
Attention-deficit/hyperactivity disorder
(ADHD), 348, 354–355
AUDIT, see Alcohol use disorders
identification test (AUDIT)
Austin, A. A., 366
Autonomic nervous system activation, 220
Avoidance theory of worry, 187
Avoidant personality disorder (APD), 170–171,
175, 181, 255, 257
Ayers, C. R., 13
Ayonrinde, O., 88
B
Babor, T. F., 276–277
BABS, see Brown assessment of beliefs scale
(BABS)
Back, S. E., 283
Baer, L., 127, 133–135
Baeyens, F., 43
Bailey, G. K., 35
Bakker, A., 21
Ballenger, J. C., 68, 293
Ball, S. G., 232
Balluz, L., 333
Bandura, A., 71, 213
Bankier, B., 326
Bannon, Y., 293, 298
Barad, M., 41, 77
Barber, J. P., 119
Bar, F. W., 329
Barkham, M., 53
Barlow, D., 33
373
Barlow, D. A., 238
Barlow, D. H., 20, 32, 61, 68, 71, 103–105,
108, 111–112, 116, 129, 163, 170,
174, 186, 197, 212, 217, 232–234,
238, 258, 277, 292–293, 306, 318,
329, 347, 357–358, 366
Barnes, E. A., 321
Barona, A., 88
Barrett, H. M., 159
Barrett, P. M., 357, 359–361
Basoglu, M., 38, 60–61, 72, 112, 134, 234
Basten, C., 237
Batten, S. V., 160, 162, 284
Baum, C., 327
Baum, M., 40
Bazile, A., 86
Beard, C., 26
Beck, A. T., 25, 131– 133, 149, 153, 172,
186–187, 194, 242
Becker, C. B., 4, 148, 150–152, 154, 156, 160,
291–313
Becker, E., 175
Becker, E. S., 209–210, 214, 218, 220
Becker, R. E., 172–173
Beckian-style CBT model, 172–173
Beck, J. G., 13
Beck, J. S., 135
BED, see Binge eating disorder (BED)
Beens, H., 132–133
Beevers, D. G., 327
Beglin, S. J., 294
Behar, E., 4, 108, 113, 185–205
Behavior therapy (BT), 131, 133, 140
Beidel, D. C., 129, 171, 175, 232, 347–348,
357, 359
Beitman, B. D., 272, 325
Belar, C., 330
Bellack, A. S., 175
Bell, J., 335
Bellodi, L., 127
Bender, B., 332–335
Bennett, P., 328
Benninghoven, D., 318, 326
Bents, H., 133
Benzer, W., 327
Benzodiazepines, 68
Beresford, J., 322
Berglund, P. A., 3, 260, 317
Berkman, L. F., 328
Berk, M. S., 241–242
Berman, S. L., 349, 350
Bernal, G., 83, 85–88, 95
Bernal, M. E., 94
374
Bernstein, D. A., 192
Bernstein, G. A., 349
Berry, J. W., 89, 92
Bhugra, D., 83
Bhui, K., 83
Bichard, S., 219
Bickman, L., 56–58
Bicultural evaluation method (Evans and
Paewai), 91
Biemond, R., 215
Biernat, M., 86
Binge eating disorder (BED), 293–294,
297, 302
Biondi, M., 60–61, 72
Bird, H. R., 352–353
Biswas, A., 186–187, 191
BITE, see Bulimic investigatory test,
Edinburgh (BITE)
Bittinger, J. N., 152
Bjornsson, E., 332
Black, B., 175
Black, D. W., 112, 234
Blacker, K. H., 112, 234
Blais, F., 203
Blake, D., 156
Blanchard, E. B., 149, 213, 237
Bland, R., 127
Blaszczynski, A., 210
Bleiberg, K. L., 23
Blomhoff, S., 69
Blood/injury/injection (BII), 209
Blouin, A. M., 41, 77
Blumenthal, J. A., 326
BMI, see Body mass index (BMI)
BN, see Bulimia nervosa (BN)
Boath, K., 333
Body dysmorphic disorder, 12, 128, 130,
170–171
Body mass index (BMI), 298, 304
Boersma, S. N., 327
Bögels, S. M., 176, 350
Bogetto, F., 128
Bohn, K. S., 292, 298
Bohn, M. J., 276
Bohr, Y., 294
Boman, G., 332
Bomyea, J., 26
Bonala, S. B., 333
Bond, F. W., 25
Bonner, B. L., 59
Booth, R., 212, 216
Bootzin, R. R., 193
Index
Borderline personality disorder (BPD), 24, 58,
115, 135, 252, 255–257, 262, 264
effects, 135
Bordin, E. S., 52
Borgeat, F., 130
Borges, G., 258, 260
Borkovec, M., 200
Borkovec, T., 43
Borkovec, T. D., 4, 23, 43, 55, 57, 108, 113,
129, 185–205, 237
Bornovalova, M. A., 284
Borson, S., 333
Bosley, C. M., 333
Boulet, L. P., 333
Boulougouris, J., 43
Boulougouris, J. C., 40
Bourdon, K. H., 210
Bourland, S., 358
Bourne, L., 212
Bouton, M. E., 31, 34–36, 71, 104, 221
Bouvard, M., 70
Bowers, W., 112, 234
Bowker, J. L., 36
Boyce, C. A., 92
Boyd-Franklin, N., 86
Boyd, J. H., 210
Boyle, C., 218
Boyle, S. H., 326
BPD, see Borderline personality disorder
(BPD)
Bradley, B. P., 148, 189
Bradley, S., 359
Brady, E. U., 349, 351, 353
Brady, K. T., 275–276, 281–283
Brandberg, M., 214
Brault, M., 130
Braunwald, E., 325
Brawman-Mintzer, O., 68
Brechman-Toussaint, M., 347
Breitholtz, E., 237
Breslau, N., 161
Breton, S., 263
Brewerton, T., 292–293
Brewerton, T. D., 292
Brewin, C., 59
Brewin, C. R., 60, 72, 156
Brief, D. J., 293
Briere, J., 54
Bromet, E., 161, 273
Bronchoconstriction, 331, 333, 336
Bronik, M. D., 351
Brooks, D. C., 35–36
Broome, K., 279
Index
Brouwers, C., 115
Brown assessment of beliefs scale (BABS), 134
Brown, E. J., 175
Brown, G. K., 242, 260–261
Brown, M. Z., 260
Brown, P. J., 274
Brown, S. A., 275
Brown, T. A., 68, 111– 113, 129, 170, 176,
186, 211, 232, 234, 238, 293, 357
Brown, T. M., 175
Brozovich, F., 112
Bruce, N., 57
Bruce, S. E., 70
Bruce, T. J., 73, 216
Bruch, M. A., 232
Bruera, E., 321, 324
Bryan, C. J., 260
Bryant, B., 61
Bryant, R. A., 150–151, 232, 236–238
BT, see Behavior therapy (BT)
Buckminster, S., 68
Building Confidence program, 361
Bulik, C. M., 292
Bulimia nervosa (BN), 23, 290–292, 294,
299–300, 309, 311–312
Bulimia Test-Revised (BULIT-R), 292
Bulimic investigatory test, Edinburgh (BITE),
294
BULIT-R, see Bulimia Test-Revised
(BULIT-R)
Bullet points, 354
Bunde, J., 326
Buodo, G., 218
Burke, B. L., 22, 55
Burnam, A., 274
Burns, B. J., 210
Burns, D. D., 32
Butcher, G., 127
Butler, G., 186
Bystritsky, A., 38, 59, 72, 108
C
Cahill, S. P., 150, 158
Cain, C. K., 41, 77
Calamari, J. E., 127
California Psychotherapy Alliance Scale
(CALPAS), 61–62
CALPAS, see California Psychotherapy
Alliance Scale (CALPAS)
Calton, J. L., 34
Cambron, S., 358
Cameron, L. D., 321
Campbell, D. A., 333
375
Campbell, L., 26, 330
Campbell, L. A., 176, 211, 244
Campbell, P., 131
Campbell-Sills, L., 238
Campeas, R., 175
Camp, P., 317
Cancer-related symptoms, 321
Canestrari, R., 104
Cantor-Graae, E., 327
Capreol, M. J., 175
Capstick, C., 283
Carey, K. B., 276–277
Carey, M. P., 277
Carlsson, R., 327
Carmin, C., 204
Carroll, D., 327
Carroll, K. M., 283
Carr, R. E., 333, 335
Cartwright-Hatton, S., 348
Case formulation, OCD, 305–307
diagnoses, 305
E.coli precipitants, 307
nomothetic formulations, 306
problem list, 305
steps of construction, 303f
templates, individualizing, 304–306
biological/somatic factors, 306
cognitive factors, 306
working hypotheses, 306–307
Castle, D. J., 133
Castonguay, L. G., 52, 129, 200–201
Catastrophic misinterpretations, 13–14,
104–105
Caucasians, 83, 85–87, 90, 94, 125, 147
Caudill, M., 331
CAVE technology, 42
CBGT, see Cognitive behavioral group therapy
(CBGT)
CBT, see Cognitive-behavioral therapy (CBT);
Cognitive-behavioral treatment
(CBT)
CBT-BED, see Cognitive behaviour therapy for
binge eating disorder (CBT-BED)
CBT-BN, see Cognitive behavioural
therapy-bulimia nervosa (CBT-BN)
CBT-E, see CBT-enhanced (CBT-E) model
CBT-enhanced (CBT-E) model, 298
CBT treatment strategies, 113
CCBT, see Comprehensive cognitive
behavioral therapy (CCBT)
CD, see Conduct disorder (CD)
CDurrett, C. A., 253
Centanni, S., 332
376
Center for Anxiety and Related Disorders
and Massachusetts General
Hospital, 348
Cerny, J. A., 116, 163
Chait, I., 320
Chambers, A., 192
Chambless, D. L., 7, 40, 51, 56–57, 61, 112,
115, 133, 175–176, 234–235
Chandrasekhar, C., 134
Chansky, T. E., 351
Chaplin, E. W., 40
Chapman, D. P., 333
Chapman, M., 92
Chard, K. M., 160
Charney, D. A., 274
Chattopadhyay, P. K., 186–187, 191
Cheavens, J., 56
Chelonis, J. J., 34
Chemtob, C. M., 54
Cherry, S., 23
Cheung, F. K., 90
Cheung, M., 94
Cheung, M. K., 94
Chilcoat, H. D., 161, 273
Chin, S. B., 321
Chitsabesan, P., 348
Chiu, W. T., 3, 210, 317
Choate, M. L., 20, 238
Chopey, I. V., 331
Chorpita, B. F., 357, 366
Chow, E., 322
Choy, Y., 212–213, 215
Christensen, B., 55
Christianson, H. F., 156
Chronic worriers, 187, 189, 193, 199–200
treatment, 203
emotion dysregulation model,
GAD, 204
intolerance of uncertainty, 203
metacognitive model, GAD, 204
Chu, B. C., 358, 360, 364
Churchill, R., 69, 111
CIFA, see Culturally Informed Functional
Assessment Interview (CIFA)
Clara, I., 317
Clare, A. W., 127
Clark, D., 8, 12, 149, 159
Clark, D. A., 25
Clark, D. M., 8, 12, 18, 104, 108, 111–112,
153, 172–174, 176, 236
Clarkin, J. F., 21
Clark, J. V., 176
Clark, L. A., 359
Index
Claustrophobia, 35, 59, 210, 213, 217, 219,
221, 320
Claustrophobia questionnaire (CLQ), 213f
Clinical disorders (mental disorders), 10
Clinical Global Impressions scale, 173
Clinical severity rating (CSR), 170
Clinician Administered PTSD Scale (CAPS),
156, 283
Clinician-rated assessments, 61, 259
Clinician’s dysfunctional thought record, 264
Cloitre, M., 24, 53–54, 72, 159–161, 237
CLQ, see Claustrophobia questionnaire (CLQ)
Cluley, S., 333
Cluster C personality symptoms, 119
Cobb, J., 69
Cobham, V. E., 360
Cocco, K. M., 276
Cochran, B. N., 58
Cochrane Collaboration, 328
Cochrane, G. M., 328, 333–334
Cognitive avoidance, 188, 204, 219
Cognitive behavior
case formulation
five-axis DSM diagnoses, 10
formulation, individualizing, 14–15
nomothetic formulation, 12–14
precipitants of illness, 17–19
primary diagnosis, 11–12
problem list, 8–10
model, 91, 104, 149, 153, 262, 306, 359
of bulimia nervosa, 310
of social phobia, 308–311
and pharmacological treatments, efficacy
of, 67–68
anxiety disorders, acute treatment of,
74f
see also Cognitive behavioral/pharmacologic treatment
strategies
primary diagnosis of, 11–12
dysmorphic disorder symptoms, 12
problem-solving process, 12
therapist, task of, 32, 120
Cognitive behavioral group therapy (CBGT),
172, 251, 283
Cognitive behavioral/pharmacologic treatment
strategies
acute-phase combined treatments, efficacy
of, 68–70
minimal therapist contact, 70
positive effects, 69
short-term advantages, 69
Index
CBT strategy for discontinuation of
pharmacotherapy, 72–73
clinical considerations, 73–76
anxiety disorders, acute treatment of, 74
medication discontinuation, strategies,
76
novel combination strategies, 76–77
treatment discontinuation
mechanisms of relapse, 71–72
outcomes, 70–71
self-efficacy theory, 71
Cognitive-behavioral therapy (CBT), 3–4,
8–9, 11–12, 15, 17, 20–22, 25,
35, 40, 52–61, 53, 67–77, 83, 91,
93–95, 108, 111–119, 130–131,
134–135, 139, 148–152, 154, 157,
160, 162–163, 172–176, 185–186,
188, 194–, 200, 204, 214, 216,
221, 231, 234–244, 251, 259, 262,
297, 299–302, 306, 308, 310–311,
318, 319, 322–324, 329, 334–337,
347–366
treatment programs, 148
relaxation/stress management
components, 149
Cognitive-behavioral treatment (CBT), 112,
172, 185, 188, 257, 263, 335
Cognitive behavioural therapy-bulimia nervosa
(CBT-BN), 299–300, 311–312
Cognitive behaviour therapy for binge eating
disorder (CBT-BED), 302
Cognitive fear networks, 149
Cognitive interventions, 22, 105, 150, 187,
216, 218
Cognitive model of BN, 299
Cognitive restructuring (CR), 60
Cognitive therapy (CT), 8, 32, 61, 130–131,
133, 150–151, 157, 160–161, 172,
175, 178, 187, 193–194, 197, 212,
241, 243, 261
complication, 197
knee-jerk reactions, 195
OCD, 133
Socratic method, 197
technique
ABAB single-subject designs, 197
cost–benefit analysis, 198
“thinking traps,” 195
Cohen, J., 53
Cohen, J. A., 148, 353
Cohen-Kettenis, P. T., 72
Cohen, L., 320
Cohen, L. R., 24, 53, 159, 237, 283
377
Cole, D., 326
Cole, P. M., 54
Coles, M. E., 128
Cole, S. R., 326
Collaborative empiricism, 11
Collaborative longitudinal personality disorder
study, 254
Comorbid anxiety/substance use disorders,
resolving treatment complications
anxiety disorders/SUDs, correlation, 271
assessment through treatment, recommendations, 273–274
issues, 274
treatment, 279
Comorbid axis I disorder, 118t, 185, 293
Comorbid depression, 69, 112, 156, 176,
231–245
anxiety treatment outcome, impact on
OCD, 235
panic disorder, 233
PTSD, 236
social anxiety disorder, 234
treatment outcome literature, 236
reduced motivation for treatment, 232
treatment for anxiety, impact, 231
Comorbid dysthymia, 186
Comorbid eating disorders, 291–313
anxiety patients, likelihood of encountering, 291–294
AN, 292
structured clinical interview (DSM-IV),
292
EDs in anxiety patients, 294–298
caffeine, use, 298
dental enamel erosion, 297
“gold standard,” assessment of
EDs, 294
mental health clinicians, 298
electrolyte imbalance, dizziness, 313
formulation approach to guide treatment
planning, 303–308
OCD case example, 303–308
case description, 303–305
case formulation, 305–307
treatment plan, 307–308
ordering of treatment, 311–313
social phobia case example, 308–311
“obsessing” (negative reactions), 308
treatments for EDs, 298–299
CBT-BN/CBT-E, 299–300
CBT strategies for treating EDs,
300–302
cognitive model of BN, 299
378
Comorbid eating disorders (cont.)
