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Library of Congress Cataloging-in-Publication Data
Names: Storch, Eric A., editor. | Abramowitz, Jonathan S., editor. | McKay, Dean, 1966– editor.
Title: Complexities in obsessive-compulsive and related disorders : advances in conceptualization and treatment / [edited by] Eric A. Storch, Jonathan S. Abramowitz, and Dean McKay.
Description: New York, NY : Oxford University Press, [2022] | Includes bibliographical references and index.
Identifiers: LCCN 2021016363 (print) | LCCN 2021016364 (ebook) | ISBN 9780190052775 (hardback) | ISBN 9780190052799 (epub) | ISBN 9780190052805
Subjects: LCSH: Compulsive behavior. | Obsessive-compulsive disorder.
Classification: LCC RC533 .C658 2022 (print) | LCC RC533 (ebook) | DDC 616.85/227—dc23
LC record available at https://lccn.loc.gov/2021016363
LC ebook record available at https://lccn.loc.gov/2021016364
DOI: 10.1093/med-psych/9780190052775.001.0001
9 8 7 6 5 4 3 2 1
Printed by Integrated Books International, United States of America
To Ellie, Noah, Maya, and Jill for their love and being life co-pilots. EAS
To Stacy, Emily, and Miriam with all my love. JA
To my loving wife Dawn, and our wonderful daughter Rebecca. DM
CONTENTS
Contributors ix
1. Introduction: What Is Obsessive-Compulsive Disorder? What Is Not? And Why This Book? 1
Jonathan S. Abramowitz, Dean McKay, and Eric A. Storch
2. Body Dysmorphic Disorder 15
Sophie C. Schneider, Amita Jassi, Lauren Peile, D. Luis Ordaz, and Eric A. Storch
3. Hair-Pulling Disorder 32
Kara N. Kelley, Devin Dattolico, Caroline Strang, and Martha J. Falkenstein
4. Excoriation Disorder 44
Hae-Joon Kim, Kelsey L. Luks, Ana Rabasco, Justyna Jurska, and Margaret Andover
5. Hoarding Disorder 63
Blaise Worden and David F. Tolin
6. Misophonia: An Obsessive-Compulsive Disorder? 87
Lisa Clark and Dean McKay
7. Orthorexia Nervosa and the Use of Exposure and Response Prevention to Treat Eating-Related Obsessions and Compulsions 103
Hana F. Zickgraf
8. Sensory Processing and Intolerance in Obsessive-Compulsive Disorder 125
Katherine A. Collins, Stephanie J. Grimaldi, and Emily R. Stern
9. Incompleteness, Not Just Right Experiences, and Reward Sensitivity in Obsessive-Compulsive Disorder 142
Charlene Minaya and Dean McKay
10. The Hunt for “Perfect” Jolly Green (Cannabis): Examining the Complex Relationship Between Obsessive-Compulsive Disorder and Substance Use 155
Charlene Minaya and Dean McKay
11. Stress, Trauma, and Obsessive-Compulsive and Related Disorders 173
Jennifer Forte, Christal L. Badour, C. Alex Brake, Jordyn M. Tipsword, and Thomas G. Adams, Jr.
