Exposure Therapy for Children with Anxiety and OCD: Clinician's Guide to Integrated Treatment

Many providers have difficulty implementing exposure-based cognitive behavioral therapy for youth with anxiety and obsessive-compulsive disorder (OCD), despite it being the leading treatment for this condition. Exposure Therapy for Children with Anxiety and OCD: Clinician's Guide to Integrated Treatment provides a step-by-step framework for how providers apply exposure therapy in practice. The book begins with empirical support for the treatment followed by suggested implementation of exposures for specific conditions and ages. Tables of sample exposures and case illustrations are provided throughout the book and common challenges that may complicate implementation are addressed. Intended for busy providers to implement directly into practice, chapters provide clinical excerpts and illustrate techniques in an easy "how-to" format.

• Summarizes empirical support for exposure treatment efficacy
• Recommends how to implement exposure therapy treatment for anxiety and OCD
• Provides guidance on overcoming common challenges when implementing exposures in practice
• Offers separate treatment guidelines for children and adolescents
• Integrates exposure therapy with other therapy modalities
• Includes case studies and clinical excerpts illustrating techniques

• Language: English
• Publisher: Academic Press
• Release date: Jan 11, 2020
• ISBN: 9780128162750

Book preview

States

Preface

Over the last two decades, the treatment literature for child and adolescent anxiety and obsessive-compulsive disorder (OCD) has grown immensely (Comer, Hong, Poznanski, Silva, & Wilson, 2019; Freeman et al., 2018; Higa-McMillan, Nakamura, Morris, Jackson, & Slavin, 2015). Using increasingly rigorous methods, this body of research has cemented the status of cognitive-behavior therapy (CBT) as a well-established treatment for both child and adolescent anxiety and OCD. Moreover, it has begun to examine novel applications (e.g., internet-based delivery; Spence et al., 2011), augmentation (D-Cycloserine for OCD (Storch et al., 2016), and modular intervention strategies (Chorpita & Weisz, 2009) that are meant to expand access to evidence-based care and to optimize clinical outcomes. Yet, as the field continues to evolve, one feature remains constant and that is the emphasis on the role of exposure in treatment.

Exposure is among the most important basic principles in psychology. Dating to the work of Joseph Wolpe in the 1960s, and Mary Cover Jones before him, it has evolved in both theory and practice through decades of study in learning and behavior, clinical intervention, and behavioral neuroscience. Today, exposure is incorporated in virtually every evidence-based protocol for child and adolescent anxiety and OCD (Chorpita, Daleiden, & Weisz, 2005). Significant clinical improvements are observed following its introduction in treatment (Peris et al., 2015), and the technique is viewed widely as the key to successful treatment (Barlow, Gorman, Shear, & Woods, 2000; Bouchard, Mendlowitz, Coles, & Franklin, 2004; Hudson, 2005; Öst, Svensson, Hellström, & Lindwall, 2001; Schniering, Hudson, & Rapee, 2000). Yet as the literature related to exposure has evolved, the guidance for practicing clinicians has not always kept pace.

Our goal in developing this book was to provide up-to-date, empirically informed guidance on best practices for implementing exposure with youth with anxiety and OCD. Despite its central role in treatment for youth anxiety and OCD, technique, we were struck by how few resources exist to guide clinicians in its practical application. Beyond knowing that exposure is the technique one should use when treating anxiety and OCD, there is little to guide clinicians in what it should actually look like in practice. There are few guides that offer practical strategies for maximizing success, tailoring by age, and anticipating and troubleshooting common difficulties that arise. Given that exposure, at the most basic level, involves encouraging young clients to practice and tolerate scary situations, this is no small matter.

The oversight is also unfortunate, given the many recent advances in basic science and experimental research that might inform how these techniques can and should be used in treatment (Craske et al., 2008; Kircanski, Lieberman, & Craske, 2012). Indeed, a growing body of research has examined the mechanisms underlying how we learn to be fearful or distressed and how we unlearn these associations (McGuire et al., 2016). Such work has debunked many of the prevailing theories of how and why exposure tasks work, in turn offering new evidence-based models with direct implications for practicing clinicians (Baker et al., 2010; Culver, Stoyanova, & Craske, 2012; Hayes, 2008; Kircanski et al., 2012; Norton, Hayes-Skelton, & Klenck, 2011). Related work in developmental neuroscience offers further guidance for how we might tailor our approach based on the age of the patient (Pattwell et al., 2016; Schiller, Raio, & Phelps, 2012).

With these advances in mind, we have structured this book to provide both a foundation of understanding about how and why exposure works and the evidence supporting its application and also a users’ guide for treating children of different ages and clinical presentations. The first part of this book provides background information important for all practicing clinicians. As effective implementation is predicated on understanding the principles of learning and behavior that underlie exposure therapy, we begin with a historical overview of the theory guiding exposure practice (Chapter 2: Efficacy of exposure-based cognitive behavioral therapy for youth anxiety and obsessive-compulsive disorder). We then provide an overview of the evidence-base for exposure therapy in treating child and adolescent OCD and anxiety (Chapter 3: Psychoeducation for exposure therapy) and strategies for getting started in treatment, including psychoeducation (Chapter 4: Charting the course of treatment: strategies for developing and optimizing a symptom hierarchy), developing a symptom hierarchy (Chapter 5: Developing and implementing successful exposure-based interventions), and crafting individual exposure exercises (Chapter 6: Exposure therapy for childhood selective mutism: principles, practices, and procedures).