comorbid anxiety, formulations for,
298–299
ED treatments with empirical
support, 302
idiographic model, psychopathological
features, 300
“keep an eye,” self-monitoring of
eating, 301
transdiagnostic model, 300
Comorbidities, OCD, 127
OCPD, 128
PTSD, 128
Comorbid medical conditions, treatment
complications, 317–337
anxiety comorbid with asthma, 331
anxiety effect on quality of life,
333–334
hypotheses between asthma and anxiety
disorders, 332–333
psychological interventions, 334
resolving treatment complications,
335–336
treatment complications, 334–335
anxiety comorbid with cancer/malignant
neoplasm, 319–321
complications in treating, 322–323
psychological interventions, 322
symptoms/side effects, 321–322
anxiety comorbid with coronary heart
disease, 327–328
anxiety as risk factor, 326–327
complications in treating, 328–329
persistent effects/quality of life in
patients, 327
psychological interventions, 327–328
resolving treatment complications,
329–331
Comorbid personality disorder, complications
clinical severity, 256
poorer response to treatment, 256
premature termination of treatment,
257–258
self-injurious thoughts/behaviors,
likelihood, 258
Comorbid social phobia, 113
Complicate exposure therapy, 160
Comprehensive cognitive behavioral therapy
(CCBT), 173
Compton, W., 272
Comtois, K. A., 260–261
Concurrent treatment of PTSD and cocaine
dependence (CTPCD), 283
Index
Conduct disorder (CD), 273, 352–352
Confidence-building activity (martial arts
classes), 352
Connolly, C. K., 324
Conoley, C. W., 55
Constantino, M. J., 52, 57
Context effects, 34–36, 61
generalization decrement, 36
Conti, S., 104
Conway, E., 331
Cook, B., 68
Cook, J. M., 151, 152
Cook, M., 211
Cooley, M. R., 92
Cooper, Z., 294–295, 299
Cootie, 304
Coplan, J. D., 68
Cordioli, A. V., 133
Cord, J. J., 358
Cormier, H. J., 112, 234
Coronary artery disease, see Coronary heart
disease (CHD)
Coronary heart disease (CHD), 326
anxiety as risk factor, 326–327
anxiety effects and quality of life, 327
psychological interventions, 327–328
symptoms, 323
heart palpitations, 329
treatment complications, 329–331
Corson, J. A., 218
Coryell, W., 326
Cossich, T., 322
Costello, E., 57, 237
Costello, E. J., 353
Costin, J., 354–365
Cote, G., 112, 234
Cottraux, J., 69–70, 130, 132–133
Cougle, J. R., 42, 219
Council of national psychological associations
for advancement of ethnic minority
interests, 85
Cournoyer, I., 333
Cowan, P. A., 42
Cowley, D. S., 70
Cox, B. J., 103, 317
Cox, G. B., 85
CR, see Cognitive restructuring (CR)
Craig, T. J., 275
Craske, M., 33, 35
Craske, M. G., 34–35, 41–42, 105, 108, 111,
113, 116, 212, 220–221, 237, 258,
334, 359
Creer, T., 332, 334–335
Index
Crick, N. R., 355
Crits-Cristoph, P., 186
Crombez, G., 43
Crowley, M., 263
Crum, R. M., 276
Cruz-Neira, C., 42
Crystal, D., 212
CSR, see Clinical severity rating (CSR)
CT, see Cognitive therapy (CT)
CTPCD, see Concurrent treatment of PTSD
and cocaine dependence (CTPCD)
Culturally Informed Functional Assessment
Interview (CIFA), 91
Culturally responsive assessment
paradigms, 91
ADDRESSING Framework, 91
Bicultural Evaluation, 91
CIFA, 91
DSM-IV-TR Outline for Cultural
Formulation, 91
Explanatory Model Interview Catalogue, 91
functional analysis, 91
MAP, 91
Culture and treatment complications, 83–96
culture and language, 88–89
culture and treatment resistance, 86–88
idioms of distress and culture, 89–91
acculturative stress, 89
anxiety sensitivity, 90
culture-bound syndrome, 89
language and culture, 88–89
psychological disorders among ethnic and
racial minorities, 84–85
resolving treatment complications, 91
psychological assessment, 91–92
treatment adaptations, 92–96
treatment resistance and culture, 86–88
Culture-bound syndrome, 89
Curbow, B., 320
Curry, C., 322
Curtis, G. C., 210, 212
D
Dadds, M. M., 357, 359
Dadds, M. R., 360
Dahl, A. A., 218, 321
Dahlen, I., 333
Dahlloef, O., 218
Dancu, C. V., 171
Dang, S. T., 150, 232, 237
Daniels, J. A., 55
Dansky, B. S., 283, 292
DAST, see Drug abuse screening test (DAST)
379
Daughters, S. B., 283
Davey, S. G., 217, 328
Davidson, A. L., 218
Davidson, J. R. T., 70, 173
Davidson, K. W., 326
Davidson, M., 211
Davies, D. H., 332
Davies, R. D., 92
Davis, K. E., 93
Davis, M., 40
Davis, M. K., 20, 52
Davis, N. R., 36
Davison, G. C., 60
Davis, T. M., 334
Day, L., 59
DBT, see Dialectical behavior therapy
(DBT)
D-cycloserine (DCS), 76–77, 221
Deane, F. P., 219
De Araujo, L., 133
Deardorff, W., 329
Deblinger, E., 347
De Bono, J., 189
Decision analysis strategy, 301, 308
DeFanti, T. A., 42
de Haan, E., 133
De Leon, G., 279
Deliberto, T. L., 4, 251–265
Delsignore, A., 56, 57
Demler, O., 3, 210, 317
Demoncada, A. C., 322
Denniston, J. C., 34, 221
Denollet, J., 327
Depression symptoms, impact of CBT on, 237
Depressive disorder, 70, 84, 125, 151, 153,
170, 232, 251, 260, 348–349
Derogatis, L. R., 277
DeRubeis, R. J., 53, 112, 186, 257
Desai, R. A., 90
DeSanctis, R. W., 326
Deschesnes, F., 333
Deshmukh, V. M., 334–336
Dettmer, E. L., 260
Detweiler-Bedell, J., 9
Detweiler, M. F., 9, 218
Detweiler-Shostak, G., 218
Deuser, W., 353
Devilly, G. J., 57
Devine, D., 320
Devine, E. C., 322
DeViva, J. C., 147–164, 293
Dew, M. A., 331
Dew, S. E., 56–58
380
Diabetes/HIV/irritable bowel syndrome, 337
clinical recommendations, 337
Diaferia, G., 115, 127
Diagnostic and statistical manual of mental
disorders (DSM), 8, 126, 185
Diagnostic challenges, OCD, 128
antisocial personality disorder, 129
body dysmorphic disorder, 130
OC- or OCD-spectrum disorders, 129
postpartum psychotic symptoms, 129
Tourette’s disorder, 129
Diagnostic/statistical manual of mental
disorders, 126, 185
Diala, C., 85
Dialectical behavior therapy (DBT), 20–21,
24, 115, 118t, 154, 160, 284, 302
Diaphragmatic breathing, 107, 191–192
Diaz, M. L., 197
Dickens, C. M., 321, 327
Dickerson, M., 220
Dickinson, D., 86
DiClemente, C. C., 22, 279
Diefenbach, G. J., 134
Dimensional assessment of personality
pathology-basic questionnaire
(DAPP-BQ), 259
Dimidjian, S., 238
Dinan, T. D., 127
Di Nardo, P. A., 170, 211, 277, 291
Disability (fainting or going crazy), 3, 104,
108, 112, 231, 317–318, 325,
329–331
Discrete pathological entities, 20
Disorder-based model, 14
Disorders, anxiety, 7, 8, 11–13, 20–21, 24–25,
32, 53, 55–56, 59, 67–68, 70,
72–77, 84–86, 90–92, 103, 113,
115, 127–128, 170–173, 176,
187–188, 191, 210–211, 218,
231–233, 235–237, 244–245,
252–258, 264, 270–286, 291,
299, 311–313, 317–318, 320–321,
325, 332–336, 347–348, 352–353,
357–365
Disorder-specific nomothetic formulation, 20
Distressing memories, 155
Dixon, D., 93
Dobkin, P. L., 274
Dodge, K. A., 355
Doering, S., 327
Dohm, F., 292
Donohue, B., 90
Donovan, C., 347
Index
Dovidio, J. F., 86
Dozois, D. J. A., 22, 55–56, 242
Dracup, K., 327
Drake, R. E., 269
Dreessen, L., 175, 257
Drug abuse screening test (DAST), 276
DSM, see Diagnostic and statistical manual of
mental disorders (DSM)
Dubovsky, S. L., 92
Duffy, M., 236
Dugas, M. J., 73, 203, 218, 233
Dunn, C., 22
DuPont, C. M., 3
DuPont, R. L., 3
Duration/spacing, exposure parameters, 40
Durham, R. C., 186–187
Dusseldorp, E., 21
Dyadic/triadic interaction, 358
Dyck, I. R., 186
Dyckman, J. M., 42
Dysfunctional anxiety
features/patients report, 320
ineffective behavioral responses, 320
Dysfunctional Attitude Scale, 194
Dyspnea, 317, 323, 332, 336
E
Earle, C. C., 322
Early adulthood research project (EARP), 273
EARP, see Early adulthood research project
(EARP)
Eastman, K., 94
EAT, see Eating attitudes test (EAT)
Eating attitudes test (EAT), 294
Eating disorder diagnostic scale, 294
Eating disorder examination (EDE),
294–295, 297
Eating Disorder Examination-Questionnaire
(EDE-Q), 294
Eating disorder not otherwise specified
(EDNOS), 292–293, 298–299,
302, 305
Eating disorders (EDs), 12, 152, 193, 281,
291–313
in anxiety patients, 294–298
dental enamel erosion, 297
“gold standard,” assessment of EDs, 294
mental health clinicians, 298
Eaton, W. W., 85, 113, 210
Eaves, L. J., 211, 356
Ebrahimi, S., 192
Ebrahim, S., 328
Ebsworthy, G., 26
Index
ECA, see Epidemiological catchment area
(ECA)
Echiverri, A. M., 35
EDE, see Eating disorder examination (EDE)
EDE-Q, see Eating Disorder ExaminationQuestionnaire (EDE-Q)
Eder, W., 331
Edlund, M. J., 186
EDNOS, see Eating disorder not otherwise
specified (EDNOS)
EDs, see Eating disorders (EDs)
Educational Support Group Therapy, 172
Edwards, S., 218
Eelen, P., 36, 43, 221
Eells, T. D., 7, 17, 20
Effective therapy relationship, 160
Effting, M., 35
Ege, M. J., 331
Ehlers, A., 61, 149, 153, 159, 173, 212, 217,
236–237
Ehrenreich, J. T., 4, 347–366
Eifert, G. H., 38, 244
Eisen, J. L., 127–128, 134
Eisenthal, S., 239
Eley, T. C., 357
Elie, R., 176
Elkind, G., 333
Emery, G., 149, 153, 172
Emery, R., 239
Emmelkamp, P. M., 40, 42, 72, 132–133
Emmelkamp, P. M. G., 77, 175–176, 215, 221,
235, 360
Emotional distress, 325, 334
Emotional processing therapy, 200
Emotion dysregulation model, 204
Emotion-focused psychotherapy, 119
Emotion regulation difficulties, 23–24
Emotion regulation therapy, 185
Emotions, influence of, 156–159
anger, 158
imaginal exposure, 158
non-verbal behavior, 158
non-anxiety emotions, 156
overcoming guilt, shame, and anger,
158–159
cognitive restructuring or imagery
rescripting, 158
empowering effects of anger, 159
loss/shame/powerlessness, 159
validating anger, 159
sadness, 156–157
cognitive restructuring, 157
exposure or cognitive therapy, 157
381
shame and guilt, 157–158
behavior and entire self, 157
cognitive processing therapy, 157
traumatic events, 157
worthlessness and powerlessness, 157
sources of distress, 156
Empirical support, 52–55
patient expectancies, 57–59
therapeutic alliance, 52–55
anger symptoms, 54
emotional regulation, 54
interpretations, 53
physical or sexual abuse, 54
Empty-chair technique, 200
Engel, G. L., 330
Epidemiological catchment area (ECA),
272–273
Epstein, D. R., 193
Erhardt, L., 327
Erickson, T. M., 186
ERP, see Exposure and response prevention
(ERP)