12. Tourette’s Disorder 201
Kesley Ramsey and Joseph F. McGuire
13. Pediatric Acute-Onset Neuropsychiatric Syndrome: Diagnostic and Therapeutic Considerations with Abrupt-Onset ObsessiveCompulsive Disorder 231
Kirti Saxena, Sherin Kurian, Johanna Saxena, and Eyal Muscal
14. Perinatal and Postpartum Obsessive-Compulsive Disorder 249
Nichole Fairbrother, Fiona L. Challacombe, Fanie Collardeau, and Thanh Thuy Truong
15. The Inhibitory Learning Approach to Exposure and Response Prevention for Obsessive-Compulsive Disorder 270
Samantha N. Hellberg, Heidi J. Ojalehto, Jennifer L. Buchholz, and Jonathan S. Abramowitz
16. Childhood Obsessive-Compulsive and Related Disorders 285
Andrew G. Guzick, Sophie C. Schneider, and Eric A. Storch
17. Technology-Based Psychotherapies for Obsessive-Compulsive Disorder 311
Terri L. Fletcher, Anthony H. Ecker, Derrecka M. Boykin, Darius B. Dawson, Fenan Rassu, and Natalie E. Hundt
18. Co-occurrence of Obsessive-Compulsive Disorder and Autism Spectrum Disorder: Differentiation, Assessment, and Treatment 332
Saashi A. Bedford, Michelle Hunsche, and Connor M. Kerns
19. Acceptance and Commitment Therapy for Obsessive-Compulsive and Related Disorders 352
Jennifer Krafft, Julie M. Petersen, and Michael P. Twohig
20. Couple-Based Cognitive-Behavioral Therapy for Obsessive-Compulsive Disorder 370
Jennifer L. Buchholz, Jonathan S. Abramowitz, Samantha N. Hellberg, and Heidi J. Ojalehto
21. Advances in Treating Obsessive-Compulsive Related Disorders Other than OCD? 384
Abel S. Mathew, Ivar Snorrason, Martha J. Falkenstein, and Han-Joo Lee
22. Distress Tolerance 407
Shannon M. Blakey and Megan K. Lanier
23. Prevention of Obsessive-Compulsive Disorder 424
Shiu F. Wong, John H. Riskind, and Frederick Aardema
Index 443
Natalie E. Hundt, PhD
Michael E. DeBakey VA Medical Center
Michelle Hunsche, MA University of British Columbia
Amita Jassi, BSc, DClinPsy
South London and Maudsley NHS Trust
Justyna Jurska, MA Fordham University
Kara N. Kelley, BA American University
Connor M. Kerns, PhD University of British Columbia
Hae-Joon Kim, MA Fordham University
Jennifer Krafft, MS Utah State University
Sherin Kurian, PhD Baylor College of Medicine
Megan K. Lanier, BS Duke University
Han-Joo Lee, PhD University of Wisconsin-Milwaukee
Kelsey L. Luks, MS Fordham University
Abel S. Mathew, MS University of Wisconsin-Milwaukee
Joseph F. McGuire, PhD Johns Hopkins University School of Medicine
Dean McKay, PhD Fordham University
Charlene Minaya, BA Fordham University
Eyal Muscal, MD, MS Baylor College of Medicine
Heidi J. Ojalehto, BS University of North Carolina at Chapel Hill
D. Luis Ordaz, PhD
Baylor College of Medicine
Lauren Peile, DClinPsych, BSc (Hons) Psychology
South London and Maudsley NHS Trust
Julie M. Petersen, MS Utah State University
Ana Rabasco, MA Fordham University
Kesley Ramsey, PhD Johns Hopkins University School of Medicine
Fenan Rassu, PhD Johns Hopkins University School of Medicine
John H. Riskind, PhD George Mason University
Johanna Saxena, BS, BA Baylor College of Medicine
Kirti Saxena, MD
Baylor College of Medicine
Sophie C. Schneider, PhD Baylor College of Medicine
Ivar Snorrason, PhD Massachusetts General Hospital
Emily R. Stern, PhD
New York University School of Medicine
Eric A. Storch, PhD
Baylor College of Medicine
Caroline Strang, PhD Scripps College
Jordyn M. Tipsword, MS University of Kentucky
David F. Tolin, PhD
The Institute of Living
Thanh Thuy Truong, MD
Baylor College of Medicine
Michael P. Twohig, PhD
Utah State University
Shiu F. Wong, PhD Concordia University
Blaise Worden, PhD Institute of Living/Hartford Hospital
Hana F. Zickgraf, PhD University of South Alabama
Frederick Aardema, PhD University of Montreal
Jonathan S. Abramowitz, PhD UNC-Chapel Hill
Thomas G. Adams, Jr., PhD University of Kentucky
Margaret Andover, PhD Fordham University
Christal L. Badour, PhD University of Kentucky
Saashi A. Bedford, MSc University of British Columbia
Shannon M. Blakey, PhD Durham VA Health Care System
Derrecka M. Boykin, PhD Baylor College of Medicine
C. Alex Brake, PhD
Warren Alpert Medical School of Brown University
Jennifer L. Buchholz, MA
University of North Carolina at Chapel Hill
Fiona L. Challacombe, PhD, DClinPsy King’s College London
Lisa Clark, BS Fordham University
CONTRIBUTORS
Fanie Collardeau, MSc, PhD
Candidate
University of Victoria
Katherine A. Collins, MSW, PhD
Nathan S. Kline Institute for Psychiatric Research
Devin Dattolico, BS McLean Hospital
Darius B. Dawson, PhD
Baylor College of Medicine
Anthony H. Ecker, PhD
Baylor College of Medicine
Nichole Fairbrother, PhD University of British Columbia
Martha J. Falkenstein, PhD McLean Hospital/Harvard Medical School
Terri L. Fletcher, PhD Baylor College of Medicine
Jennifer Forte, BA Binghamton University
Stephanie J. Grimaldi, MA Hofstra University
Andrew G. Guzick, PhD Baylor College of Medicine
Samantha N. Hellberg, BA UNC Chapel Hill
What Is Obsessive-Compulsive Disorder? What Is Not? And
Why
This Book?