The second part of the book considers how to apply the technique to different disorders. What do you do when your client will not speak to you (as in selective mutism)? How do you develop an exposure for future-oriented concerns where the outcome cannot be assessed immediately (as in generalized anxiety disorder [GAD]-related anxiety about the environment or the economy)? Covering selective mutism (Chapter 7: Exposure therapy for separation anxiety disorder), separation anxiety disorder (Chapter 8: Exposure therapy for specific phobias in children and adolescents), specific phobia (Chapter 9: Exposure therapy for children and adolescents with social anxiety disorder), social phobia (Chapter 10: Exposure therapy for generalized anxiety disorder in children and adolescents), GAD (Chapter 11: Exposure with response prevention for obsessive-compulsive disorder in children and adolescents), and OCD (Chapter 12: Using exposure with young children), this section of the book explicates strategies for designing and implementing exposures across the most common disorders for children and adolescents.

The third section of the book tackles developmental considerations in depth. Focusing on treatment adaptations for very young children (Chapter 13: Using exposure with adolescents and youth adults) and also on those transitioning to adulthood (Chapter 14: Involving family members in exposure therapy for children and adolescents), these chapters guide practitioners in how to individualize treatment and maintain engagement and buy-in. Chapter 15, Transdiagnostic exposure-based intervention for anxiety and depression in children and adolescents provides an overview of how to involve family members in treatment for anxiety and OCD, recognizing that parents are often anxious and highly stressed themselves.

In the final section of the book, we consider adaptations that may be needed for more complex cases. This includes a discussion of the use of exposure in transdiagnostic treatment (Chapter 16: Overcoming challenges in exposure therapy) as well as ACT-enhanced approaches (Chapter 17: Acceptance and commitment therapy–enhanced exposures for children and adolescents) and clinical troubleshooting (Chapter 18).

In undertaking all of this, our goal was to draw on the expertise of leaders in the field of youth anxiety and OCD treatment. We are immensely fortunate and grateful that they so readily agreed to participate, and their work here speaks for itself. As seasoned clinicians ourselves, we were amazed by their clinical wisdom, and by how much we continued to learn from their excellent work and advice in this process. We hope that you, too, find this guide valuable, and that it informs the rewarding, fun, and often challenging work that exposure therapy involves.

References

1. Baker A, Mystkowski J, Culver N, Yi R, Mortazavi A, Craske MG. Does habituation matter? Emotional processing theory and exposure therapy for acrophobia. Behaviour Research and Therapy. 2010;48(11):1139–1143 https://doi.org/10.1016/j.brat.2010.07.009.

2. Barlow DH, Gorman JM, Shear MK, Woods SW. Cognitive-behavioral therapy, imipramine, or their corn or their combination for panic disorder: A randomized controlled trial. Journal of the American Medical Association. 2000;283(19):2529–2536 https://doi.org/10.1001/jama.283.19.2529.

3. Bouchard S, Mendlowitz SL, Coles ME, Franklin M. Considerations in the use of exposure with children. Cognitive and Behavioral Practice. 2004;11(1):56–65 https://doi.org/10.1016/S1077-7229(04)80007-5.

4. Chorpita BF, Daleiden EL, Weisz JR. Identifying and selecting the common elements of evidence based interventions: A distillation and matching model. Mental Health Services Research. 2005;7(1):5–20 https://doi.org/10.1007/s11020-005-1962-6.

5. Chorpita BF, Weisz JR. Modular approach to therapy for children with anxiety, depression, trauma, or conduct problems (MATCH-ADTC). PracticeWise 2009.

6. Comer JS, Hong N, Poznanski B, Silva K, Wilson M. Evidence base update on the treatment of early childhood anxiety and related problems. Journal of Clinical Child and Adolescent Psychology. 2019;48(1):1–15 https://doi.org/10.1080/15374416.2018.1534208.

7. Craske MG, Kircanski K, Zelikowsky M, Mystkowski J, Chowdhury N, Baker A. Optimizing inhibitory learning during exposure therapy. Behaviour Research and Therapy. 2008;46(1):5–27 https://doi.org/10.1016/j.brat.2007.10.003.

8. Culver NC, Stoyanova M, Craske MG. Emotional variability and sustained arousal during exposure. Journal of Behavior Therapy and Experimental Psychiatry. 2012;43(2):787–793 https://doi.org/10.1016/j.jbtep.2011.10.009.

9. Freeman J, Benito K, Herren J, et al. Evidence base update of psychosocial treatments for pediatric obsessive-compulsive disorder: Evaluating, improving, and transporting what works. Journal of Clinical Child and Adolescent Psychology. 2018;47(5):669–698 https://doi.org/10.1080/15374416.2018.1496443.

10. Hayes SC. Climbing our hills: A beginning conversation on the comparison of acceptance and commitment therapy and traditional cognitive behavioral therapy. Clinical Psychology: Science and Practice. 2008;15(4):286–295 https://doi.org/10.1111/j.1468-2850.2008.00139.x.

