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Treatment of Anxiety Disorders 

Treatment of Anxiety Disorders
Chapter:
Treatment of Anxiety Disorders
DOI:
10.1093/9780195173642.003.0011
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date: 15 October 2018

Concurrent with the emergence of a growing psychopathology literature, child and adolescent clinical psychology and psychiatry have moved away from nonspecific interventions toward problem-focused treatments keyed to specific diagnoses in the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (American Psychiatric Association, 1994; DSM-IV) and, within diagnoses, targets (Kazdin, 1997). The past 40 years have seen the emergence of diverse, sophisticated, empirically supported, cognitive-behavioral and pharmacological therapies that cover the range of childhood-onset anxiety disorders (Ollendick & March, 2004). Before reviewing what is known about the treatment of anxiety disorders in adolescence, we first provide a brief overview of the history and rationale for cognitive-behavioral therapy (CBT), for pharmacotherapy, and for the combination of the two in the treatment of youth with anxiety disorders. Because of increasing emphasis in the field on evidence-based approaches, those interventions that have not been subjected to treatment outcome study by means of accepted research methodology, such as psychodynamic approaches, “play therapy,” and other approaches, are not reviewed in this chapter.

COGNITIVE-BEHAVIORAL THERAPY

Current cognitive-behavioral theories regarding the etiology and maintenance of anxiety disorders posit that internal mental phenomena play an important role in mediating pathological anxiety. Foa and Kozak (1985, 1986) proposed that specific “fear structures” which contain erroneous information about the fear stimuli, fear responses, and their meaning underlie the anxiety disorders. Kendall (2000b) also referred to “cognitive structures” as being important in anxiety disorders in childhood. Accordingly, the goal of cognitive-behavioral treatment is to provide information that is incompatible with the erroneous elements of the fear structure.

Most mental health clinicians are familiar with treatments that assume psychological distress stems from historical relationship problems that must be uncovered in therapy. In contrast to this approach, the CBT clinician addresses the anxiety symptoms directly by confrontation with the feared stimuli in a therapeutic environment and by teaching the patient a set of adaptive coping skills for specific symptoms associated with distress and impairment (Kendall, 2000b). Thus, unlike some other psychotherapeutic approaches, CBT fits into a problem management framework in which the symptoms of the disorder and associated functional impairments are specifically targeted for treatment.

The cognitive-behavioral approach is not a single, monolithic approach. Quite the contrary is true. The generic approach labeled “cognitive-behavioral” involves working with parents, enhancing emotional processing, changing social and peer influences, and using behavioral contingencies and cognitive processing. Similarly, CBT is not one treatment. Rather, treatments of childhood anxiety disorders, though held together by common components and guiding theory, have emerged from different clinics, in different countries, and with variations in the length and specifics of treatment. Nevertheless, there are numerous common themes, strategies, and guiding principles.

One CBT program has received research attention, and though not exactly prototypic, serves as an illustrative example of this approach. (For futher discussion of CBT programs, the reader is referred to the several programs that are described in detail within each of the sections on the several disorders.) This program is manual based and time limited (Kendall, 2000b). This program integrates elements of cognitive information processing associated with anxiety with behavioral techniques (e.g., relaxation, imaginal and in vivo exposure, role-playing) that are known to be useful in the reduction of anxiety. In this program, children with anxiety typically participate in a structured 16-to 20-week treatment program divided into two phases: education and practice.

The first phase includes training, education, and skill-building, during which the therapist works with the child to recognize signs of anxiety, acquire relaxation skills, and identify anxious cognitive processing. Through self-monitoring homework assignments and in-session role-playing, the child learns about anxiety and, more importantly, the cognitive, somatic, emotional, and behavioral aspects of his or her own personal anxious experience. These sessions also allow the child to begin to think about various ways to overcome his or her anxiety.

Education and Skill-Building

During initial sessions, the anxious child learns to distinguish between various bodily reactions to emotions as well as the somatic reactions that are specific to his or her anxiety. Coupled with this awareness, the child is taught relaxation exercises designed to help the child develop further awareness of and control over physiological and muscular reactions to anxiety (see King, Hamilton, & Ollendick, 1994). This segment may be especially beneficial for children whose worry is accompanied by more severe somatic symptoms (see also Eisen & Silverman, 1998). In this way, anxious children may develop an awareness of their physiological responses to anxiety and use this as an “early warning signal” to initiate relaxation procedures.