Erwin, B. A., 176, 232, 234
Escherichia coli, 304
Evans, I. M., 91–92
Evans, L. A., 95
Everett, F. L., 59
Evers, S. M. A. A., 57
Expectancy
control, 57–58
outcome, 57
role, 56
Explanatory Model Interview Catalogue, 91
Exposure and response prevention (ERP),
55–56, 69, 130, 133, 214, 221, 307
Exposure and ritual prevention (EX/RP), 69
Exposure-based interventions, 31, 221
Exposure-based therapy, 55, 177, 318, 329, 337
Exposure-based treatments, 71, 160, 187
Exposure parameters, 40
attention/behavior during extinction, focus
of, 43
duration/spacing, 40
mean subjective anxiety ratings during
exposure sessions, 41
fear activation, 43, 45, 217, 221
gradation of exposure, 42
sessions, distribution of, 41
stimulus properties (imaginal, in vivo,
virtual reality), 42
EX/RP, see Exposure and ritual prevention
(EX/RP)
Eysenck, M. W., 220
382
Eysenck’s (1992) hypervigilance theory, 220
Ezdinli, E. Z., 321
F
Faddis, S., 324
FAH, see Fear and avoidance hierarchy (FAH)
Fairburn, C. G., 23, 292, 294–295, 297–300,
302, 306, 310, 312
“Fair-quality” trials, 322
Falcomata, T. S., 193
Fals-Stewart, W., 133
Family-based treatment (FBT), 302
Family Cognitive Behavior Therapy (FCBT),
360–361, 366
Faragher, B., 233
Farmer, J., 294
Faust, D., 191
Fava, G. A., 104
Fava, M., 232
Favilla, L., 349
Fawzy, F. I., 322
Fawzy, N. W., 322
FBT, see Family-based treatment (FBT)
FCBT, see Family Cognitive Behavior Therapy
(FCBT)
Fear activation, 43, 45, 217, 221
Fear and avoidance hierarchy (FAH), 110, 352,
356, 362–363
Fear-of-fear cycle, 13, 18, 104
Feeny, N. C., 151
Feigenbaum, W., 42
Feldman, J. M., 333, 335–336
Fellenius, J., 218
Fennell, M., 236
Fenton, B. T., 274
Ferguson, B., 186
Fergusson, D. M., 332
Fergusson, W., 332
Feske, U., 175
Feuer, C., 232
Feuer, C. A., 150
Feuerstein, M., 322
FEV1 , see Forced expiratory volume in one
second (FEV1 )
Field, A. P., 211
Fight-or-flight response, 104
Finkelstein, R., 352–353
Finney, J. W., 274
First-line treatment, CBT, 70, 149, 299, 318
First, M. B., 62, 277
Fisak, B., 357
Fischer, H., 210
Fischman, D., 238
Index
Fisher, A., 201
Fisher, M., 294
Fishman, R., 128
Fiske, S., 14
Flack, W. F., 43
Flament, M. F., 292
Flannery-Schroeder, E., 353, 365
Fleet, R., 325–327
Fleet, R. P., 326–327
Fleisig, W., 90
Fleming, S. L., 334
Fletcher, K., 25
Fluent, T. E., 212
Fluoxetine
combined with placebo, 175
combined with self-exposure, 175
Foa, E. B., 13, 26, 40, 42–43, 55, 69–70, 126,
130, 133–134, 148–149, 150–151,
156–158, 162–163, 173, 188, 220,
235, 237, 283
Foa’s treatment (efficacy rates), 173
Foddy, M., 176
Folensbee, R., 193
Follette, V. M., 25, 204
Foote, B., 293
Forced expiratory volume in one second
(FEV1 ), 332, 335
Ford, E. S., 333
Forner, F., 128
Forsyth, J. P., 38
Fortner, B. V., 322
Fosbury, J. A., 333
Fossa, S. D., 321
Foster, V. L., 36
Fothergill, C., 348
Fouladi, R. T., 320
Frame, C. L., 349
Francis, G., 349, 353
Francis, S. E., 366
Frank, E., 157
Frank, J. B., 56, 58
Frank, J. D., 56, 58
Franklin, C. L., 160
Franklin, M. E., 4, 26, 55, 69, 127, 134,
173, 235
Fraser, D., 274
Fredrikson, M., 210
Freeman, C. P., 294
Freeston, M. H., 127, 131, 133, 203, 333
Fresco, D. M., 200
Freud, S., 52
Frey, K., 43
Frick, P., 349
Index
Friedman, B. H., 191
Friedman, M. J., 148
Friedman, S., 324
Frost, R. O., 8, 132–133
Frye, B., 210
Fujii, M., 321
Fujino, D. C., 94
Fulton, C., 320
Furman, J. M., 218
Furr, J. M., 127
Furukawa, T. A., 69, 111
Fyer, A. J., 175, 211–212, 214
G
Gabbert, S., 92
Gabel, J., 112, 234
GAD, see Generalized anxiety disorder (GAD)
GAF, see Global Assessment of Functioning
(GAF)
Gagnon, F., 203
Galin, R. S., 84
Gamble, J., 331
Garb, H. N., 14
Garcia-Gutierrez, A., 34
Gardenswartz, C. A., 116
Garfield, S. L., 58
Garfinkel, P. E., 331
Garner, D. M., 294
Garrett, J., 333
Garske, J. P., 20, 52
Garvey, M. J., 68
Garvin, V., 292
Gastfriend, D. R., 277
Gaston-Johansson, F., 321
Gaston, L., 61
Gatchel, R., 331
Gatsonis, C., 349
Gauthier, J. G., 112, 234
Gega, L., 215
Gelder, M. G., 42
Generalized anxiety disorder (GAD), 3–4,
9, 12–16, 21, 23, 55, 68, 73, 90,
113, 125, 127–129, 151, 170,
185–205, 237, 257, 272–273, 275,
292–293, 312, 337, 347–349, 353,
360–361, 363
cognitive therapy, 194–199
future directions, 203–205
IEP, 199–203
predictors of response to treatment,
186–187
relaxation training, 191–193
resolving treatment complications,
185–186
383
self-control desensitization, 193
self-monitoring, 189–191
stimulus control, 193–194
symptoms, 186–187, 194
theoretical conceptualization of worry,
187–188
treatment, 186, 197
Georg, H., 209–222
Gerdes, A. B. M., 211, 220
Gerlach, A., 176
Gerlach, A. L., 209
German community clinic, 234
Gershuny, B. S., 135
Gerull, F. C., 211
Giaconia, R. M., 273
Giardino, N. D., 335
Gibbon, M., 277
Gibbons, M. B. C., 23, 62, 186
Giesen-Bloo, J., 54
Gifford, E. V., 204
Gigliotti, T., 127
Gilheany, B., 86
Gillespie, K., 236, 239
Gill, K. J., 274
Gim, R. H., 93
Ginsburg, G. S., 357–358, 360
Girodo, M., 40
Gitow, A., 72
Glaros, A. G., 60
Glasgow, R. E., 176
Glass, C. R., 56–57, 176, 235
Gleason, J. R., 277
Glimelius, B., 320
Global assessment of functioning (GAF), 10,
170, 353
Glover, S. K., 85
Glutaminergic N -methyl-D-aspartate (NMDA)
receptor, 76–77
Glynne-Jones, R., 320
Godart, N. T., , 292
Goldbloom, D. S., 297
Goldfried, M. R., 52–53, 193
Goldman, J. L., 263
Goldman, M. L., 364
Goldman, R., 20
“Gold standard,” assessment of EDs, 212,
221, 294
Goldstein, A. J., 175
Goldstein, C. R., 366
Goldston, D., 260
Gómez-Conesa, A., 235
Gomm, S. A., 321
Gonzalez, J. S., 336
384
Good, B. J., 210
Goodman, W. K., 129, 261
“Good-quality” trial, 322
Goodwin, R. D., 275, 317, 331–332
Goossens, M. E. J. B., 57
Gordon, C. M., 277
Gorman, J., 111
Gorman, J. M., 61, 68, 71, 175, 234
Gosselin, P., 73
Götestam, B., 213
Gotestam, K., 214
Götestam, K. G., 213
Gotlib, I. H., 112
Gould, M. S., 353, 364
Gould, R. A., 68, 105, 111, 119, 186, 237, 299
Graap, K., 221
Gracely, E. J., 61, 115
Gradation of exposure, 42
Graded live exposure, 60
Graf, E., 119
Graham, E., 4
Gramzow, R., 157
Grandi, S., 104
Grant, B. F., 103, 114–115
Grant, J. E., 128
Gratz, K. L., 284
Graves, K. D., 324
Gray, M. J., 55
Grayson, J. B., 40, 43, 220
Greeley, J., 161
Green, A. I., 115
Greenberg, D. B., 323
Greenberger, D., 135
Greenberg, L. S., 20, 53
Greenberg, R. L., 149
Greenberg, R. P., 57
Green, G., 86
Greeno, C., 119
Greer, J., 317–337
Greer, S., 318, 324
Gregg, S. F., 73
Greist, J. H., 130, 133
Gresenz, C. R., 87
Grey, N., 156
Grey, S., 176
Griez, E., 232
Griez, E. J., 332
Griffin, M. G., 163
Griner, D., 93, 94
Grisham, J. R., 176, 211, 244
Groom, C., 189
Gross, A. M., 358–359
Gross, D. M., 54
Index
Grothaus, L. C., 327
Grover, R. L., 358
Grunert, B. K., 156, 158
Grüter-Andrew, J., 174
Guay, J. P., 253
Gunther, L. M., 34, 221
Gur, M., 23
Guthrie, R., 150
Guthrie, R. M., 232
Guyotte, S., 325
H
Haaga, D. A., 186
Hackett, C. A., 186
Hackmann, A., 236
Ha, E. H., 70
Hafner, J., 43
Haines, A. P., 326
Hair, T., 68
Halford, K., 176
Hall, G. C. N., 87
Hallstrand, T. S., 333
Hamada, R. S., 54
Hamann, M. S., 115
Hamilton Anxiety Scale, 186
Hamilton, N., 186, 325
Ham, L. S., 272
Hammerness, P. G., 73, 111
Hand, I., 176
Han, H., 53, 159, 161, 237
Hanusa, B. H., 127
Hare, R. D., 253
Haring, M., 151
Harrington, P. J., 111
Harrington, R., 348
Harris, J. A., 35
Harrison, J., 131
Harry Potter book, 179
Harth, T., 322
Hart, J. A., 34
Hartnick, E., 293
Harvey, A. G., 153, 237, 238
Hasin, D., 277
Hasin, D. S., 277
Haslam, N., 253
Hasler, G., 292, 331
Hassett, M. J., 322
Haug, T. T., 70, 218
Hautzinger, M., 68
Haw, J., 220
Hawke, J., 279
Hawton, K., 258
Hayes, C., 86
Index
Hayes, S. A., 41
Hayes, S. C., 25, 204, 238, 284
Haynes, S. N., 92, 277
Hays, P., 93, 95
Hays, P. A., 9, 86, 91, 92
Hazlett-Stevens, H., 192, 197, 200
Heaney, L. G., 331
Heard, H. L., 260–261
Hearst-Ikeda, D., 149
Heart rate (HR), 212–213f, 221, 282, 327
Heath, A. C., 211, 357
Hecht, J., 327
Hedberg, A. G., 218
Heffner, M. E., 284
Hegel, M. T., 73
Heilbronner, R. L., 90
Heimberg, R. G., 8, 12, 41, 72, 115, 172–173,
175–176, 200, 204, 232–234, 256
Heimberg’s CBT protocol, 173
Heinrichs, N., 173
Heldt, E., 73, 111, 115
Hellstroem, K., 214
Helms, J., 86
Helzer, J. E., 128, 273
Hembree, E. A., 151–152, 158
Henderson, M., 294
Hendriks, G. J., 73, 112
Henk, H. J., 130
Hennen, J., 70
Henninger, N. J., 128
Henriques, G. R., 242
Henry, D. R., 40
Herbal supplement
anxiety-dampening effects, 59
anxiogenic effects, 59
Herbert, J. D., 173, 175
Herda, C. A., 212
Hermans, D., 35, 221
Hermesh, H., 135
Hernandez, D. H., 284
Hersen, M., 197, 348, 353
Hertel, P. T., 112
Herzog, D. B., 293
Hetta, J., 332
Hidding, A.., 57
Hiemisch, A., 173
Hien, D. A., 274, 283
Higgins, H., 326
Hill, K. M., 324
Himadi, W. G., 116
Himle, J. A., 133, 212, 214
Hirsch, C. R., 173
Hiss, H., 133
385
Hladek, D., 35
Hochron, S. M., 333
Hodgson, R., 127, 131
Hoehn-Saric, R., 191
Hoekstra, R., 133
Hofer, S., 327
Hoffart, A., 72
Hoffman, C., 325
Hoffman, K., 320
Hofmann, S., 310
Hofmann, S. G., 3–4, 25, 33–35, 40, 53, 68, 77,
153, 169–181, 212, 217, 237–238,
243–244
Hogue, A., 61
Hohagen, F., 69
Hoke, J. A., 351
Holdrinet, I., 214
Holker, L., 26
Hollander, E., 4
Holland, L., 263
Hollon, S. D., 51
Holmberg, E. B., 260
Holmes, E. A., 156
Holohan, D. R., 323
Holt, C. S., 175
Holzer, C. E., 85
Homan, S., 333
Homework compliance, 58
Honda, K., 317
Hong, J. J., 73, 112
Honig, A., 327
Hood, J., 349, 353
Hoogduin, C. A., 73, 112, 161
Hoogduin, C. A. L., 232, 234
Hooker, C., 320
Hope, R. A., 23, 312
Hopko, D. R., 244
Hopko, S. D., 244
Horowitz, J. D., 212
Horvath, A. O., 53
Horwood, L. J., 332
Houck, P., 119
Houck, P. R., 157
House, A., 320, 326
House, A. S., 166
House, J. D., 326
Houts, P., 324
Hovey, J. D., 90
Howard, L. J., 292
Hoyert, D. L., 320
HR, see Heart rate (HR)
Hudson, J. L., 358–359
Huffman, J. C., 327
386
Index
Hu, L., 94
Hunter, S. B., 274
Huppert, J. D., 61, 129
Hu, S., 188, 191
Hüweler, R., 209
Hwang, W. C., 358
Hynd, G. W., 349