11. Higa-McMillan CK, Nakamura BJ, Morris A, Jackson DS, Slavin L. Predictors of use of evidence-based practices for children and adolescents in usual care. Administration and Policy in Mental Health and Mental Health Services Research. 2015;42(2):373–383 https://doi.org/10.1007/s10488-014-0578-9.

12. Hudson JL. Efficacy of cognitive-behavioural therapy for children and adolescents with anxiety disorders. Behaviour Change. 2005;3 https://doi.org/10.1375/bech.2005.22.2.55.

13. Kircanski K, Lieberman MD, Craske MG. Feelings into words: Contributions of language to exposure therapy. Psychological Science. 2012;23(10):1086–1091 https://doi.org/10.1177/0956797612443830.

14. McGuire JF, Orr SP, Essoe JKY, McCracken JT, Storch EA, Piacentini J. Extinction learning in childhood anxiety disorders, obsessive compulsive disorder and post-traumatic stress disorder: Implications for treatment. Expert Review of Neurotherapeutics. 2016;16(10):1155–1174 https://doi.org/10.1080/14737175.2016.1199276.

15. Norton PJ, Hayes-Skelton SA, Klenck SC. What happens in session does not stay in session: Changes within exposures predict subsequent improvement and dropout. Journal of Anxiety Disorders. 2011;225(5):654–660 https://doi.org/10.1016/j.janxdis.2011.02.006.

16. Öst LG, Svensson L, Hellström K, Lindwall R. One-session treatment of specific phobias in youths: A randomized clinical trial. Journal of Consulting and Clinical Psychology. 2001;77(3):504–516 https://doi.org/10.1037/0022-006X.69.5.814.

17. Pattwell SS, Liston C, Jing D, et al. Dynamic changes in neural circuitry during adolescence are associated with persistent attenuation of fear memories. Nature Communications. 2016;7:11475 https://doi.org/10.1038/ncomms11475.

18. Peris TS, Compton SN, Kendall PC, et al. Trajectories of change in youth anxiety during cognitive-behavior therapy. Journal of Consulting and Clinical Psychology. 2015;83(2):239–252 https://doi.org/10.1037/a0038402.

19. Schiller D, Raio CM, Phelps EA. Extinction training during the reconsolidation window prevents recovery of fear. Journal of Visualized Experiments 2012; https://doi.org/10.3791/3893.

20. Schniering CA, Hudson JL, Rapee RM. Issues in the diagnosis and assessment of anxiety disorders in children and adolescents. Clinical Psychology Review. 2000;20(4):453–478 https://doi.org/10.1016/S0272-7358(99)00037-9.

21. Spence SH, Donovan CL, March S, et al. A randomized controlled trial of online versus clinic-based CBT for adolescent anxiety. Journal of Consulting and Clinical Psychology. 2011;79(5):629–642 https://doi.org/10.1037/a0024512.

22. Storch EA, Wilhelm S, Sprich S, et al. Efficacy of augmentation of cognitive behavior therapy with weight-adjusted D-cycloserine vs placebo in pediatric obsessive-compulsive disorder: A randomized clinical trial. JAMA Psychiatry. 2016;73(8):779–788 https://doi.org/10.1001/jamapsychiatry.2016.1128.

Section I

Basics of exposure therapy for children and adolescents

Outline

Chapter 1 History and theoretical underpinnings of exposure therapy*

Chapter 2 Efficacy of exposure-based cognitive behavioral therapy for youth anxiety and obsessive-compulsive disorder

Chapter 3 Psychoeducation for exposure therapy

Chapter 4 Charting the course of treatment: strategies for developing and optimizing a symptom hierarchy

Chapter 5 Developing and implementing successful exposure-based interventions

Chapter 1

History and theoretical underpinnings of exposure therapy*

Meghan Vinograd¹ and Michelle G. Craske²,    ¹Department of Psychology, University of California, Los Angeles, CA, United States,    ²Departments of Psychology and Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, United States

Abstract

The practice of exposure therapy has evolved over time in conjunction with shifts in the theory that is used to explain how and why it is effective. The purpose of this chapter is to provide the reader with foundational knowledge of the history and theoretical underpinnings of exposure therapy so as to aid in successful treatment delivery. First, the theory and procedure of systematic desensitization, considered a precursor to modern exposure therapy, are presented. The habituation and inhibitory learning models of exposure therapy are then described. For each, we discuss how theory influences the clinical practice of exposure therapy under the given model. Lastly, we review some of the key considerations for conducting exposure therapy with children and adolescents as related to the inhibitory learning model.