JONATHAN S. ABRAMOWITZ, DEAN MCKAY, AND ERIC A. STORCH ■
Obsessive-compulsive disorder (OCD) was once considered a rare and untreatable condition (Kringlen, 1965). Over the past half-century, however, a dramatic surge in clinical research has led not only to a clearer understanding of this problem but also to the realization that it is fairly common, afflicting up to about 3% of the population (i.e., Adam et al., 2012; Ruscio et al., 2010). Further, research has shown that those with OCD have high rates of disability and occupational and social role dysfunction (Markarian et al., 2010). When the prevalence and functional impairment are considered together with the anxiety and distress that individuals with OCD experience, one recognizes that this condition represents a significant public health concern. With this in mind, the present volume focuses on advances and emerging clinical implications in the field of OCD and related disorders with respect to assessment, treatment, treatment augmentation, and basic science.
WHAT IS OCD?
OCD is classified in the DSM-5 (American Psychiatric Association, 2013) as an obsessive-compulsive and related disorder (OCRD) and characterized by obsessions or compulsions. Obsessions are persistent intrusive thoughts, ideas, images, or doubts that are experienced as senseless or unacceptable (e.g., the idea that one could murder loved ones in their sleep). Such intrusions evoke subjective distress
in the form of fear, doubt, or guilt and are not simply everyday worries about work, relationships, or finances. Although highly person-specific, obsessions usually focus on the following general themes: aggression and violence, responsibility for harm or mistakes, contamination, sex, religion, the need for exactness or completeness, and concerns about serious illnesses. Most people with OCD report multiple types of obsessions.
Because individuals with OCD perceive their obsessions as unpleasant and unwanted, they attempt to control these thoughts (and reduce the associated distress) by avoiding trigger stimuli (e.g., knives, in the case of violence-related obsessions). If such stimuli cannot be avoided, the person might perform compulsive rituals—behavioral or mental acts that are completed according to self-generated “rules.” These rituals are deliberate, yet senseless or excessive in relation to the obsessional fear they aim to neutralize (e.g., checking the roadway for 30 minutes to be sure one hasn’t hit a pedestrian without realizing it). As with obsessions, rituals are highly individualized. Common rituals include excessive washing and cleaning, checking, seeking reassurance, counting, and repeating routine actions (e.g., going through doorways). Rituals can also be covert, such as excessive prayer and using “good” words or phrases to neutralize “bad” thoughts (e.g., thinking a happy thought to “undo” the effect of number 13). A hallmark of OCD is therefore that obsessions and compulsions are functionally related: Obsessions provoke subjective distress, and rituals are performed to reduce this distress.
Individuals with OCD display a range of insight into the senselessness of their symptoms: Some acknowledge the irrationality of their obsessions and compulsions, and others are firmly convinced that these symptoms are realistic. Often, the degree of insight varies across time and obsessional themes. For example, one person might recognize her obsessional thoughts of harm as senseless yet have poor insight into the irrationality of her contamination obsessions.
PREVALENCE, COURSE, ASSOCIATED FEATURES, AND TREATMENT
The lifetime prevalence of OCD in the general adult population is between 2% and 3% (e.g., Kessler et al., 2005). Symptoms typically develop gradually, often beginning in childhood; a noteworthy exception is the abrupt onset sometimes observed during the perinatal period (e.g., Fairbrother & Abramowitz, 2007). Left untreated, OCD usually follows a chronic course with waxing and waning symptoms over time, often dependent upon levels of stress (e.g., Skoog & Skoog, 1999). Most people with OCD also suffer from depressive and anxiety symptoms, which can exacerbate obsessional problems and attenuate response to treatment (e.g., Abramowitz & Foa, 2000).