Hyperventilation, 68, 106, 108, 110, 114, 163,
332, 335–336
Hypochondriasis, 104
Hypokalemia, 306
Hypothesis-testing approach, 153, 303
biopsychosocial problem list, 23
Interpersonal psychotherapy (IPT), 20, 23,
54, 302
Interpersonal therapy, 53, 185, 200
Intolerance of uncertainty, 185, 203
Inz, J., 188
IPT, see Interpersonal psychotherapy (IPT)
Irritable bowel syndrome, 337
Ischemia, 325, 328–330
Ito, L., 133
Ivey, A. E., 85
Iwamasa, G. Y., 84, 91–92
I
Ialongo, N., 358
ICD-9 anxiety disorder, 320
Idiographic model, psychopathological
features, 300
IEP, see Interpersonal and emotional
processing therapy (IEP)
Ilardi, S., 56
Illness-related worry, 323
algorithm, 319f
Imagery rescripting, see Cognitive
restructuring (CR)
Imaginal exposure, 60
Imeson, J. D., 326
Impending death (heart attack or stroke), 104
In-Albon, T., 237
Individualize formulation, cognitive
behavioral, 14–15
disorder-based model, 14
“screwing up treatment,” 15
Information processing training, 26
Information transfer (process), 359
Inglehart, M., 43
Inhibitory mechanism, 36
Initial symptom change, 58
Insel, T. R., 77
Insomnia, 193, 321
Institute on Alcohol Abuse and Alcoholism,
272
Interoceptive exposure, 10, 32–34, 37–38,
68, 75–76, 106–108, 110–111,
114–115, 163, 217, 329–330, 333,
335–337, 357
avoiding treatment failures in social anxiety
disorder, 33
Interpersonal and emotional processing therapy
(IEP), 199–203
empty-chair technique, 200
Interpersonal problems, 23, 187, 200, 306
treatment complications, 23
J
Jackson, C. A., 317
Jackson, R. J., 103
Jacobi, F., 331
Jacob, R. G., 218, 232
Jacobs, D. G., 260
Jacobson, N. S., 61, 238
Jacobs, W. J., 40
Jacquin, K. M., 111
Jaimez, T. L., 111
Jainchill, N., 279
Jameson, J. S., 40
Janeck, A. S., 127
Janis, I. B., 260
Janis, I. L., 301
Janoff, D., 60
Jansen, M. A., 175
Janson, C., 332–333
Jansson, L., 234
Januzzi, J. L. Jr, 326
Jaycox, L. H., 158, 162–163
Jeammet, P., 292
Jefferson, J. W., 130
Jeffrey, D. B., 60
Jenike, M. A., 134–135
Jenike, M. A. M. D., 127
Jenkins, C. R., 334
Jerremalm, A., 218, 234
Jobes, D. A., 260
Joe, G., 279
Joe, G. W., 279
Joekes, K., 327
Johansson, J., 219
Johnson, A. L., 186
Johnson, D. M., 283
Johnson, T., 186
Johnstone, K. A., 43
Joiner, T. E. Jr, 260
Jones, M. L., 35
Jones, R., 23, 312
Index
Joormann, J., 112, 232, 234, 237
Juster, H., 176
Juster, H. R., 175, 232–233
K
Kabat-Zinn, J., 25, 325
Kadden, R., 277
Kadden, R. M., 275
Kaelber, C. T., 272
Kaiser, G., 176
Kamphuis, J. H., 43, 220
Kampman, M., 73, 112, 161, 234
Kandil, F., 209
Kanel, K., 89
Kaplan, D., 364
Kaplan, J., 274
Karamanlian, B. R., 36
Karver, M., 53
Kashani, J. H., 349, 353, 357
Kasimatis, M., 43
Kaspi, S. P., 73, 111
Kasvikis, Y., 61, 134
Katon, W. J., 327, 331–332
Katzelnick, D. J., 130
Katz, I. R., 13
Kawachi, I., 326
Kaye, W. H., 292
Kazdin, A., 348, 353
Kazdin, A. E., 51, 57–58, 260, 263–264, 348
Keane, T. M., 148
Keefe, F. J., 330
Keefer, L., 218
Keijsers, G., 161
Keijsers, G. P., 73, 112
Keijsers, G. P. J., 73, 151, 232, 234
Keir, R., 211
Keller, M. B., 186, 236
Kelly, C., 331
Kelly, S., 17–19, 87, 94
Kelso, T. M., 332
Kendall, P. C., 347– 351, 353, 358,
360–361, 364
Kendler, K. S., 210–211, 357
Kennedy, S. H., 297
Kenney, F. A., 35
Kent, J. M., 68
Kenwright, M., 215
Kessler, R., 103, 113
Kessler, R. C., 3, 85, 103, 113, 161, 176, 185,
210–211, 244, 252, 255, 260, 272,
317, 357
Ketter, T. A., 275
Keuler, D. J., 129
387
Kilic, C., 60, 72
Kilpatrick, D. G., 292
Kim, P., 322
Kim, S. J., 93
Kindt, M., 35, 158
King, C. A., 90
King, D. A., 35
King, N. J., 347
King, P., 204
Kirby, P. G., 321
Kirkeby, J., 85
Kirk, M., 156
Kirsch, I., 43, 215
Kishore, V., 134
Kitzman, H., 325
Kleespies, P. M., 260
Klein, D. F., 175, 214, 274
Klein, D. N., 53, 61
Kleinman, A. M., 210
Klerman, G. L., 23
Knee-jerk reactions, 195
Knight, R. A., 253
Knutson, J. L., 43
Kobak, K. A., 130, 133
Koch, E. I., 214
Koch, W., 237
Koch, W. J., 112, 151, 232
Koenen, K. C., 24, 53, 159, 237
Koerner, K., 21, 61
Kohls, S., 133
Kolbe, J., 333
Kop, W. J., 326, 329
Kortlander, E., 351
Kosfelder, J., 232
Kosten, T. R., 275, 276
Kotov, R., 103
Kovacs, M., 349
Kozak, M. J., 40, 43, 126, 130, 133–134, 188,
220, 235
Kozak, M. S., 220
Kranzler, H., 276
Kranzler, H. R., 276, 277
Krijn, M., 215
Krone, K. P., 133
Krueger, R., 210
Krystal, J., 276
Krystal, J. H., 77
Kubany, E. S., 156–157
Kubzansky, L., 326
Kubzansky, L. D., 326
Kucuk, O., 321
Kumar, R., 68
Kung, H. C., 320
388
Kunzel, R., 13
Kurtines, W. M., 364
Kushner, M. G., 77, 210, 272
L
Laberge, B., 112, 234
LaCroix, A. Z., 327
Lahey, B. B., 349
Lambert, M. J., 95
Lambert, R. G., 95
Lane, D., 327
Lang, A. J., 41
Lange, W. G. T., 220
Langmeyer, D. B., 364
Lang, P. J., 220
Lannon, R. A., 275
Lanugo (body hair), 297
Larsen, R. J., 43
Last, C. G., 116, 348–349, 353, 360
Lauchlan, F., 218
Lauritzen, T., 55
Lavie, C. J., 327, 330
Lavoie, K., 325
Lavoie, K. L., 327, 333
Lawson, J., 211
Lawson, W. B., 84
Lax, T., 61, 134
Lazare, A., 239
Lazarus, A. A., 52
Leary, M. R., 172–173
Lease, C. A., 353
Leckman, J. F. M. D., 127
Ledley, D. R., 217
Lee, D., 163
Leen-Feldner, E. W., 103
Leeuw, I., 220
Leger, E., 127
Le Grange, D., 302
Lehman, C. I., 176, 244
Lehman, C. L., 211, 217
Lehrer, P. M., 333, 335
Leitenberg, H., 42
Lejuez, C. W., 4, 115, 244, 271–286
Lemko, I. S., 331
Leon, A. C., 119
Leonhard, C., 277
Lerew, D. R., 103
Lerman, C., 193
Leskin, G. A., 113
Lev, E. L., 321
Levensky, E. R., 58
Leventhal, H., 321
Levine, B. A., 40
Index
Levin, F. R., 274
Levis, D. J., 40
Levitt, J. T., 235
Levitt, K., 216
Levy, K. N., 21
Lewin, M. R., 113
Lewis, G., 274
Ley, R., 332
Leyro, T. M., 71
Liebowitz, M. R., 72, 130, 173, 175
Liese, B. S., 283
Life stressors, 116, 118t, 326
Lilenfeld, L. R. R., 292
Lillis, J., 25
Lim, L., 176
Lincoln, T. M., 75, 234
Lindahl, I. -L., 218
Linden, W., 193
Linehan, M. M., 24–25, 58, 115, 154, 160,
258, 260– 262, 264, 284, 302
Lip, G. Y., 327
Lips, C., 176
Lipschitz, D. S., 293
Lipsitz, J. D., 23, 212, 214, 218–219
Liss, A., 217
Litt, L. C., 283
Littman, A. B., 326
Litvak, S. B., 42
Livanou, M., 60, 150, 237
Lochman, J. E., 355
Lock, J., 302
Loeb, K. L., 54
Loge, J. H., 321
Lopez, B., 273
Lopez, S. R., 14
Loss of control (inability to escape), 18,
104, 297
Louie, A. K., 275
Lousberg, R., 327
Lovell, K., 150, 237
Love, R. R., 321
Lovibond, P. F., 36
Lowe, D., 332
Lozano, P., 331
Luborsky, L., 277
Lucas, D., 332
Lucey, J. V., 127
Luck, A. J., 294
Lundberg, I., 274
Luoma, J. B., 25
Luterek, J. A., 200
Lydiard, R. B., 68, 293
Lynch, T., 321
Index
Lynch, T. R., 284
Lytle, R., 185
M
MacDonald, G. F., 334
MacKinnon, K. J., 218
Mackintosh, N. J., 36, 40, 43
MacLeod, C., 26, 220
Maddock, R. J., 112, 234
Maes, S., 327
Magee, W. J., 210
Magrath, K. H., 216
Maguire, P., 322
Maidenberg, E., 108
Maina, G., 128
Maisto, S. A., 276
Major depressive disorder (MDD), 75, 125,
128, 134, 151, 153, 232, 237–241,
244, 251, 260, 348–349
Maki, K. M., 70, 112
Malan, J., 103
Malgady, R. G., 89
Mallott, M., 103
Malnutrition, 305–306
Manassis, K., 347, 351, 356
Mancebo, M. C., 128, 135
Mancill, R. B., 176, 211, 244
Mancini, C., 293
Mannarino, A. P., 347
Mann, L., 301
Mannuzza, S., 212, 214
Mansueto, C. S., 129–130
Manualized psychodynamic therapy, 119
Manzo, P. A. M. S. W., 127
MAOI, see Monoamine oxidase inhibitors
(MAOI)
MAP, see Multicultural Assessment Procedure
(MAP)
March, J. S., 348
Marciniak, M. D., 317
Mar, C. M., 58
Marcus, M., 56
Marcus, M. D., 299, 310
Margraf, J., 111–112
Marin, G., 92
Marı́n-Martı́nez, A., 23, 25
Mark, M. M., 322
Markowitz, J. C., 20, 23, 119
Marks, A. P., 133
Marks, D. F., 320
Marks, I., 40, 42–43, 70, 133, 150–151, 176,
216, 237
Marks, I. M., 60–61, 69–70, 72, 111, 133–134,
209, 215, 232
389
Marks, M., 127
Marmar, C. R., 61
Marset, P., 43
Marshall, W. L., 216
Marsteller, F., 42
Martell, C. R., 238
Martin, D. J., 53
Martinez, E., 235, 294
Martin, J. R., 25
Martin, L. L., 43
Martinsen, E. W., 72
Masi, G., 349
Massie, E. D., 151
Massie, M. J., 323
Massion, A. O., 187, 257
MAST, see Michigan alcohol screening test
(MAST)
Masters, S., 119
Mastery of your anxiety and panic (patient
manual), 108
Masuda, A., 25, 284
Mataix-Cols, D., 215
Mataix-Cols, D. P., 127, 133
Mathews, A., 26, 220
Matthews, J. P., 322
Mattia, J. I., 232
Mattis, S. G., 347
Maudsley approach, 302
Mavissakalian, M., 115
Mavissakalian, M. R., 68, 70, 111, 115
Mawson, D., 69
Mayou, R. A., 61
Mays, V. M., 83
McCabe, R. E., 220
McCarthy, P. R., 13, 134
McCauley, E., 331
McCutcheon, B. A., 40
McDonagh, A., 151, 232, 236–237
McDonald, R., 69
McEvoy, L., 128, 273
McFadden, E., 331
McFall, M. E., 132
McGee, R., 349, 353
McGinn, L. K., 187
McGlashan, T. H., 255
McGonagle, K. A., 210
McGovern, M. P., 269
McHugh, R. K., 4, 70, 103–120
McIsaac, H. K., 213
McKenna, K., 326
McKnight, P. E., 332
McLachlan, S. A., 322
McLean, P. D., 112, 133, 217, 232, 234, 237
390
McLellan, A. T., 277
McLeod, B. D., 358, 361
McLeod, D. R., 191
McManus, F., 236
MCMI, see Millon clinical multiaxial inventory
(MCMI)
McMillan, E. S., 159
McNally, R. J., 75, 103, 211
McNeil, D. W., 175
McNeil, T., 327
MDD, see Major depressive disorder (MDD)
Meade, T. W., 326
Medical model (categorical approach), 20
Medoro, L., 103
Meigs, J. B., 70
Mellings, M. B., 174
Melnick, G., 279
Menard, C., 273
Menchola, M., 55
Mendelsohn, R. A., 158
Mendes de Leon, C. F., 329
Mendlowitz, S. L., 360
Menna, R., 349
Mennin, D. S., 24, 115, 200, 204
Mental disorders, 3, 10, 126, 185, 209–210,
255, 260–261, 277
Menzies, R. G., 211
Merckelbach, H., 214
Meredith, L. S., 317
Merikangas, K. R., 3, 252, 272, 274, 317
Mersch, P. P. A., 175–176
Metacognitive therapy, 185, 204
Meta-worry, 204
Meyer, L., 321
Meyer, T. J., 322
MI, see Motivational interviewing (MI)
Micco, J. A., 4, 347–366
Michael, S., 56
Michael, S. T., 56
Michalek, J. E., 326
Michel, B. D., 260
Michigan alcohol screening test (MAST),
276–277
Miele, G. M., 283
Milad, M. R., 35
Milani, R. V., 327, 330
Millepiedi, S., 349
Miller, B. V., 40
Miller, J. J., 25