Keywords

Exposure therapy; anxiety; youth; theory

Exposure therapy is an empirically supported treatment for anxiety, posttraumatic stress, and obsessive–compulsive disorders. The Society of Clinical Psychology of the American Psychological Association (APA) designates exposure therapy for specific phobias as having strong research support, indicating that it is a well-established treatment (APA Presidential Task Force on Evidence-Based Practice, 2006). Prolonged exposure for posttraumatic stress disorder and exposure and response prevention for obsessive–compulsive disorder, two forms of exposure therapy, similarly have strong research support per these criteria. In a meta-analysis of 111 treatment outcome studies, exposure was designated as a well-established and first-line treatment for childhood and adolescent anxiety (Higa-McMillan, Francis, Rith-Najarian, & Chorpita, 2016). Exposure has been identified as an essential component of cognitive behavior therapy for successfully treating anxious youth (Kazdin & Weisz, 1998; Kendall et al., 2005). Indeed, in a sample of anxious youth, the introduction of exposure exercises was followed by a significant increase in the rate of progress during subsequent treatment as indexed by measures of anxiety symptom severity and global functioning (Peris et al., 2015). One study found that the percentage of sessions focused on exposures was positively related to improvement in functioning from pre- to post-treatment among youth with anxiety disorders, whereas the use of other anxiety management strategies was negatively related to this improvement (Voort, Svecova, Jacobsen, & Whiteside, 2010). Finally, greater time spent on more difficult exposure exercises during treatment predicted better outcomes in a sample of children and adolescents with anxiety disorders (Peris et al., 2017).

The practice of exposure therapy has evolved over time in conjunction with shifts in the theory that is used to explain how and why it is effective. It has been argued that a clinician’s understanding of the theory that underlies exposure therapy is important in order for the treatment to be most successful (Abramowitz, 2013). The purpose of this chapter is to provide the reader with foundational knowledge of the history and theoretical underpinnings of exposure therapy. First, we review the theory and procedure of systematic desensitization, considered a precursor to modern exposure therapy. Second, we describe the habituation model of exposure therapy. We then present the most recent model of exposure therapy: the inhibitory learning model. For each, we discuss how theory influences the clinical practice of exposure therapy under the given model. Lastly, we review considerations for conducting exposure therapy with children and adolescents as related to current theory.

Systematic desensitization

In the early- to mid-20th century, behaviorism emerged as a contrast to psychoanalytic theory, which until that point was the predominant theoretical framework used for the explanation and treatment of mental disorders. Behaviorists argued the importance of examining overt behavior, rather than unconscious or covert processes. At this time, there was a renewed interest in the principles of Pavlovian conditioning, sometimes referred to as classical conditioning. In Pavlovian conditioning, when a neutral stimulus (known as the conditional stimulus or CS) is repeatedly paired with an aversive stimulus (unconditional stimulus or US), it will come to elicit a conditional response (CR) even in the absence of the US. For example, the presentation of a neutral tone paired with an electric shock will eventually elicit a fear response in the organism, even when the tone is presented without the shock. This procedure is known as fear acquisition. In fear extinction, the repeated presentation of the CS without the US will lead to an eventual decline in the CR. Specifically, extinction is thought to occur when there is a mismatch between the expectancy of an event and its nonoccurrence (Rescorla & Wagner, 1972). Exposure therapy is largely based on the principles of Pavlovian conditioning.

Joseph Wolpe began disseminating systematic desensitization as a treatment for phobias and other types of anxiety in the 1960s, alongside the emergence of behaviorism. The experimental work of Mary Cover Jones decades earlier, however, provided an important empirical basis for systematic desensitization. In a case study of a young child named Peter who had a fear of rats, Jones demonstrated that presenting stimuli that resembled rats (e.g., a fur coat, a rabbit) to Peter while he was eating led to a reduced fear response (1924a, 1924b).¹ The studies of Peter are an illustration of the principle of reciprocal inhibition, on which systematic desensitization is based. Reciprocal inhibition dictates that the pairing of a fear-provoking stimulus with a response that is physiologically incompatible with fear will inhibit the fear response, thereby reducing it (Wolpe, 1968). In her experiments with Peter, Jones used feeding as the response incompatible with fear. Wolpe tested this same technique in cats that had undergone a Pavlovian fear-conditioning procedure. By administering electric shocks to the cats while in their cages, they eventually grew to fear the cage alone. Wolpe then fed the cats while in their cages as a test of reciprocal inhibition, and indeed, the cats eventually demonstrated a reduced fear response (Wolpe, 1952, 1954).

Next, Wolpe began to conduct systematic desensitization with adult human subjects, most of whom had phobias. Wolpe hypothesized that after this procedure, the association between the stimulus and the anxiety response would be weakened, or inhibited, so that encountering the stimulus in vivo would no longer evoke anxiety (1961). Wolpe’s systematic desensitization procedure involved three stages: relaxation training, construction of anxiety hierarchies, and desensitization (1961). In the first stage, patients were trained in deep muscle relaxation, which was to thought to be physiologically incompatible with a fearful state. Wolpe argued that deep muscle relaxation was a convenient behavior to inhibit the anxiety response (1961), and he modeled the relaxation procedures off of those used by Edmund Jacobson (1939). Over the course of six sessions, the clinician would guide the patient in tensing and then relaxing various muscle groups, encouraging the patient to go beyond the point of typical relaxation (Wolpe, 1961). Patients were also encouraged to practice the relaxation procedure at home between sessions.