OCD as an Anxiety Disorder
Through DSM- IV- TR, OCD was considered an anxiety disorder along with social and specific phobias, panic disorder and agoraphobia, posttraumatic stress disorder (PTSD), and generalized anxiety disorder (GAD). Indeed, at a descriptive level, OCD symptoms are similar to the main features of these conditions: excessive and irrational fear, apprehension, and avoidance behavior. Although not mentioned in DSM, “rituals” such as checking for safety (in PTSD), asking for reassurance (in GAD), and seeking repeated medical evaluations (in panic disorder) also appear in both OCD and the anxiety disorders. But OCD and the anxiety disorders are also all maintained by the same psychological mechanisms involving (a) overestimates of the likelihood and severity of threat and (b) escape and avoidance behaviors that reduce anxiety in the short term but prevent long- term fear extinction. Moreover, these conditions all respond to a specific intervention that promotes fear extinction— exposure therapy (Abramowitz, Deacon, & Whiteside, 2011; Barlow, 2004).
OCD in the DSM-5
Some of the DSM-5 architects, however, felt that OCD was incorrectly classified as an anxiety disorder because it bears even greater similarity to disorders— including hoarding, trichotillomania, body dysmorphic disorder (BDD), and compulsive skin picking—that appear to share “compulsive behavior and failures in behavioral inhibition” (Fineberg et al., 2011, p. 21). These authors (e.g., Fineberg et al., 2011; Hollander et al., 2005) provided the following arguments for moving OCD out of the anxiety disorders and creating the new OCRD classification in DSM-5:
(a) The distinguishing features of OCD and the other OCRDs are repetitive thoughts and behaviors and a failure of behavior inhibition,
(b) OCD and the OCRDs overlap in demographic features such as their age of onset, comorbidity, and family loading,
(c) OCD and the OCRDs share brain circuitry and neurotransmitter abnormalities, and
(d) OCD and the OCRDs share similar treatment response profiles.
This shift has implications for how clinicians and scientists understand, treat, and study OCD and the other OCRDs. Thus, it is worth taking a closer look at these arguments.
Repetitive Thoughts and Behaviors Are Distinguishing Features of OCD and the OCRDs
The DSM-5 labels OCD and the other OCRDs as “characterized by preoccupations and by repetitive behaviors or mental acts in response to the preoccupations” and “recurrent body-focused repetitive behaviors (e.g., hair pulling, skin picking) and repeated attempts to decrease or stop the behaviors” (American Psychiatric Association, 2013, p. 235). Thus, the unifying factor among the OCRDs appears to be repetitive thoughts and behaviors that the person cannot stop.
To be sure, the OCRDs have repetitive thinking and/or repetitive behavior in common. But such a description of the form of observable signs and symptoms is only one way to think about how mental health problems may relate to one another. Another perspective focuses on the function of the repetitive behavior. In OCD, repetitive rituals are performed in response to obsessional thoughts that are misinterpreted as danger signals. Rituals thus function as a “safety behaviors” in that they provide a temporary escape from distress and are negatively reinforced. This is an important mechanism by which OCD is maintained. But is it present in the other OCRDs?
The answer is generally not. Hair pulling disorder (HPD) and skin picking disorder (SPD) are characterized by repetitive behavior, yet these behaviors are distinct from rituals in OCD. First, there are no obsessional fears in HPD and SPD; thus there is no safety behavior function. Second, urges to pull and pick are precipitated by feelings of general tension, depression, anger, boredom, frustration, indecision, or fatigue (Diefenbach et al., 2002), and the behavior leads to pleasurable feelings (Grant & Potenza, 2004; Schreiber et al., 2011), which is not observed with rituals in OCD (Stanley et al., 1992). Even the excessive acquisition behavior in hoarding disorder—if one could call this repetitive—is not motivated by intrusive obsessive fears but rather by beliefs about the potential usefulness of possessions and other exaggerated cognitions about loss or sentimentality. Moreover, excessive saving does not result in an escape from obsessional anxiety in the way that OCD rituals do and thus cannot be conceptualized as “compulsive” or “ritualistic” in the OCD sense. BDD, on the other hand, is the one OCRD that does conform to the OCD functional template. As with obsessions, the appearance-related preoccupations in BDD are intrusive and anxiety-provoking; and as with rituals in OCD, the repetitive checking and other appearance-related behaviors in BDD have an anxiety-reduction function (Phillips et al., 2010).
The logical and scientific problem with grouping the OCRDs together on the basis of the mere presence of repetitive behaviors and thoughts is easy to spot if we consider the following absurdity:
• Vomiting is a symptom of bulimia nervosa.