Next, children are taught how to identify and modify anxious cognition (their internal dialogue). Therapist and child then discuss such thoughts and the child is encouraged to ask himself or herself the various possibilities that may occur in a given situation. It is believed that helping children to challenge their distorted or unrealistic cognition will promote more constructive ways of thinking and less dysfunctional emotional and behavioral responses. For example, the “perfectionistic” nature of many anxious children can be challenged as these children become better able to examine, test out, and reduce their negative self-talk, modify unrealistic expectations, generate more realistic and less negative self-statements, and create a plan to cope with their concerns. Importantly, the idea here is not necessarily to fill the child with positive self-talk. Rather, the ameliorative power rests in the reduction of negative self-talk, or the “power of non-negative thinking” (Kendall, 1984). This phenomenon is supported by recent evidence indicating that changing children's anxiety-ridden and negative self-talk—but not positive self-talk—mediates the changes in anxiety that are associated with treatment-produced gains (Treadwell & Kendall, 1996). Children learn problem-solving skills that help them to devise a behavioral plan to cope with their anxiety. This includes learning to recognize the problem, brainstorming and generating alternatives to managing their anxiety, weighing the consequences of each possible alternative, and then choosing and following through with their plan (see D'Zurilla & Goldfried, 1971). The therapist serves as a model during each phase of problem solving by, for example, reminding the child that problems and challenges are part of life or by brainstorming ideas without judgment. With the acquisition of problem-solving skills, children develop confidence in their ability to handle anxiety-provoking situations as well as everyday challenges that arise. They learn to judge the effectiveness of their efforts and reward themselves for these efforts. They also learn to identify those things they liked about how they handled a situation and those things that they may want to do differently. Here, children are encouraged to reward both complete and partial successes. Children with anxiety may have exceedingly high standards for achievement and be unforgiving and critical of themselves if they fail to meet these standards. Therefore, it is important for the therapist to emphasize and encourage self-reward for effort and partial success.

Exposure Exercises

The second phase of treatment focuses on exposure exercises in which children practice the newly acquired skills. In these sessions, participant youth are prepared for and exposed to various situations that induce anxiety. They are first exposed to imaginary and low-anxiety situations and gradually are exposed to moderate-and then high-anxiety situations. Through imaginal and in vivo exposures, the therapist assists the child in preparing for the exposure by, for example, discussing aspects of the situation that are likely to be troubling, working through the steps of the plan, and rehearsing. The in vivo exposures are extremely important, as these situations provide the child real opportunities to practice. Thus, they should be tailored to address the spe cific worries (sources of anxious distress) of the child.

The therapist also facilitates children's postexperience processing of the exposures, helping them to evaluate their performances and think of a reward. In so doing, the therapist helps to frame the current exposure experience in terms of a pattern for future coping. When designing the graduated hierarchy of exposures, it is beneficial for the therapist and child to collaborate to create in vivo exposures that are meaningful and memorable for the child. Homework assignments are an important feature of this program. Throughout the treatment, children complete tasks in a personal notebook, which allow them to practice their steps and to use their skills outside of session. Rewards are provided upon completion of the assignments.

As the end of the time-limited treatment approaches (starting with 3 weeks left), the therapist and child begin to discuss how the child will create and produce a “commercial” about his or her experiences in the program to be presented and videotaped during the last session of the treatment. Children are encouraged to use their imagination and create a videotape, audiotape, or booklet describing their experiences to help in telling other children about strategies for coping with anxiety. This effort is designed to not only help children organize their experiences but also afford them the opportunity to “go public” with their newly acquired skills and recognize their accomplishments. The commercial also serves as a tangible reward that children can take home with them once the treatment is completed and, although it may not be described as such, it is an in vivo exposure task with emotional, social, creative, and organizational features.

Developmental Considerations

The treatment manuals that have been written and evaluated in research (e.g., Kendall, Chu, Pimentel, & Choudhury, 2000) were designed for children between the ages of 8 and 13 years. Also designed for this age range, The Coping Cat Workbook (Kendall, 2000a) contains exercises that parallel treatment sessions in an effort to facilitate the child's involvement in the program and the acquisition of skills. Although some manual-based treatments have acquired the reputation of being somewhat rigid, the therapist working with this program is allowed flexibility, as life can be “breathed” into the manual to better fit the needs and functioning of the child (Kendall, Chu, Gifford, Hayes, & Nauta, 1998). Although adaptations can be made when working with older children, younger children may not have yet developed the cognitive skills necessary to participate fully in or benefit maximally from this intervention and children with an IQ below 80 may not have the prerequisite skills. Additionally, with developmental considerations, it is important to be cognizant of possible age-related increases in physiological functioning, emotional vulnerability, social and peer pressures, and comorbid conditions, as well as any other changes that these children may be experiencing. Accordingly, a CBT therapist manual and a related workbook for teenagers (Kendall, 2000a) are also available.