In the second stage of Wolpe’s systematic desensitization procedure, clinicians would guide patients in creating anxiety hierarchies. Wolpe noted that this stage could be conducted in the same sessions as the relaxation training (1961). After a thorough discussion of feared stimuli and situations, items were then ordered from most to least anxiety-provoking and grouped thematically, meaning that a given patient may have had more than one anxiety hierarchy. Wolpe noted the importance of including items on the hierarchy that evoke only a minimal fear response and can therefore be counteracted by the patient’s relaxation ability (1961). Systematic desensitization was conducted in a graduated fashion, that is, anxiety reduction was achieved for the items lower on the hierarchy before moving on to higher items. This graduated approach resulted in items higher on the hierarchy provoking less anxiety than they had at the start of treatment. The patient’s relaxation response could therefore successfully inhibit the anxiety response to higher order items, a necessary element of systematic desensitization.

The third and final stage was the desensitization procedure. In contrast to the research on children and animals, Wolpe’s procedure for adults typically utilized imaginal techniques rather than in vivo exposure. Patients were asked to vividly call to mind the feared stimulus and then relax in an alternating fashion, and indicate any anxiety experienced by lifting their finger (Wolpe, 1961). Therapists would move to the next hierarchy item when the patient indicated experiencing no distress to the previous item. Wolpe reported significant success in treating anxious patients with this procedure, with 90% of his cases either apparently cured or much improved according to one report (1954). Treatment success was typically measured via patients’ reports of their responses to feared stimuli outside the therapy setting and as such, was relatively unstandardized (Wolpe, 1961).²

Wolpe argued that reciprocal inhibition was the mechanism of change underlying systematic desensitization, rather than extinction or psychoanalytical processes (1954).³ According to reciprocal inhibition, imagining the feared stimuli while in a relaxed state was integral to the procedure’s success. In an experimental study of Wolpe’s procedure using a sample of individuals with snake phobia, the systematic desensitization group demonstrated a significantly greater reduction in posttreatment avoidance behavior than the graded exposure and no-treatment control groups, as well as a group that completed systematic desensitization using nonsnake stimuli (Davison, 1968). This study lent support to reciprocal inhibition (referred to as counterconditioning by the author) as the key mechanism underlying systematic desensitization, rather than exposure or relaxation alone.

Later work, however, demonstrated that exposure to feared stimuli led to fear reduction without the relaxation component (Dawson & McMurray, 1978; Gillan & Rachman, 1974; Waters, McDonald, & Koresko, 1972), suggesting that reciprocal inhibition may not have been the key mechanism underlying systematic desensitization.⁴ Further, there exists mixed evidence for the utility of imaginal exposure over in vivo exposure (Foa & Kozak, 1986), including in the case of phobias (Mathews, 1978). For these reasons, systematic desensitization fell out of favor as a frontline treatment for anxiety disorders, leading to the development of modern-day exposure therapy.

The habituation model

As the use of systematic desensitization declined, the habituation model emerged as the predominant approach to exposure therapy (Mathews, 1971). Habituation in the context of exposure therapy refers to response decrement, namely, a decrease in fear or anxiety. Exposure therapy using the habituation model begins with the creation of a fear hierarchy, similar to stage two of Wolpe’s systematic desensitization procedure. Throughout construction of the hierarchy, clinicians elicit subjective units of distress (SUDs; Wolpe, 1973) ratings for each trigger. SUDs ratings can be on any scale, although a smaller range of values (e.g., 0–10) may be useful when working with children and adolescents (Kendall et al., 2005). Similar to systematic desensitization, exposure therapy under the habituation model is conducted in a graduated fashion, in which the initial exposures are associated with a low SUDs rating. Treatment protocols based in part on the habituation model suggest that exposures should be terminated when at least a 50% reduction in SUDs is achieved (Foa, Hembree, & Rothbaum, 2007). Clinicians also use SUDs ratings as indicators to move on to the next item on the patient’s fear hierarchy. Therefore the patient’s level of fear or anxiety guides each individual exposure as well as the overall course of therapy under the habituation model.

Emotional processing theory (EPT; Foa & Kozak, 1986; Foa & McNally, 1996; Rachman, 1980) proposes that habituation is one mechanism underlying exposure therapy. In EPT, it is posited that fear is represented in memory as a set of propositions about the feared stimulus, the associated response, and the meaning of the stimulus and response (together referred to as a fear structure; Foa & Kozak, 1986). Exposure therapy activates fear structures and integrates information that is incompatible with them as a form of corrective learning. This incompatible information may take the form of habituation of physiological arousal to the feared stimulus or a change in the meaning of the feared stimulus or the response, such as a reduction in the perceived likelihood of harm (Foa & Kozak, 1986). Within-session physiological habituation to the feared stimulus may enable the integration of corrective information about the meaning of the stimulus or response, leading to between-session habituation.

According to EPT, three of the most important predictors of exposure therapy outcome are initial fear activation, between-session habituation, and within-session habituation (Foa & Kozak, 1986). Initial fear activation refers to the patient’s level of fear to the object or situation during the first exposure trial. Greater initial fear of the given exposure target is thought to be predictive of treatment success because activation of the fear structure is a necessary element of emotional processing (Foa & Kozak, 1986). Fear reduction over both the course of individual therapy sessions (within-session habituation) and treatment (between-session habituation) are proposed as two additional predictors of favorable treatment outcome. Both forms of habituation are thought to indicate successful integration of new information toward the formation of a new nonfear structure. In the laboratory, habituation may be indexed via decreased psychophysiological responding or lower SUDs ratings over time (Foa & Kozak, 1986). In the therapy setting, habituation is measured via SUDs ratings, given that tools for measuring physiological responding are not always available for use in treatment.