• Vomiting is a symptom of salmonella poisoning.
• Therefore, bulimia and salmonella poisoning are part of the same family of disorders.
Obviously bulimia and salmonella are not related, and we would not put them in the same diagnostic class. It is similarly easy to see how, however, from this perspective, repetitive hair pulling and skin picking could end up seeming as if they are related to OCD. On the other hand, a functional approach provides better resolution and reveals that of the OCRDs, only BDD actually “works” like OCD. Moreover, both OCD and BDD are more similar to anxiety disorders than to the other OCRDs. Both respond to a similar treatment (exposure and response prevention [ERP]) that is based on this functional perspective. From this viewpoint, skin picking and hair pulling operate quite differently from OCD, BDD, and anxiety disorders and also respond to different treatment approaches, as we will discuss later in this chapter.
The OCRDs Overlap in Terms of Their Demographic Features
Age of Onset
Although OCD may begin at any age, it has a mean age of onset in early adulthood (e.g., Anholt et al., 2014; Antony et al., 1998). The other OCRDs also typically have their onset in adolescence through early adulthood and follow similar courses (e.g., Bjornsson et al., 2013; Flessner et al., 2010; Grisham et al., 2006; Odlaug & Grant, 2012; Wilhelm et al., 1999). Yet similarity in age of onset and course is not a persuasive argument for grouping DSM disorders together: Indeed, most mood, anxiety, somatic symptom, dissociative, sexual, sleep, personality, substancerelated, psychotic, and eating disorders also begin during this time of life! Thus, the fact that the OCRDs share these nonspecific characteristics does not indicate the presence of a unique relationship.
Comorbidity
Are the OCRDs highly comorbid with one another, and is this a compelling reason to group them together? Again, the answer is “no” to both questions. Studies fail to support the claim of high comorbidity; Bienvenu et al. (2000), for example, found that while the comorbidity rate between OCD and BDD was 15%, it was only 4% with HPD. Other studies have reported largely similar results (Jaisoorya et al., 2003; Lovato et al., 2012), suggesting that other than BDD, the OCRDs are quite uncommon among people with OCD. Interestingly, 13% of OCD patients meet criteria for GAD, 20.8% for panic disorder, 16.7% for agoraphobia, 36% for social phobia, and 30.7% for specific phobias (Nestadt et al., 2001). Thus, using the DSM- 5 committee’s own reasoning, OCD is 5- to 10- fold more closely related to the anxiety disorders than to most of the OCRDs!
There’s also a logical problem with using comorbidity to group disorders into categories: Comorbidity does not indicate etiologically meaningful relationships among disorders. Substance use disorders and PTSD, for example, are highly comorbid (Kramer et al., 2014), yet they are not part of the same diagnostic category. Similarly, at least half of OCD sufferers also meet criteria for depression, yet this does not mean depression should be part of the OCRDs.
Family Patterns
Proponents of the OCRD approach assert that if OCRDs occur frequently in relatives of people with OCD, then such disorders share a common genetic etiology. Research, however, does not support this claim. Bienvenu et al. (2000), for example, found that the lifetime prevalence of HPD in first-degree relatives of adults with OCD was only 1%. In contrast, the rates of anxiety disorders among first-degree relatives of people with OCD are far higher than the rates of OCRDs among relatives of OCD sufferers (e.g., Bienvenu et al., 2000; Nestadt et al., 2001). So, the assertion that familial pattern represents a valid basis for grouping together the OCRDs again more strongly supports the notion that OCD should be grouped with the anxiety disorders.
The OCRDs Have Overlapping Neurobiological Etiologies
Brain Structure and Function
Neuroimaging studies sometimes (but not always) find that individuals with and without OCD show differences in variables related to brain structure and function (for a review and consensus statement see Bandelow et al., 2016). Much less brain imaging research, however, has been conducted with the other OCRDs, yet the few comparisons to healthy control groups also show some differences (e.g., Buchanan et al., 2013; Chamberlain et al., 2008; Grant et al., 2013; Mataix‐Cols et al., 2011). OCRD proponents interpret these findings to suggest a common causal brain abnormality or deficit across the OCRDs (e.g., Fineberg et al., 2011). Examination of the evidence (and logic), however, indicates no basis for such causal inferences, or for using brain imaging studies as a basis for grouping the OCRDs together.