Miller, N. L., 23
Miller, R. R., 34
Miller, S., 55
Miller, T., 189
Index
Miller, W. R., 55
Millon clinical multiaxial inventory (MCMI),
259
Mills, R. S., 357
Milosevic, I., 220
Milrod, B., 21, 119
Milrod, B. L., 21, 119
Minderaa, R. B., 360
Mindfulness-based therapy, 185, 204
Mindlin, M., 176, 232
Mind-reading, 324
Mineka, S., 35, 71, 104, 211
Minhas, F. A., 89
Minichiello, W. E., 134–135
Miranda, J., 85
Miranda, R., 54, 161
Mitchell, J. E., 292, 294, 297
Mitte, K., 68
Modulatory mechanism, 35–36
Moffitt, C., 366
Mogg, K., 189
Mokdad, A. H., 333
Molina, S., 23
Mollard, E., 70
Molnar, C., 200
Monahan, P., 112
Monahan, P. J., 234
Monoamine oxidase inhibitors (MAOI),
68, 172
Moody, E. W., 34
Moore, P. S., 358–359
Moore, S. A., 152
Moorey, S., 318, 324
Moos, R. H., 274
Moran, C., 275
Moras, K., 129
Morin, C. M., 73
Morral, A. R., 162
Morris, E. P., 272
Morris, R. J., 216
Morris, T. L., 347
Morrow, C., 358
Moscovitch, D. A., 237, 241
Moser, D. K., 327
Moser, J., 69
Motivational interviewing (MI), 7, 22, 55
Motoric avoidance of feared stimuli, 188
Moulds, M. L., 150, 232
Mowrer, O. H., 187, 211
Mucci, M., 349
Mueller, T., 274
Muers, M. F., 324
Mulle, K., 348
Index
Mullett, G. E., 42
Multicultural Assessment Procedure (MAP),
91, 152
Mulvey, K., 277
Munafo, M., 218
Münchau, N., 176
Munitz, H., 135
Muntaner, C., 85
Murdock, T. B., 149, 237, 283
Muris, P., 214
Murphy, S., 186
Murphy, S. L., 320
Murphy, S. T., 43
Murray, A. M., 4, 103–120, 261
Myers, H. K., 218
Myers, J., 210
Mykletun, A., 218
Myocardial infarction, 326–331
Myrick, D. H., 274, 281–282
Myrick, H., 274
Mystkowski, J. L., 35, 71, 111, 237, 312
N
Najavits, L. M., 153, 162, 283
Nakao, K., 103
Nakumura, R., 85
Narducci, J., 23
Narrow, W. E., 272
National comorbidity study, 272
National comorbidity survey – replication, 252
National Comprehensive Cancer Network, 324
National epidemiologic survey on alcohol
and related conditions (NESARC),
272–273
National Institute for Clinical Excellence
(NICE), 299
Nattiv, A., 307
Nausea, anxiety disorders, 106, 218, 318, 321,
323, 329
Nauta, M. H., 360
Neale, M. C., 211, 357
Needle phobias, see Claustrophobia
Negative affect syndrome, 20
Negrete, J. C., 274
Negy, C., 357
Nelson, C., 161
Nelson, C. B., 273
Nelson, R., 192
Nelson, T. D., 89
NESARC, see National epidemiologic survey
on alcohol and related conditions
(NESARC)
Nesse, R. M., 133
391
Newell, S. A., 322
Newhouse, J. P., 322
New learning, 31–32, 34, 43–44, 149, 157
exposure, 31
Newman, H., 185
Newman, M. G., 185
Newman, S., 127
New pre treatment (NPT), 55
Nezu, A., 324
Nezu, C., 324
NICE, see National Institute for Clinical
Excellence (NICE)
Nicholson, G., 274
Nickerson, K., 86
Nishith, P., 150, 163, 232
Nixon, R. D. V., 150, 232
Nizami, A. T., 89
Noack, P., 68
Nock, M., 264
Nock, M. K., 4, 58, 251–265
Nomothetic formulation, 12–14
purpose of selection, 13
Nomothetic model (hypothesis-testing
approach), 303, 310
Non-suicidal self-injury (NSSI), 258, 260
Norberg, M. M., 77
Norcross, J. C., 51
Nordin, K., 320
Norton, G. R., 103
Norton, P. J., 103
Noshirvani, H., 150, 237
Nouwen, A., 333
Novaco, R. W., 54
Noyes, R., Jr, 68, 185, 234, 326
NSSI, see Non-suicidal self-injury (NSSI)
Nunes, E., 274
Nunez, J., 87
Nuzzarello, A., 73
O
O’Brien, C. P., 277
O’Brien, G. T., 116
O’Brien, W. H., 92
Obsessions, 10, 13–14, 125–131, 240, 284,
292, 303–305
Obsessive compulsive cognitions working
group, 131–132t
Obsessive-compulsive disorder (OCD), 3–4,
8–16, 22, 26, 40, 55–56, 61, 68–
70, 73, 125, 126, 232, 235–241,
276, 284–285, 292–293, 303–307,
346, 366
case study, 125–126
392
Obsessive-compulsive disorder (OCD) (cont.)
CBT strategies, 130
comorbidities, 127
diagnostic challenges, 128
mood disorders, 128
related beliefs, 132t
symptoms, 127
treatment, 130–139
treatment failures, 125–130
treatment response, 132
Obsessive-compulsive personality disorder
(OCPD), 128, 135
OCD, see Obsessive-compulsive disorder
(OCD)
O’Connor, K., 130
O’Connor, M., 23, 312
OC- or OCD-spectrum disorders, 129
OCPD, see Obsessive-compulsive personality
disorder (OCPD)
ODD, see Oppositional-defiant disorder
(ODD)
Oei, T., 161
Oest, L. -G., 214, 219
O’Flaherty, A. S., 36
O’Grady, B., 334
O’Grady, J., 258
O’Hearn, T., 9
Öhman, A., 211
Okazaki, S., 91
Olafsson, R. P., 215
Oldridge, N., 327
O’Leary, K. M., 70, 172–173
Olfson, M., 331
Ollendick, T. H., 7, 51, 348
Olmsted, M. P., 294
O’Malley, A. J., 322
O’Neil, P. M., 292
Oomen, J., 115
Oppositional-defiant disorder (ODD), 348,
352–353
Orloff, L. M., 235
Ormel, J., 317
Orr, S. P., 35
Orsillo, S. M., 25, 160, 194, 204, 293
Ortega, A. N., 90
Orvaschel, H., 348, 357
Osborn, M., 258
Osborn, R. L., 322
O’Shea, M., 113, 254–255
Osofsky, S., 322
Öst, L-G., 25, 150, 214–215, 218, 234, 237
O’Sullivan, M. J., 85
Index
Otto, M. W., 3–4, 31–45, 51–62, 67–77,
103–120, 180, 186, 221, 231–245,
255, 318, 336
Ouimette, P. C., 274
Outcome expectancies, pre/duringtreatment, 57
Overbeek, T., 232
Overeating/purging behavior, 297
P
Pabico, R. R., 193
Padesky, C. A., 135
Padula, M. A., 55
Paewai, M. K., 91–92
Page, A. C., 43
Pahlman, L., 320
Pakes, J. R., 322
Palacios-Boix, J., 274
Palomba, D., 218
Panic attacks, 10–11, 17–19, 67, 103, 108,
113–114, 116, 152–153, 212, 217,
231, 239–240, 274, 285, 331–332,
335–336
disability (fainting or going crazy), 104
hypochondriasis, 104
impending death (heart attack or stroke),
104
loss of control (inability to escape), 104
Panic cycle, 104, 116
Panic disorders (PD), 3–4, 11–14, 17, 19,
21, 23, 25, 32, 41, 60, 68–73, 76,
103–120, 127–128, 186, 211–212,
216, 231–234, 237, 239–240,
242, 244, 254–258, 272, 275–276,
292–293, 312, 326, 329, 332–335,
347, 366
Panic-free rates, 112
Panic-related distress, 115
Parasympathetic deficiency, 191
Parent–child (dis)agreement, 363–365
Parenting construct
low warmth/criticism, 357
overprotection/control, 357
warmth and control, 358–359
Park, E., 321
Parker, B. T., 284
Parker, P. A., 320
Park, J. M., 216
Pasnau, R. O., 322
Pasternak, R. C., 326
Paulauskas, S. L., 349
Pauli, P., 209, 220
Paulson, A., 283
Index
Paunovic, N., 150, 237
Payne, L. L., 40
Payton, D. S., 55
PBQ, see Personality belief questionnaire
(PBQ)
PD, see Panic disorders (PD)
PDA, see PD with agoraphobia (PDA)
PD, avoiding treatment failures, 103–120
addressing inadequate treatment response,
116–119
assessment, 117
avoiding treatment, interventions, 117
noncompliance behavior, 117
re-evaluation of core fears, 117
troubleshooting non-response to CBT,
118t
alcohol/substance use/treatment resistance,
114–115
prevalence rate, 114
anxiety sensitivity, 103
cognitive-behavioral model of PD, 105f
comorbid anxiety disorders/treatment
resistance, 113–114
case example, 113–114
CBT treatment strategies, 113
comorbid social phobia, 113
physiological distress, 113
primary/secondary disorder, 113
re-designing exposures, 113
social phobia/specific phobia, 113
standard disorder-specific exposure
interventions, 113
core elements of treatment, 105–107
cognitive restructuring efforts, 105
cognitive safety strategy, 107
core interventions for PD, 105
grading of exposures, 107
hierarchy of agoraphobic situations, 106
internal sensations (induced), 105–106
key elements of exposure, 107f
psychoeducation, 105
“safety behaviors,” 106
from Smits and Otto (in press), 106f
depression comorbidity/treatment
resistance, 112
clinical impairment pretreatment, 112
factors affecting, 112
efficacy of CBT treatment, 111–112
cognitive behavior therapy, 111
cost-efficacy and effectiveness, 112
panic-free rates, 112
quality of life improvement, 111
format of treatment, 108
393
mastery of your anxiety and panic, 108
interoceptive exposure, 108
case study, 109–111
graded exposures, 110
hyperventilation, 108
patient (P), 108
situational exposures, 110
therapist (T), 108
life stressors, 116
relationship conflicts, 116
short-term/long-term benefits of
treatment, 116
medical factors, 116
medical illnesses/side effects, 116
respiratory disorders/cardiac
conditions, 116
medication treatments, 119
non-essential elements of treatment,
107–108
cognitive behavioral treatments, 107
panic attacks, 103
personality disorders and treatment
resistance, 115
axis II disorder, 115
axis I pathology, 115
DBT, 115
panic-related distress, 115
self-injurious behaviors, 115
target (frequently avoidant) behaviors,
115
psychosocial treatments, 119
cluster C personality symptoms, 119
emotion-focused psychotherapy, 119
manualized psychoanalytical
psychotherapy, 119
stress/vulnerability factor, 103
PDQ-R, see Personality diagnostic
questionnaire-revised (PDQ-R)
PD with agoraphobia (PDA), 103–104, 108,
114, 273
Pearson, M. G., 332
Peck, C. A., 35, 43
Pederson, P. B., 85
Peindl, K. S., 127
Penava, S. J., 68, 73, 111
Pepping, G., 13
Perdereau, F., 292
Perel, J. M., 68
Perrin, S., 348
Perry, K. J., 175
Personality belief questionnaire (PBQ),
259, 261
394
Personality diagnostic questionnaire-revised
(PDQ-R), 259
Personality disorders, 10, 20, 24, 58, 61, 89,
115, 125, 128–129, 135, 170, 175,
187, 252–264
and anxiety disorders, comorbidity,
254–256
evaluation (axis II), 10
nature, 252–254
cluster A, 252
cluster B, 252
cluster C, 252
Personality pathology, 115, 118t, 187, 199, 259
Persons, J. B., 8–9, 11, 13, 24, 152, 219, 257,
269, 303
Pervasive or personality conditions, 10
Peters, H., 274
Peterson, C. B., 294
Peterson, J., 210
Peterson, P. D., 85
Peterson, R., 321
Peterson, R. A., 90
Peveler, R. C., 23, 312
Pfohl, B., 259
Pharmacological/psychological placebo
treatments, 181
Pharmacotherapy (drugs in patient care),
67–69, 75–77, 111, 172–173
CBT as strategy for discontinuation of,
72–73
Phobias, 3–4, 209–222, 361
APA, 209
core elements of CBT, 214–216
cognitive preparation or psychoeducation, 214–215
fear cues, exposure to, 215
spider phobia, 215–216
factors interfere with exposure success, 216
anticipation is worse than exposure, 219
enhancing memory of success, 221
lightheadedness/fainting, 218
multiple phobias, 217