Evidence for the role of initial fear activation, between-session habituation and within-session habituation as predictors of treatment outcome is mixed. Foa and Kozak (1986) review a number of studies that lend support to the utility of these indices as predictors of successful exposure therapy in clinical samples, including specific phobia, agoraphobia, and obsessive–compulsive disorder. More recently, however, reviews have questioned the existing evidence for these indicators as useful predictors (Craske et al., 2008; Craske, Treanor, Conway, Zbozinek, & Vervliet, 2014). According to a review by Craske et al., positive evidence for the relation between initial fear activation and treatment outcomes is limited to heart rate, and other studies have demonstrated either no relation with other treatment outcome variables or did not directly test the relation (2008). Further, while research suggests that within-session habituation of self-reported fear and physiological indices typically occurs, there is limited evidence that this index relates to long-term outcomes (Craske et al., 2008). Finally, although there is some evidence in support of between-session habituation as a valid predictor of treatment outcome, other studies have not demonstrated this association. In some studies, the relation between between-session habituation and treatment outcome is not directly tested. Improvement has also been shown to occur in the absence of significant between-session habituation of physiological measures (Craske et al., 2008), suggesting that this index may not be critical to successful exposure treatment.

Of note, some studies in clinical samples have directly tested the habituation model of exposure therapy by measuring these three predictors. In a study of adults with panic disorder and agoraphobia completing an abbreviated course of exposure therapy, neither physiological activation nor within-session or between-session reduction of physiological or experiential measures of anxiety was predictive of the treatment outcome, measured as panic disorder symptom severity (Meuret, Seidel, Rosenfield, Hofmann, & Rosenfield, 2012). Similarly, a study of anxious youth found that on the whole, initial fear activation, within-session habituation, and between-session habituation did not predict anxiety-related outcomes at post-treatment or 1-year follow-up, although initial fear activation predicted less anxiety at follow-up among participants without generalized anxiety disorder (Peterman, Carper, & Kendall, 2019). The limited empirical evidence in support of elements of the habituation model, including the roles of initial fear activation, within-session habituation, and between-session habituation, led to the development of a second model of modern-day exposure therapy: the inhibitory learning model.

The inhibitory learning model

The inhibitory learning model draws on basic animal and human research in the areas of fear extinction, learning, and memory (Craske et al., 2008, 2014; Craske, Liao, Brown, & Vervliet, 2012). The principles of Pavlovian conditioning dictate that individuals with anxiety disorders have come to fear stimuli in their external or internal environment because of their perceived associations with negative outcomes. These associations, in which the CS is predictive of the US, are known as excitatory associations. One of the goals of exposure therapy is to create new, inhibitory associations as a means of extinguishing fear. Typically, inhibitory associations are between the feared stimulus and the nonoccurrence of the feared outcome, or the occurrence of the feared outcome at a rate or intensity that is lower than expected. The extinguished stimulus therefore has two meanings: excitatory and inhibitory. The prevailing meaning (and the associated response) depends on the current context, which can be either external (e.g., physical environment) or internal (e.g., drug state; Bouton, 2002). Therein lies one of the major challenges of successful exposure therapy: strengthening the inhibitory association to the point where it can successfully compete with the excitatory association.

One important caveat is that the original excitatory association is not erased from the individual’s memory following extinction (Bouton, 2002). As a consequence, individuals can often experience return of fear. Estimates of return of fear in clinical samples range from 19% to 62% of individuals who have undergone exposure therapy (Craske & Mystkowski, 2006). Forms of return of fear include reinstatement, spontaneous recovery, context renewal, and rapid reacquisition. Vervliet et al. provide an illustrative example of return of fear phenomena (Vervliet, Craske, & Hermans, 2013). Imagine a patient who has undergone successful exposure therapy for panic disorder with agoraphobia, which developed after the patient had a panic attack inside an elevator. Reinstatement can occur when the US is presented alone after extinction (Bouton, 2002). To use the above example, the patient may experience reinstatement of fear after experiencing an out-of-the-blue panic attack. Following the conclusion of extinction, spontaneous recovery of responding occurs when the CS is tested after time has passed (Bouton, 2002). Spontaneous recovery of fear may occur if the patient does not go into elevators for a period of time after the conclusion of exposure therapy. Context renewal refers to the recovery of an extinguished response when the context is changed following extinction (Bouton, 2002). Context renewal of fear might occur if the patient only completed exposures in one location and then attempts to ride an elevator in a novel location. Finally, rapid reacquisition of responding occurs when the CS is again paired with the US following extinction (Bouton, 2002). If the patient were to experience a panic attack inside an elevator after the conclusion of exposure therapy, he or she may experience rapid reacquisition.

Proponents of the inhibitory learning model have suggested a number of techniques for enhancing exposure therapy in order to reduce the likelihood of return of fear (Craske et al., 2012, 2014). Some of these techniques apply to all exposures under the inhibitory learning model (common techniques), while others may be relevant for only some exposures in a given course of treatment (specific techniques). Both common and specific techniques are detailed below.