An important limitation of most brain imaging studies is that they are correlational and therefore can merely detect associations between an OCRD diagnosis and brain structure or function. But one cannot infer the presence of abnormalities from such studies any more than one could infer that, say, an association between anorexia nervosa and being female means that being female is abnormal. That is, just because a variable is correlated with the symptoms of a mental disorder does not imply this variable indicates an “abnormality” with etiological significance. It is equally plausible that the observed differences in brain structure and function between OCRDs and controls are the result of having an OCRD, or that OCRDs and the observed differences in brain-related variables are caused by other variables.
It’s important to point out that although brain imaging is an important tool for studying brain–behavior relationships, brain scans are not snapshots of the brain’s real-time functioning (Roskies, 2007). Rather, they are highly processed representations of the brain’s activities. Thus, whereas the conclusion that people with OCRDs show enhanced activation in the basal ganglia relative to controls accurately characterizes the brain imaging data, statements such as the abnormally high activity shows that OCD is a disorder of the basal ganglia go beyond the data. Despite three decades of brain imaging studies, there have been no major advances in determining the causes of OCD (Bandelow et al., 2016, 2017).
Neurotransmitters
The most consistent (yet still overstated) neurobiological finding in OCD is that medication using serotonin reuptake inhibitors (SRIs; e.g., fluoxetine, sertraline) can be effective (Greist et al., 1995). This, and a small literature comparing serotonergic and non-serotonergic processes in OCD patients (Insel et al., 1985), led to the “serotonin hypothesis” that OCD is caused by abnormalities in the serotonergic system (Barr et al., 1993; Zohar et al., 2004). Yet it is a logical error to use the effectiveness of SRIs to infer that an abnormally functioning serotonin system is the cause of OCD/OCRDs. For one thing, the serotonin hypothesis was derived from the effectiveness of serotonin medications (making the argument circular). It also is an example of “reasoning backward from what helps,” a logical error exemplified by the following: “When I take aspirin, my toothache goes away; therefore the toothache was caused by abnormally low aspirin levels.”
Neurotransmitter models of OCRDs could be supported by evidence from experimental studies showing differences in serotonin functioning between individuals with and without OCD, or by studies in which neurotransmitters are manipulated leading to increased symptom expression. Yet despite a considerable amount of energy (and money) devoted to biological marker and challenge studies in OCD, there are no consistent findings (Bandelow et al., 2017; Barr et al., 1993; Koo et al., 2010; Zohar et al., 2004). A further problem is that virtually no neurotransmitter research has been conducted on OCRDs other than OCD.
There is no doubt that the signs and symptoms of the OCRDs involve the brain and neurotransmitter systems at some level. Yet evidence that OCRDs are caused by abnormally functioning systems is absent. Therefore, the appeal to a common neurobiological etiology as a basis for grouping the OCRDs is unjustified.
OCD and the OCRDs Share Similar Treatment
Response Profiles
Treatment response is a pivotal test of the OCRD category’s validity since effective treatment is the ultimate goal of identifying and classifying mental disorders. The DSM- 5 claims there is “clinical utility” (p. 235) in grouping OCRDs together because they respond preferentially to SRIs. This argument, however, is only useful in delineating a class of OCRDs if three conditions
are met: (a) preferential response to SRIs is observed uniformly among the OCRDs, (b) preferential response to SRIs is only observed among the OCRDs, and (c) SRIs are the best treatment for the OCRDs. We consider these conditions next.
Is There a Uniform Response to SRIs Across the OCRDs?
Numerous placebo-controlled studies indicate the efficacy of SRIs for OCD (Eddy et al., 2004; Greist et al., 1995) and BDD (Phillips et al., 2002). Yet SRI response in the other OCRDs is inconsistent. Bloch et al. (2007) found that SRIs were generally no more effective than placebo in the treatment of HPD, and patients with hoarding disorder were about 50% less likely than those with OCD to respond to SRIs (Bloch et al., 2014). Only two placebo-controlled studies have been published for SPD, one showing significant reduction with fluoxetine on only one of three outcome measures (Simeon et al., 1997), and the other finding that citalopram was no more effective than placebo (Arbabi et al., 2008). The only conclusion that can be drawn from these data is that the OCRDs do not show a uniform response to SRIs.
Is a Preferential Response to SRIs Only Observed Among the OCRDs?