patients use cognitive avoidance during
exposure, 219–220
self-report is not predictive of emotional
processing, 220–221
shame (fear), 218
skill deficits accompany the phobia,
218–219
treatment engagement, 216–217
unpleasant emotions/sensations come
into play, 217–218
vigilance to threat, 220
Index
heart rate (HR)/self-reported fear, 213f
simple phobias, situations, 209
treatment complications, 209–222
African-American individuals, 210
blood/injury/injection (BII), 209
diagnosis and comorbidity, 211–212
discrete subtypes of specific
phobias, 209
dysfunctional avoidance, 211
efficacy of exposure, 212–214
empirical data, 210
evolutionary relevant fear cues, 211
gold standard for therapy, 212
prevalence rates, ethnicity, 210
traumatic experience, 210
two-factor model, 211
vicarious learning, 210
Photos, V. I., 260
Physical or sexual abuse, 54
Physiological distress, 113
Piacentini, J. C., 360
Piantadosi, S., 320
Picardi, A., 60–61, 72
Pietrowsky, R., 133
Pigott, T. A., 134
Pilgrim, H., 233
Pilkington, K., 325
Pillay, H., 42
Pina, A. A., 364
Pina, D., 364
Pinard, G., 132
Pincus, A. L., 185
Pincus, D. P., 347
Pincus, H. A., 274
Pine, D. S., 331
Pineno, O., 31
Pinto, A., 128
Pirl, W., 321
Placebo pill, 59
Plamondon, J., 112, 234
PMR, see Progressive muscle relaxation
(PMR)
Podd, J. V., 219
Poli, P., 349
Pollack, M. H., 68, 70, 73, 75, 105, 111–112,
116, 186, 232, 234, 237, 255, 257
Pollard, C., 128
Pollard, C. A., 22, 26
Posternak, M. A., 160
Postpartum psychotic symptoms, 129
Posttraumatic stress disorder (PTSD), 3–4, 14,
16, 23–24, 33, 53–54, 60–61, 68,
73, 113, 128–129, 135, 147–148,
Index
232, 236–237, 240, 255, 273, 276,
280–281, 283, 292–293, 312, 347
Post-treatment expectancies and attributions,
59–61
Potts, H., 189
Poulton, R., 211
Powers, M. B., 4, 31–45, 59, 61, 67, 71–72, 77,
119, 212, 219, 221, 238, 293, 298
Powers, P. S., 291, 298
Pratt, E. M., 4, 291–313
Precipitants of illness, cognitive behavioral,
17–19
cognitive restructuring techniques, 18
psychoeducation component, 18
Preisig, M., 274
Prescott, C. A., 210
Preston, G. C., 36
Pre-therapy intervention, 95
Prevalence rate, 84–85, 103, 113–116, 210,
272, 292
Price, J. H., 72
Prien, R. F., 70
Prieto, J. M., 320
Primary diagnosis
anxiety disorders, challenges, 12
complications, 11
Prinstein, M. J., 258, 260
PRISM, see Psychiatric research interview
for substance and mental disorders
(PRISM)
Prochaska, J. O., 22, 279
Prognostic expectations, see Outcome
expectancies, pre/during-treatment
Programs for escaping danger, see Cognitive
fear networks
Progressive muscle relaxation (PMR), 25, 107,
191–192, 356
Prolonged exposure therapy, 148, 154
Psychiatric research interview for substance
and mental disorders (PRISM), 277,
284–285
Psychoanalytic theory, 52
Psychodynamic therapy, 21, 52, 119
Psychoeducation, 18, 105, 108, 113, 118,
118t, 126, 154, 159, 214–215, 242,
280, 283, 285, 301, 322, 354, 356,
360, 362
Psychological assessment, 84, 91–92
Psychological disorders, ethnic/racial
minorities, 84–85
issue, 85
surgeon general reports, ethnic
minorities, 83
395
Psychological flexibility, 25
Psychological interventions, 60, 86–87,
172–175, 254
for asthma, 334
for cancer, 322
Cochrane Collaboration, 328
for coronary heart disease, 327–328
Psychological placebo condition, 59–60
Psychopathology, 20, 32, 67, 70, 85, 89, 175,
278, 300, 357, 360, 364
Psychosocial and environmental factors, 10
Psychosocial history, social anxiety disorder,
169–170
Psychotherapy, 7, 20, 22–23, 54, 56–61, 74, 83,
87, 119, 125, 130, 172, 215, 257,
302, 322–323, 328–329, 334, 337
interpersonal, 54
transference-focused, 54
PTSD, see Posttraumatic stress disorder
(PTSD)
PTSD, avoiding treatment failures, 147–164
approach to guide treatment
case formulation, 153–154
CBT/PTSD implementation, challenges,
150–152
clinician barriers, 151
“concerns and misconceptions,” 151
exposure therapy, multiple contraindications, 150–151
patient barriers, 151
poor treatment outcome, 151
PTSD symptoms, 151
respondents complications, 151
trauma-focused interventions, 152
trauma survivors, 152
treatment results, 151
core components of PTSD treatment,
149–150
ameliorating symptoms, 150
CBT treatment programs, 149
cognitive-behavioral models, 149
cognitive fear networks, 149
cognitive restructuring, 149
trauma survivors, 149
in vivo exposure/cognitive therapy, 150
troubleshooting, strategies and tools,
154–164
exposure therapy, examining emotions,
162–164
facilitating affect regulation, 159–160
handling multiple trauma memories,
154–156
influence of other emotions, 156–159
396
PTSD, avoiding treatment failures (cont.)
psychosocial crises management,
160–161
SUDs, 161–162
PTSD-related anger symptoms, 54
Pulmonary function tests, 335
Pumariega, A. J., 85
Putnam, F. W., 54
Q
Quintana, S. M., 94
Quitkin, F. M., 274
R
Rabavilas, A. D., 40
Rabian, B., 90
Rabinowitz, J., 274
Rachmann, S., 174
Radomsky, A. S., 135, 213, 220
Rae, D. S., 210, 272
Rafanelli, C., 104
Ralevski, E., 255
Ramnerö, J., 237
Randall, C. L., 217, 275
Rapee, R. N., 8, 12, 103, 172, 176, 186, 211,
232, 349–350, 357– 359, 365
Rasmussen, S. A., 127–128, 134
Rauch, S. A., 158
Rauch, S. L., 35
Rauch, S. L. M. D., 127
Raue, P. J., 53–54
Rausch, L. L., 333
Ravaris, C. L., 73
Readiness intervention (RI), 56
Readiness treatment, 22
Reddy, Y., 134
Redeker, N. S., 321
Rees, C. S., 133
Reese, H. E., 4, 35, 61, 67–77, 318
Rees, K., 328
Re-experiencing symptoms, 151, 155, 158, 161
Reich, J. H., 115
Reich, T., 128
Reid, J. C., 353
Reiger, D. A., 272
Reinhardt-Rutland, A. H., 220
Relaxation and acceptance, difficulties with,
24–25
Relaxation-induced anxiety (RIA), 192
Relaxation training, 3, 38, 191–192, 212,
216, 328
complication, 192
diaphragmatic breathing, 191
parasympathetic deficiency, 191
Index
PMR, 191
sympathetic activation, 191
Renneberg, B., 175
Rentz, T. O., 42, 219–220
Resick, P. A., 149–150, 158, 160, 163, 232,
236–237
Resolving treatment complications, 91,
258–264
addressing complications, additional, 263
axis I disorder, personality disorders in
context of treating, 262
case formulation, 261
culturally appropriate
psychological assessment, 91–92
treatment adaptations, 92–96
personality disorders, assessment, 258
self-injurious thoughts/behaviors (SITB),
assessment, 258
structured clinical interview for DSM-IV
axis II disorders, 258
target behaviors in treatment, ordering
of, 261
Ressler, K. J., 77, 140, 221
Reynolds, C. F., 4, 157
Reynolds, K., 271–286
Reznikoff, M., 59
Rheaume, J., 127
RI, see Readiness intervention (RI)
RIA, see Relaxation-induced anxiety (RIA)
Rice, D. R., 3
Richards, C., 349
Richardson, J., 325
Richardson, L., 331
Richter, M. A., 127
Ricker, S. T., 35
Rief, W., 75, 234
Ries, L., 320
Rifkin, A., 274
Riggs, D. S., 149– 151, 157, 159, 161, 237, 283
Rigid thinking, information processing biases
and, 25–26
Rimington, L. D., 332
Rinck, M., 220
Ring, C., 327
Ristvedt, S. L., 320
Ritter, B., 213
Ritz, T., 332
Rizvi, S. L., 294
Roane, H. S., 193
Roberts, C., 348
Roberts, J. S., 275
Roberts, R. E., 90
Robichaud, M., 218
Index
Robillard, S., 130
Robins, L. N., 128, 273
Rodriguez, B. I., 220
Rodriguez, M., 35, 85
Roemer, L., 23, 25, 55, 159, 194, 197, 204
Rogers, C. R., 52
Rohsenow, D. J., 283
Role expectancies, 56
Rollnick, S., 7, 22, 55
Romano, R., 349
Romero, A. J., 90
Ronchi, P., 127
Ronquillo, J. G., 127
Rosa-Alcázar, A. I., 235, 237
Ros, E., 328
Rosenbaum, J. F., 73, 111, 232
Rosen, C. S., 148
Rosengard, C., 35
Rosengren, A., 326
Rosenheck, R., 90
Rosenheck, R. A., 292
Rosen, M. I., 275
Rosenthal, M. Z., 284
Rose, S., 156
Ross, C. J., 334
Ross, D. C., 214
Rothbaum, B. O., 42, 77, 149, 221,
237, 283
Roth, W. T., 175–176, 209, 212
Round, C. E., 324
Rounsaville, B., 277
Rounsaville, B. J., 277
Rowan-Szal, G. A., 279
Rowe, M. K., 34, 41–42
Rowles, J. R., 321
Roy-Byrne, P. P., 74, 108, 112, 232, 334
Rozanski, A., 326
Rubak, S., 55
Rubin, K. H., 357
Rudd, M. D., 260
Ruffin, R. E., 333
Ruggiero, J., 321
Ruggiero, K. J., 244
Ruiz, J., 326
Rumbak, M. J., 332
Rumbaut, R. G., 89
Rumpold, G., 327
Rusch, M. D., 158
Ruscio, A. M., 185, 323
Ruscio, J., 253
Rush, A. J., 153
Russell, G. L., 94
Rutherford, E., 26
397
Ryan, H., 322
Ryan, S. M., 357
S
Saab, P. G., 326
Saavedra, L. M., 273, 350
Sabatino, S. A., 234
Sachs, G. S., 257
Sackville, T., 237
SAD, see Social anxiety disorder (SAD)
Saez-Santiago, E., 83, 87–88, 95
Safety behaviors, 36–40, 106–108, 110, 114,
117, 119, 174, 179, 220, 310
avoiding treatment failures in social anxiety
disorder, 40
understanding exposure cues/contexts, 39
Safran, J. D., 61
Safren, S. A., 112, 233, 317–337
Salkovskis, P., 131
Salkovskis, P. M., 104, 131, 214, 218
Salters-Pedneault, K., 194
Salzman, C., 13
Samar, R., 134
Samuels, J., 128
Sánchez-Meca, J., 235
Sandboek, A., 55
Sander, J. B., 351
Sanders, C., 77, 221
Sanderson, W., 216, 255–257
Sanderson, W. C., 187
Sandin, D. J., 42
Sano, N., 220
Sanson-Fisher, R. W., 322
Santiago, H. T., 73, 111
Santos de Barona, M., 88
Sareen, J., 317
Sarlo, M., 218
SASII, see Suicide attempt self-injury
interview (SASII)
Sasson, Y., 135
Saviotti, F. M., 104
Savolainen, N. J., 322
SCD, see Self-control desensitization (SCD)
Scepkowski, L., 169, 171, 175, 310
Schaap, C. P. D. R., 232
Schachtman, T. R., 34
Schafer, A., 133
Scharron-del-Rio, M. R., 83
Schatzberg, A. F., 272
Schema questionnaire (SQ), 259, 261
Schizophrenia, 84, 92
Schizotypal personality disorder, 135
Schlossberg, M. C., 357, 360
Schmaling, K. B., 332, 335
398
Schmidt, N. B., 38, 73, 103, 107–108, 111, 283
Schnicke, M. K., 149–150, 237
Schniering, C. A., 350
Schnurr, P. P., 150–151
Schnyder, U., 56–57
Scholing, A., 175, 234–235, 360
Schreier, A. M., 321
Schroeder-Hartwig, K., 176
Schruers, K., 232
Schruers, K. R., 332
Schuckit, M. A., 275
Schulberg, H. C., 239
Schul, D., 232
Schulte, D., 13
Schulzinger, D., 283
Schut, A. J., 52, 129
Schwalberg, M. D., 292
Schwartz, S. A., 127
SCID, see Structured clinical interview for
DSM-IV (SCID)
SCL, see Symptom checklist (SCL)