Common techniques

One of the major implications of the inhibitory learning model is a shift in focus from habituation to expectancy violation in the design and implementation of exposures. The Rescorla–Wagner model (1972) posits that extinction learning occurs when there is a mismatch between the expectancy of an event and the absence of its occurrence, that is, when the organism’s expectancy is violated. Expectancy violation is thought to strengthen the inhibitory association, the association that the CS is no longer a predictor of the US. An exposure under this model would be designed to disconfirm the patient’s expectations about the rate or intensity of the feared outcome. Exposures may be designed to last a predetermined length of time (e.g., I will make small talk with a stranger for 5 minutes) based on how long the patient believes it will take for the feared outcome to occur. The therapist can also have the patient rate his or her expectancy of the feared outcome before and after the exposure to further illustrate expectancy violation.

Expectancy violation requires the individual to clearly articulate the feared outcome, as well as the predictors (CS) and protectors (conditional inhibitors, including safety objects and behaviors, described in detail subsequently) of the feared outcome prior to the completion of the exposure. It is crucial that the indicators of the feared outcome are objective, given the known attentional and interpretive biases that many individuals with anxiety disorders possess (Mathews & MacLeod, 2005). During in-session exposures, the therapist can act as another judge of these indicators, but this is not possible for between-session exposures. Specificity is critical. For example, an exposure for a patient with public speaking anxiety should explicate the verbal and nonverbal indicators that audience members are judging or rejecting the patient. Alternatively, when the feared outcome is intolerable distress, the therapist should work with the patient to clearly operationalize intolerable distress. For example, the patient may fear that they will be unable to function if the feared outcome occurs. An exposure to test this would ask the patient to specify what task he or she fears she will not be able to complete should the feared outcome occur and then incorporate this task into the exposure exercise (e.g., completing an hour’s worth of work, completing household chores).

If an exposure is designed to test the association between the CS and nonoccurrence of the US, the therapist should monitor the patient’s level of attention to both throughout the exposure. The goal of these types of exposures is to make the CS and nonoccurrence of the US salient, as research suggests that extinction learning will be directed to the most salient cue (Mackintosh, 1975; Pearce & Hall, 1980). The therapist may notice the patient attempting to distract or otherwise distance himself or herself from the CS, in which case coaching the patient to redirect his or her attention may be necessary.

Postexposure consolidation of learning is also critical under the inhibitory learning model. Therapists should guide patients in identifying if the feared outcome occurred or not and discuss the related objective evidence. For exposures in which the feared outcome did not occur, the focus of the discussion should be on this new association between the stimulus and the absence of the outcome. For exposures in which the feared outcome did occur, the focus should be on the patient’s ability to tolerate the anxiety associated with the outcome. Oftentimes, patients overestimate the likelihood that the feared outcome will occur or catastrophize the consequences (e.g., I will go crazy or have a heart attack). If relevant, postexposure discussions should highlight these patterns. In a study of children and young adolescents with anxiety disorders, postevent processing of exposure tasks was significantly associated with clinician-rated diagnostic improvements following cognitive behavior therapy (Tiwari, Kendall, Hoff, Harrison, & Fizur, 2013).

Under the inhibitory learning model, the principle of variability can be used to guide the design of individual exposures and the overall course of treatment. Research has demonstrated that inhibitory associations are context-dependent, whereas excitatory associations are not context-dependent (Bouton, 2004). Therefore exposures should be conducted across varied external and internal contexts to increase the likelihood that the inhibitory association will generalize to these other contexts. Varying the external context would require exposures to be conducted in different locations, both with and without the therapist present. To ensure that the internal context is varied, the patient can practice exposures at different times of day, for example. Using a sample of students with a fear of spiders, the completion of exposures to videos of spiders in multiple contexts reduced fear renewal when participants were tested in a novel context, demonstrating generalization of extinction learning (Vansteenwegen et al., 2007).

Research also suggests that the specific stimuli used in exposures should be varied (Lang & Craske, 2000; Rowe & Craske, 1998). In a nonclinical sample, participants were conditioned to fear a CS and then received extinction either to the CS, a single generalization stimulus (a stimulus similar to the CS), or several generalization stimuli. At test, the group who underwent extinction with several generalization stimuli demonstrated less fear than those who underwent extinction with only one generalization stimulus (Zbozinek & Craske, 2018), demonstrating the importance of variability of stimuli during exposure. For example, if an individual has a specific phobia of spiders, spiders of varying sizes, colors, and shapes should be used. Variability of within-exposure fear levels has also been shown to predict positive outcomes among young adults with contamination anxiety and public speaking anxiety (Culver, Stoyanova, & Craske, 2012; Kircanski et al., 2012) and among youths with obsessive–compulsive disorder (Kircanski & Peris, 2015), again suggesting that within-session habituation of fear may not be a necessary element of exposure therapy. Rather than using habituation to guide the course of treatment, exposures can be conducted in random order from the hierarchy, with varying stimuli, duration, and intensities (Craske et al., 2014).