The previous problem aside, numerous controlled studies show that SRIs are efficacious in the treatment of unipolar depressive disorders (e.g., Fournier et al., 2010; Schatzberg & Nemeroff, 2013) and anxiety disorders such as social anxiety disorder (Hedges et al., 2007). Thus, because SRIs help numerous conditions, even if the OCRDs all responded preferentially to these agents (which they don’t), it would not call for grouping these disorders together based on SRI response.
Are SRIs the Best Treatment for OCRDs?
A meta-analysis of 13 randomized controlled trials directly comparing SRIs and cognitive-behavioral therapy (CBT) (mainly using ERP) for OCD revealed that CBT is at least as effective (if not more so) than SRIs (Romanelli et al., 2014). No studies to date have compared SRIs with CBT in an exclusively hoarding disorder sample. In BDD, although larger effect sizes and more consistently positive findings are reported in studies of CBT (usually ERP) compared to those evaluating SRIs, there are no direct comparison studies (Ipser et al., 2009; Williams et al., 2006). Similarly, the skin-picking treatment literature indicates greater consistency in response to CBT (e.g., habit reversal training) than to SRIs (e.g., Grant et al., 2012), although there are as yet no direct comparison studies. Finally, in HPD, Bloch et al.’s (2007) meta-analysis revealed that habit reversal training had a larger effect size on hair-pulling symptoms than did SRIs. Thus, research suggests that SRIs are not the most effective treatment for any of the OCRDs.
The scientific evidence suggests CBT is at least as effective as SRIs across the OCRDs. A noteworthy aspect of CBT interventions apparently overlooked by the DSM-5 is that these treatments are derived from specific models of psychopathology that have a sound empirical basis. The use of ERP for OCD and BDD, for example, originated from experimental research demonstrating that these conditions are characterized by conditioned fear that is maintained by anxietyreduction strategies that impede long-term fear extinction (e.g., Rachman & Hodgson, 1980; Veale & Riley, 2001)—which happen to be the same processes that maintain the anxiety disorders (e.g., Barlow, 2004). The use of habit reversal training for SPD and HPD is also guided by research on the function of these behaviors and their controlling variables (e.g., Grant et al., 2012). This is in contrast to SRI medications, which were discovered serendipitously and which gave rise to (circular) theories about serotonin (which have also turned out to be invalid), primarily on the basis of treatment response (Whitaker, 2011). All of this leaves pharmacotherapy response of little value in classifying mental disorders, whereas response to CBT—because it targets specific processes—has a better chance of helping to identify useful boundaries and classes of disorders. Thus, if we consider CBT response as a litmus test of the OCRD approach, the only conclusion to be drawn is that whereas OCD and BDD overlap and could be considered “related,” hoarding disorder, HPD, and SPD would not fit into the same category. Moreover, OCD and BDD fit best with the anxiety disorders.
WHY THIS BOOK?
The scientific difficulties we’ve noted with the OCRD classification aside, the last decade has witnessed a dramatic surge in research on OCRDs, some of which were understudied. And this has also led to more people seeking help for these and other putatively related problems. We view these consequences as positive outcomes resulting from the OCRD classification. Yet they have come at a price: Many researchers and clinicians assume that because disorders such as HPD, hoarding disorder, and SPD are classified as OCRDs, they have overlapping mechanisms and respond to the same treatments. This, however, is not the case. Moreover, although the DSM-5 is most closely aligned with a medical model in which psychiatric disorders are considered brain diseases that require medication, research on the psychological mechanisms and treatments for these problems has eclipsed any advances in biological approaches—especially when it comes to understanding the nuances and complexities that often present barriers to successfully treating these problems. These fast-moving clinical and research advances set the stage for this book, which aims to bring together state-of-the-art practical implications and research advances under one cover.
The volume is organized into four sections. Chapters in the first section cover the phenomenology and assessment of putative OCRDs (other than OCD) to provide the reader with a comprehensive understanding of psychological mechanisms of these conditions. The second section comprises chapters addressing additional mental and behavioral health problems that remain under-researched yet are often considered related to OCD in one way or another. The focus of the third section is complex presentations of these conditions, including co-occurring problems (e.g., trauma, substance abuse, autism spectrum symptoms) and special populations (e.g., postpartum onset, pediatric acute onset). Finally, section four covers novel applications of existing interventions (e.g., the use of technology, involving a partner in treatment). We believe these various sets of chapters provide unique and up-to-date collections of material to help clinicians and researchers apply psychological approaches to understanding, assessing, and treating a collection of problems that are often misunderstood, misdiagnosed, and mistreated in clinical practice.
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