Scuito, G., 127
Segal, S. R., 269
Segrin, C., 350
Seivewright, H., 186
Selar, D. A., 84
Selby, P. J., 321
Selective serotonin reuptake inhibitor (SSRI),
68– 70, 73, 125
Self-control desensitization (SCD), 193, 197
Self-efficacy theory, 71
Self-injurious behaviors, 115, 260–261
Self-monitoring, 189–192, 194, 300–301, 311
chronic worriers, 189
non-adaptive awareness step, 189
Self-reported anxiety, 186, 332
Self, T. H., 332
Seligman, L. D., 348
Seligman, M. E. P., 211
Sell, R., 209, 213, 219, 221
Selwyn, A., 325, 329
Separation anxiety disorder, 347, 349, 353,
355, 360–361
Serotonergic reuptake inhibitions (SRIs), 130
Shaffer, D., 364
Shafran, R., 131, 174, 216, 299
Shahar, A., 135
Shapiro, J. P., 59
Shapiro, L. J., 134
Shapiro, S. J., 56
Shapiro, T., 320
Sharp, T. J., 153
Shaw, B. F., 153
Index
Shea, M. T., 113
Sheard, T., 322
Shearer, D. K., 156
Shear, K., 111
Shear, M. K., 61, 71, 111, 157, 234
Shea, S., 254–255
Shedler, J., 253, 259
Shedler-Westen assessment procedure, 259
Sheikh, J. I., 13, 113
Shen, Y. -C., 210
Sherbourne, C. D., 317
Sher, K. J., 272
Sherman, A. R., 42
Shirk, S. R., 53
Shuldham, C. M., 53
Shuman, A. L., 59
Shwartz, M., 277
Siddique, M. I., 333
Siembab, L., 269
Sigman, M., 358, 360
Sijsenaar, M., 214
Silva, P. A., 349
Silverman, W. K., 90, 347, 350, 364
Simmonds, S., 186
Simon, G. E., 326
Simple phobias, 209, 221
Simpson, D., 279
Simpson, D. D., 279
Siqueland, L., 358
Sirey, J. A., 70
Situational exposures, 110, 351
Sjoden, P. O., 320
Skaer, T. L., 84
Skeketee, G., 112
“ Skip-out” condition, 294
SL, see Supportive listening (SL)
Slagle, D. M., 55
Sloan, T., 220
Smeraldi, E., 127
Smith, E. M., 321
Smith, J. E., 326, 333
Smith, M., 294
Smith, T., 325
Smits, J. A. J., 3–4, 31–45, 53, 59, 61, 67–77,
106, 119, 217, 219, 221
Smoller, J. W., 68
Smucker, M. R., 156, 158
Snaith, P. R., 321
Snowden, L. R., 85, 87, 94
Snyder, C. R., 56
Social anxiety disorder (SAD), 3–4, 31–34, 37,
37f, 40, 68–70, 104, 113–114, 127,
169–177, 218, 232–235, 237–238,
Index
242–244, 251–252, 254–257,
263, 272, 276, 347, 349, 351,
360–361, 366
avoiding treatment failures, 33, 40, 169
case study, 169–172
conceptualization, 170–172
diagnostic information, 170
psychosocial history, 169–170
treatment in social phobia/anxiety
inventory, 171f
character, 32
common sticking-points in therapy/core
elements of treatment, 176–180
challenging cognitive errors, 178
eliminating avoidance behaviors,
179–180
motivation for therapy, 177–178
flexibility for dealing with challenging
cases, 180–181
potential predictors, 175–176
depression, 176
generalized subtype/avoidant
personality disorder, 175
social skills, 176
psychological interventions, 172–175
Beckian CBT model, 172
cognitive processes, 173
factors of social anxiety disorder, 174f
Foa’s treatment (efficacy rates), 173
Heimberg’s CBT protocol, 173
pharmacotherapy, 172
psychotherapy placebo condition, 172
target disorder-specific factors, 173
“traditional” CBT approaches, 173
safety behaviors, 179
“social mishap,” 34
Social phobia, 8, 11–16, 23, 113, 153,
169–172, 176, 235, 292–293,
308–312, 347
Social phobia and anxiety inventory (SPAI),
171
Social Phobic Disorders, 173
Socratic method, 178, 197
Sommerfield, C., 233
Sonnega, A., 161, 273
Sonne, J., 60
Sookman, D., 132, 140
Sorlie, P. D., 85
Soroudi, N., 336
Sorrell, J. T., 13
Southam-Gerow, M., 360
Southwick, S. M., 293
Southworth, S., 215
399
SPAI, see Social phobia and anxiety inventory
(SPAI)
Sparrow, D., 326
Spates, C., 214
Spaulding, S., 232
Specific phobias, subtypes, 206
animal type, 206
BII type, 206
natural environment, 206
situational type, 206
see also Phobias
Spence, S. H., 347, 360
Sperry, J. A., 284
Sperry, L., 323
Spertus, J. A., 327
Spider phobia, 211, 215, 220
Spiegel, D. A., 73
Spinhoven, P., 21, 54, 155, 332–333
Spitzer, R. L., 62, 277
Spivak, M. Y., 331
SRIs, see Serotonergic reuptake inhibitions
(SRIs)
SSRI, see Selective serotonin reuptake
inhibitor (SSRI)
Stafford, R. S., 70
Staghezza, B. M., 353
Standard worry control treatment protocol, 14
Stang, P., 176
Stang, P. E., 317
Stanley, M. A., 13, 129, 171
Stark, D., 320–321
Stark, D. P., 320
Stark, K. D., 351
Steer, R. A., 347
Stefanis, C., 40
Stegagno, L., 218
Steinberg, L., 358
Stein, D. J., 68
Stein, M. B., 176, 317, 334
Steketee, G., 8, 56, 75, 128–129, 131–135,
220, 234–235
Steketee, G. S., 40, 131, 306
Stepper, S., 43
Steptoe, A., 332
Sterk, P. J., 332–333
Sterner, U., 218
Stern, R., 40, 42, 216
Stern, R. S., 69
Stern, T. A., 326
Stevens, D. E., 274
Stewart, A., 133
Stewart, B. L., 186
Stewart, J. W., 236
400
Stewart, S. H., 272
Stice, E., 294
Stigmatization, 86
Stimulus control treatments, 193–194
insomnia, 193
variations, 194
worry-free zones, 194
worry time, 194
Stimulus properties (imaginal/in vivo/virtual
reality), 42
Stinson, F. S., 210–211, 217, 272
Stith, S., 87
Stockdale, S. E., 87
Stopa, L., 176
Story, K. T., 321
Stout, R. L., 274
Stovall-McClough, K. C., 54, 161
Strack, F., 43
Strasser, F., 324
Strauss, C. C., 348–349, 353
Strauss, J. L., 61
Stravynski, A., 176
Street, G. P., 151, 235
Stridh, B. M., 215
Striegel-Moore, R. H., 292
Strik, J. J., 327
Strine, T. W., 333
Strosahl, K., 204
Strosahl, K. D., 25, 238
Structured clinical interview for DSM-IV
(SCID), 61, 156, 175, 259, 277, 292
Stuart, G. L., 112, 234
Stunkard, A. J., 298
Styan, G., 293
Suarez, A., 260–261
Suarez, E. C., 326
Subjective units of distress (SUD), 42, 213,
271–272, 279, 280
Substance use disorders (SUDs), 4, 41, 114,
161–162, 271–286
SUD, see Subjective units of distress (SUD)
SUDs, see Substance use disorders (SUDs)
Sue, D. W., 85
Suelzer, M., 68
Sue, S., 85, 87, 89, 93–95
Sugarman, A., 364
Suicide attempt self-injury interview (SASII),
260
Sullivan, G. M., 68
Sullivan, M. D., 327
Suls, J., 326
Summerfeldt, L. J., 127
Supportive listening (SL), 200
Index
Suvak, M., 237
Swartz, H. A., 20
Swavely, S., 274
Swendsen, J. D., 274
Swinson, R. P., 60, 72, 127, 217, 220
Symonds, B. D., 53
Symptom checklist (SCL), 277
T
T, see Therapist (T)
Takeda, M., 103
Takeuchi, D. T., 91
Tanaka-Matsumi, J., 93–94
Tancer, M. E., 175
Tangney, J. P., 157
Tang, T. Z., 53
Tannenbaum, L., 221
Target (frequently avoidant) behaviors, 115,
261–263
Tarrier, N., 150, 233, 236, 238
Taylor, A. A., 366
Taylor, C. B., 175
Taylor, C. T., 26
Taylor, J. E., 219
Taylor, R. R., 323– 325
Taylor, S., 68, 112, 158, 232, 236–237
Taylor, S. E., 14
Teachman, B. A., 4, 7–27, 213
Teitelbaum, L. M., 276
Telch, C., 302
Telch, C. F., 294
Telch, M. J., 38, 42–43, 59, 72, 108, 111, 212,
217, 219–220, 232
Temel, J., 321
Tennen, H., 277
Terrell, F., 86
Thayer, J. F., 191
Thefeld, W., 331
Thelen, M., 294
Thennarasu, K., 134
Theobald, D. E., 321
Therapeutic alliance and factors, 51–62
changing expectancies, 59
concept of, 51–62
factor, 52
empirical support, 52–55
patient expectancies, 57–59
therapeutic alliance, 52–55
motivation for treatment, 55–56
nonspecific/common treatment factors, 51
outcome expectancies, 57
post-treatment expectancies and
attributions, 59–61
Index
role expectancies, 56
specific treatment factors, 51
treatment adherence, 61–62
Therapist (T), 108
Therapy-interfering behaviors, 9, 139
Thevos, A. K., 275
Thewissen, R., 221
Thielking, P. D., 321
Thomason, T. C., 84, 87
Thomas, S. E., 275
Thomas, S. F., 320
Thompson, C. E., 93
Thompson, V. L., 86–88, 93
Thomson, A., 321
Thordarson, D. S., 133, 213
Thorpe, S. J., 214
Thorp, S. R., 13
Thrasher, S., 150, 237
Thulin, U., 237
TIBs, see Treatment-interfering behaviors
(TIBs)
Tierney, K. J., 220
Tiesema, M., 158
Tishk, L., 193
Todorov, C., 130
Toelle, B. G., 334
Tokuyama, M., 103
Tolerance of uncertainty, 185, 218
Tolin, D. F., 55–56, 77, 134, 140
Tompkins, M. A., 8, 11, 13, 152, 303
Tourette’s disorder, 129
Tovt-Korshynska, M. I., 331
Townsley, R. M., 175
Trakowski, J. H., 111
Tran, G. Q., 57, 112, 133, 176, 234–235
Transdiagnostic CBT model of EDs, 306, 310
Transference-focused psychotherapy, 54
Transtheoretical model of change (TTM),
22, 279
Trauma-Related Guilt Inventory (TRGI), 156
Treatment adherence/integrity, 61–62
Treatment coach (parents), 360
Treatment complications, 7
add or change treatment strategies, case
formulation, 20–26
difficulties with relaxation and
acceptance, 24–25
emotion regulation difficulties, 23–24
information processing biases and rigid
thinking, 25–26
interpersonal problems, 23
lack of motivation or difficulty with
follow-through, 22
401
low self-efficacy and losing treatment
gains, 26
clinical decision-making, 7
motivational interviewing, 7
psychotherapy case formulation, 7
using cognitive behavioral, 8–19
five-axis DSM diagnoses, 10
hypotheses, mechanisms maintaining
disorder, 15–17
individualize formulation, 14–15
nomothetic formulation, 12–14
precipitants of illness, 17–19
primary diagnosis, 11–12
problem list, 8–10
using different modalities, 20–21
Treatment complications, case formulation
approach
cognitive behavioral
five-axis DSM diagnoses, 10
individualize the formulation, 14–15
nomothetic formulation, 12–14
precipitants of illness, 17–19
primary diagnosis, 11–12
problem list, 8–10
different modalities of case formulation,
20–21
difficulties with relaxation and acceptance,
24–25
emotion regulation difficulties, 23–24
hypotheses about basis of mechanisms
maintaining disorder, 15–17
information processing biases and rigid
thinking, 25–26
interpersonal problems, 22
lack of motivation or difficulty with
follow-through, 22
low self-efficacy and losing treatment
gains, 26
Treatment complications, comorbid depression
CBT for anxiety disorders on depression
symptoms, impact, 237
comorbid anxiety/depression, treatment
considerations, 239
comorbid depression, impact of, 232
panic disorder, 233
PTSD, 236
social anxiety disorder, 234
treatment outcome literature, 236
Treatment complications, personality disorders
complications associated, 256–258
personality disorders
anxiety disorders, comorbidity,
254–256
402
Treatment complications, personality (cont.)