Specific techniques

The elimination of safety signals is a specific technique used in some exposures conducted under the inhibitory learning model. Safety signals can be objects (e.g., medications, cell phone) or people (e.g., therapist, friend or family member). These signals are thought to be detrimental to long-term exposure therapy outcomes because they prevent the patient from learning the inhibitory association (Craske et al., 2014). For example, a patient who takes a benzodiazepine when he or she feels the first physical sensations of anxiety will not have the opportunity to learn that he or she can tolerate the anxiety. Although these safety signals often lessen the fear response during an individual exposure exercise, they ultimately interfere with the long-term goal of inhibitory learning (Craske et al., 2008). Research on the effects of safety signal usage has been mixed, with some studies demonstrating detrimental effects for exposure therapy (Sloan & Telch, 2002), while other studies of individuals with contamination and claustrophobic fears have not found detrimental effects (Deacon, Sy, Lickel, & Nelson, 2010; Rachman, Shafran, Radomsky, & Zysk, 2011; Sy, Dixon, Lickel, Nelson, & Deacon, 2011). In a study of anxious youth, use of safety-seeking behavior during exposure was significantly predictive of poorer outcome (Hedtke, Kendall, & Tiwari, 2009). In order to facilitate the patient remaining in treatment, the elimination of safety signals may be incorporated into the fear hierarchy, in which early exposures allow for the use of safety signals, whereas later exposures do not (Vorstenbosch, Newman, & Antony, 2014).

Another technique that can be used in exposures is the inclusion of multiple CS in a single exposure after the patient’s fear to each stimulus has been extinguished independently. This technique is known as deepened extinction (Rescorla, 2006). Deepened extinction requires that both stimuli predict the same outcome. In a nonclinical sample, participants who were presented with single extinction trials followed by compound extinction trials demonstrated significantly less spontaneous recovery of fear responding than participants who were presented with single extinction trials only (Culver, Vervliet, & Craske, 2015). Panic disorder with agoraphobia is particularly amenable to deepened extinction, although exposures targeting other feared outcomes can also make use of this technique. For example, interoceptive exposures that target feared physiological sensations and in vivo exposures that target feared situations may be combined after extinguished in isolation (Barlow & Craske, 1994).

Another implication of the inhibitory learning model is the inclusion of exposures in which the feared outcome does occur, known as occasional reinforcement. Occasional reinforcement may exert its beneficial effects through expectancy violation or enhanced salience of the CS (Craske et al., 2014). Social anxiety disorder is particularly amenable to this type of exposure, in which feared outcomes such as being embarrassed or rejected are part of daily life. An exposure of this type may involve the patient doing something purposefully embarrassing or silly in front of other people in order to increase the likelihood that they will be judged. For example, the patient may ask for directions to a building that they are standing directly in front of or sing loudly in public. It should be noted, however, that the use of these types of exposures has yet to be examined in the treatment of anxious youth (Peterman, Read, Wei, & Kendall, 2015) and should only be used if deemed ethically appropriate. Further, these exposures should be attempted after building sufficient rapport with the patient and clearly explaining the rationale behind occasional reinforcement to prevent treatment dropout.

For some patients, it may be useful to incorporate the use of retrieval cues into treatment. Retrieval cues are introduced during extinction and aid the patient in recalling the inhibitory association following the conclusion of extinction. It is important that retrieval cues do not come to function as safety signals. Retrieval cues are meant to be used solely to recall the inhibitory association, whereas safety signals are associated with the nonoccurrence of the US (Craske et al., 2014). For example, individuals with fear of spiders who were instructed to mentally reinstate the treatment context before encountering a spider in a new context demonstrated less return of fear than those who were not instructed to use mental reinstatement (Mystkowski, Craske, Echiverri, & Labus, 2006). The use of retrieval cues should be introduced later in treatment so that they do not reduce expectancy violation effects. Therefore retrieval cues may be best used as a relapse prevention strategy (Craske et al., 2014).

Exposure therapy for children and adolescents

Exposure therapy is an evidence-based treatment for children and adolescents with anxiety disorders, including generalized anxiety disorder, social anxiety disorder, separation anxiety disorder, specific phobias, panic disorder, and obsessive–compulsive disorder (Peterman et al., 2015). There are, however, several important considerations to be made in conducting exposure therapy with anxious youth, given their developmental stage (Kingery et al., 2006). We focus here on considerations that relate to the inhibitory learning model of exposure therapy.

Exposures conducted using an inhibitory learning approach rely on expectancy violation rather than habituation. Expectancy violation requires the identification of the feared outcome, the predictors, and protectors of that outcome, as well as the objective indicators that the outcome did or did not occur. Depending on the age of the patient, this may prove difficult. It may be that the child is unable to articulate what outcome he or she is afraid of, or if able to do so, unable to explicate truly objective markers of the outcome. Indeed, the goal of many exposures with children may be less focused on expectancy violation and more on tolerance of distress. In these cases, the new association to be learned is the ability to tolerate the fear or anxiety in the presence of the feared stimulus. Beyond mere tolerance, an additional goal for patients is to learn that they can function even when experiencing anxiety (Abramowitz, 2013). An exposure may be designed in which the patient attempts to complete a predetermined task after becoming anxious, such as carrying on a conversation with a stranger or completing a homework assignment. The goal of this type of exposure is to illustrate that the patient can function in spite of his or her anxiety. It has been suggested that therapists present exposure as a technique for coping with anxiety, with an emphasis on the goals of improved approach behavior and daily functioning (Peterman et al.,