nature, 252–254
resolving treatment complications,
258–264
see also PD, avoiding treatment failures
Treatment complications, problem list, 8–10
CBT strategies, 9
school/occupational functioning, 9
Treatment expectancies, see Outcome
expectancies, pre/during-treatment
Treatment guidance for PTSD
case formulation, 153–154
dialectical behavior therapy, 154
examining evidence-based formulations, 153
factors affecting, 153
hopelessness, 154
problem list, 153
prolonged exposure therapy, 154
psychoeducation, 154
treatment planning, 153
Treatment-interfering behaviors (TIBs), 22
Treatment, OCD, 130–139
BT, 130
CBT strategies, 130
CT, 131
treatment delivery, challenges, 135
treatment non-response, predictors, 133
treatment response, 132
Treatment, recommendations from assessment
case illustrations
presenting problem of heroin
dependence, 285
presenting problem of obsessive
compulsive disorder, 284
combining stand-alone treatments for
anxiety disorders and SUDs
issues with treating both disorders
simultaneously, 281
issues with treating one disorder at a
time, 281
treating one disorder in prognosis of
other disorder, benefits, 282
integrative treatments, specialized, 282
anxiety sensitivity treatment for heroin
users, 283
concurrent treatment of PTSD and
cocaine dependence, 283
seeking safety, 283
willingness to change
maintenance, 280
precontemplation and contemplation,
280
Index
preparation and action, 280
Treatment resistance/relapse, learning theory
perspectives, 31
context effects, 34
exposure parameters, considering, 40
attention/behavior during extinction,
focus of, 43
duration/spacing, 40
fear activation, 43
gradation of exposure, 42
sessions, distribution of, 41
stimulus properties (imaginal/in
vivo/virtual reality), 42
learning perspectives on treatment
resistance and relapse, 44f
new learning, exposure, 31
safety behaviors, 37
Treat, T. A., 234
TRGI, see Trauma-Related Guilt Inventory
(TRGI)
Tricyclic antidepressants, 68
Trinkaus, K. M., 320
Troubleshooting, tools/strategies, 154–164
exposure therapy, examining emotions,
162–164
advantage and disadvantage to initiate
exposure, 163
emotional engagement, 162
“flash back,”, 164
interoceptive exposure exercises, 163
losing control of emotions, 163
over-engaged patients, 163
self-reported emotional arousal, 163
steps to titrate anxiety, 163
facilitating affect regulation, 159–160
acceptance and commitment
therapy, 160
complicate exposure therapy, 160
dialectical behavior therapy, 160
effective therapy relationship, 160
poor affect-regulation skills, 160
trauma-focused therapies, 159
trauma survivors, emotion-regulation
skills, 159
handling multiple trauma memories,
154–156
distressing memories, 155
less distressing events, 155
painful event, 155
re-experiencing symptoms, 155
standardized self-report measure, 155
symptoms relating to more than one
memory, 154–155
Index
veterans affairs medical center, 155
influence of other emotions, 156–159
anger, 158
overcoming guilt, shame, and anger,
158–159
sadness, 156–157
shame and guilt, 157–158
psychosocial crises management, 160–161
emotional or pragmatic crises, 160
pre-treatment functioning, 161
session attendance or homework
compliance, 160
targeting symptoms, 160
substance use disorders (SUDs), 161–162
abstinence, 162
assessment information, 161
higher rates of PTSD, 161
sobriety, 162
trauma-focused treatment, 162
treatment approaches, 162
Trull, T. J., 253
Tsao, J. C. I., 41, 111, 113, 237, 312
Tsao, M. N., 322
Tsuang, M. T., 127
Tsujimoto, R. N., 60
TTM, see Transtheoretical model of change
(TTM)
Tull, M. T., 159, 269–284
Turk, C. L., 200, 204
Turk, D., 331
Turner, R. J., 273
Turner, R. M., 40
Turner, S., 357, 359
Turner, S. M., 129, 171, 175, 232, 234, 347
Twohig, M. P., 25, 284
Tyrer, P., 186–187
U
Uccello, R., 232
Udin, H., 239
Uhde, T. W., 175
Uhl, G., 211
Ultee, K. A., 42
Unger, D. L., 156
U.S. Department of Health and Human
Services (USDHHS), 83–89, 94
USDHHS, see U.S.Department of Health and
Human Services (USDHHS)
Usherwood, T., 334
V
VA health care providers, 148
Vamos, M., 73, 111, 237, 333
Van Ameringen, M., 293
403
Van Balkom, A. J., 130, 133
Van Balkom, A. J. L. M., 21
Van Beek, N., 332
Van Blakom, A. J., 130, 133
Van den Bergh, O., 43
Van den Brink, R. H. S., 186
Van den Hout, M., 115
Van der Does, A. J., 332–333
Van der Sleen, J., 176
VanDoren, T., 128
Van Dyck, R., 21, 54
VanDyke, M. M., 22, 26
Van Etten, M. L., 68
Van Oppen, P., 133
Van Peski-Oosterbaan, A. S., 332–333
Vansteenwegen, D., 34–36, 221
Van Velzen, C. J., 234
Van Velzen, C. J. M., 175
Varela, E. R., 90
Varra, A. A., 25
Vasey, M., 73, 111
Vasile, R. G., 115
Vega, W. A., 89
Velikova, G., 321
Velting, O. N., 348
Verbraak, M. J. P. M., 73
Verduin, T. L., 348–349, 353
Vermetten, E., 232
Vernon, L. L., 35, 71
Versiani, M., 68
Vervliet, B., 4, 31–45, 221
Virtual reality exposure treatment (VRET), 42
Visser, S., 133
Vitousek, K., 302
Vivekananda-Schmidt, P., 200
Vlaeyen, J. W. S., 57
Vokonas, P. S., 326
Volkow, N. D., 274
Von Mutius, E., 331
VRET, see Virtual reality exposure treatment
(VRET)
W
Wade, W. A., 112, 234
Wagner, A., 260
Wagner, A. R., 42–43
Wagner, A. W., 284
Wagner, P., 157
WAI, see Working Alliance Inventory (WAI)
Waitlist (WL), 56
control condition, 59
Walker, J. R., 68
Walker, R. L., 260
404
Wallace, S. T., 176
Walters, E. E., 3, 176, 210, 317
Waltz, J., 61
Wampold, B. E., 93
Wang, P. S., 260
Wang, Y., 263
Warman, D. M., 242
Warshaw, M., 186
Warwick, H. M., 104
Wasteson, E., 320
Watanabe, A., 103
Watanabe, N., 69, 111
Watkins, K. E., 274, 282
Watkins, L. L., 327
Watson, D., 350
Watson, J. P., 42
Watson, M., 321
Watson, S., 302
Watson, S. B., 157
Watts, F. N., 26
Weaver, T. L., 150, 160, 232
Weber, G., 26
Wedig, M. M., 260
Weems, C. F., 350, 364
Weilburg, J. B., 70
Weinmann, S., 320
Weis, J. M., 56
Weiss, B., 364
Weiss, D. S., 61
Weissman, M. M., 23, 127, 210
Weiss, R. D., 283
Weisz, J. R., 364
Well-done social performance, 34
Wells, A., 8, 12, 32, 37, 174, 204
Wells, K. B., 87, 317
Welner, A., 128
Wender, A., 176
Wesner, R. B., 112, 234
Wessels, H., 42
Westbrook, R. F., 35
Westen, D., 145, 253, 259
Westermann, R., 173
Westin, L., 327
Westlake, S. K., 322
West, R., 328
Westra, H. A., 22, 56, 58, 242
Wetherell, J. L., 13
Whaley, A. L., 93
Whaley, S. E., 358–359
White, C., 175
White, C. A., 323–324, 330
White, J., 189
“White knuckled,” (through anxiety), 113
Index
Whitley, D., 38, 59, 72
Whitney, S. L., 218
Whittaker, A., 86
Whittal, M., 299
Whittal, M. L., 73, 112, 133
Widiger, T. A., 20
Wiegartz, P. S., 127
Wik, G., 210
Wilfley, D., 302
Wilfley, D. E., 302
Wilhelm, F. H., 209
Wilhelm, S., 77, 125–140
Wilkinson, L., 193
Wilkins, W., 51
Willems, L. N., 332–333
Williams, J. B., 62
Williams, J. B. W., 277
Williams, J. M. G., 26
Williams, S. A., 321
Williams, S. M., 349
Wilson, G. T., 14, 297–299, 302–303, 312
Wilson, J. K., 232
Wilson, K. A., 135
Wilson, K. G., 25, 204, 238
Wilson, L. L., 87
Wilson, R., 42
Wincze, J. P., 42
Winegar, R. K., 293
Wise, B. K., 85
Wisner, K. L., 127
Wittchen, H. U., 113, 176, 210
WL, see Waitlist (WL)
Wlazlo, Z., 176
Wolfe, B. E., 52
Wolff, P. L., 232
Wolf, M., 215
Wolitzky, K. B., 43
Wolitzky-Taylor, K. B., 212– 215
Wollaway-Bickel, K., 73, 111
Wollersheim, J. P., 132
Wolpe, J., 212
Wolpin, M., 43
Wonderlich, S. A., 292, 294
Wood, J. J., 358, 360–361, 365
Woodruff-Borden, J., 358
Woods, A. M., 31
Woods, C. M., 56
Woods, S. W., 61, 71, 111, 234
Woody, G. E., 277
Woody, S., 9, 11, 13, 112, 217, 232, 237
Woody, S. R., 173
Working Alliance Inventory (WAI), 53
“Worry-free zone” techniques, 113, 194
Index
Worry, theoretical conceptualization of,
187–188
avoidance theory, GAD, 187
cognitive, 188
motoric, 188
inhibitory effect, 188
Worry time, 118t, 194
Worthington, R., 93
Worth, J. L., 336
Wright, L. R., 366
X
Xie, H., 269
Xu, J. Q., 320
Y
Yale-Brown Obsessive Compulsive Scale
(YBOCS), 129, 133, 134
Yamamoto, J., 95
Yamas, K., 200
Yancy, M. B., 351
Yap, L., 68, 186, 237
Yarczower, M., 151
Yaryura-Tobias, J. A., 127–128
YBOCS, see Yale-Brown Obsessive
Compulsive Scale (YBOCS)
Yeager, K. K., 307
Yeh, M., 93–94, 364
Yonkers, K. A., 103, 186–187
Yorke, J., 334
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405
Young, J. E., 261
Young, K., 87
Young, K. A. D., 156
Yule, W., 176
Yusuf, S., 326
Z
Zabora, J., 320
Zajonc, R. B., 43
Zalewski, M., 193
Zammit, S., 274
Zane, N., 87, 88, 90, 94
Zayas, L. H., 88, 89
Zayfert, C., 4, 147–164, 291–313
Zhang, A. Y., 85
Zhang, N., 93
Zhao, S., 113
Zigterman, D., 350
Zilski, J., 34
Zimand, E., 221
Zimmerli, W. D., 191
Zimmerman, L., 321
Zimmerman, M., 160, 259
Zinbarg, R. E., 35, 129
Zlotnick, C., 258, 283
Zoellner, L. A., 151–152
Zucker, B. G., 73, 111, 237, 312
Zuellig, A. R., 188
Zvolensky, M. J., 103, 284