PHARMACOTHERAPY

Progress in the neurobiology of anxiety has focused on (1) identifying the central nervous system (CNS) substrates of anxiety and (2) the effects of rearing and environment in the progression of anxiety states with reference to their somatic substrates (Pine & Grun, 1999) in an evolutionary context (Leckman & Mayes, 1998). Convergent evidence from both child studies of stress and trauma as well as primate rearing and deprivation studies suggests that the effects of stress in the genesis of anxiety disorder can be profound. Important substrates for this “stress-response system” include brainstem arousal centers, particularly the locus ceruleus, which provides noradrenergic input to brainstem and more rostral arousal mechanisms (McCracken, Walkup, & Koplewicz, 2002); the amygdala located in the anterior temporal lobe, which processes threat cues and safety signals, with particular emphasis on social threat (Bremner, Krystal, Charney, & Southwick, 1996); the septal–hippocampal system that mediates glucorticoid sensitive context-conditioning within the framework of learned experience; striatal and neoriatal structures, such as the caudate nucleus, which with their cortical targets comprise the circuitry that mediates habitual automatic behaviors, such as those seen in obsessive-compulsive disorder (OCD; Rosenberg & Hanna, 2000); the orbital-frontal cortex, which assigns complex negative affective valence to cognitive attributions (Graybiel & Rauch, 2000); paralimbic structures, such as the anterior cingulate gyrus, which play an important role in directed and selective attention to threatening stimuli (Davidson, Abercrombie, Nitschke, & Putnam, 1999); and the dorsolateral and ventromedial prefrontal cortex, which respond to and modulate subcortical input and output, generating adaptive responses or, in the case of disease states, maladaptive anxiety-maintaining behaviors (Davidson et al., 1999). From an integrationist point of view, extensive afferent and efferent connections between these brain regions process a wide variety of internal and external threat cues and safety signals, integrate current experience with previous experience, and generate affective and cognitively mediated approach and avoidance behaviors that are either appropriate or inappropriate to the individual's current context.

The understanding of the neurobiology of anxiety has been propelled by new pharmacologic agents that impact CNS receptors within the stress–response system (Heim, Owens, Plotsky, & Nemeroff, 1997). For example, the serotonin system is involved in generating and maintaining normal and pathological fear (Stein, Westenberg, & Liebowitz, 2002). Modulation of this system with a serotonin reuptake inhibitor provides an effective treatment for OCD (March, Biederman, et al., 1998) and may be useful for separation anxiety, panic, and social phobia (Research Units of Pediatric Psychopharmacology (RUPP) Anxiety Group, 2001). Other major neurotransmitter systems that appear to be involved in pathological anxiety include the GABAergic/glutamergic, noradrenergic, and dopaminergic systems, with recent evidence also suggesting important roles for the neuropeptides cholecystokinin, neuropeptide Y, and corticotropin-releasing hormone (CRH) (Sallee & March, 2001). These neurotransmitter systems appear to work in concert to provide homeostasis with respect to the phasic management of threat, and dysregulation in the information processes linked to these substrates may be linked to anxiety states in children and adolescents. They also appear to interface with Kagan's notion of “behavioral inhibition,” which as a stable temperamental characteristic appears to be an index of biological vulnerability that under certain circumstances (e.g., separation-stress exposure) can contribute to the generation of an anxiety disorder (Biederman, Rosenbaum, Chaloff, & Kagan, 1995).

Brain mechanisms of response to threat that are highly conserved in evolutionary terms and are exquisitely sensitive to learned experience provide the CNS substrate for the information processes that, when dysregulated, produce pathological anxiety, as well as for normal fears and worry. Pharmacotherapy presumably biases these processes directly by influencing the neurotransmitter milieu within which these hierarchically distributed neural networks operate.

COMBINED TREATMENT

In a biopsychosocial approach, combined treatment may be the rule rather than the exception (e.g., the treatment of juvenile rheumatoid arthritis with ibuprofen and physical therapy). In a perfectly evidence-based world, selecting an appropriate treatment for the anxious child or adolescent from among the many possible options would be reasonably straightforward. In the complex world of research and clinical practice, choices are rarely clear-cut. In this regard, the treatment of the anxious child can be thought of as being partially analogous to the treatment of juvenile-onset diabetes, with the caveat that the target organ, the brain in the case of mental disorders, requires psychosocial interventions of much greater complexity. The treatment of diabetes and anxiety disorder can both involve medication—insulin in diabetes and in anxiety, typically a serotonin reuptake inhibitor. Each also involves an evidence-based psychosocial intervention. In diabetes, the psychosocial treatment of choice is diet and exercise, and in anxiety, exposure-based CBT. Depending on the presence of risk and protective factors, not every participant has the same outcome. Bright youngsters from well-adjusted, two-parent families typically may do better with either diabetes or anxiety than those beset with tremendous psychosocial adversity and family hardship. Also, not everybody recovers completely even with the best of available treatment, so some interventions need to target coping with residual symptoms, such as diabetic foot care in diabetes and helping patients and their families cope skillfully with residual symptoms in anxiety disorders.

Psychosocial treatments may be combined with a medication for one of several reasons. First, in the acute treatment of the severely anxious child, two treatments may provide a greater “dose” and thus, may promise a better and perhaps speedier outcome. For example, patients with OCD may opt for a combined treatment even though CBT alone may offer equal benefit (March & Leonard, 1998). Second, comorbidity may require two treatments, since different targets may require varied treatments. For example, treating an 8-year-old who has attention-deficit hyperactivity disorder (ADHD) and separation anxiety disorder (SAD) with a psychostimulant and CBT is a reasonable treatment strategy. Third, in the face of partial response, an augmenting treatment can be added to the initial treatment to improve the outcome. A selective serotonic reuptake inhibitor (SSRI) can be added to CBT or CBT can be added to an SSRI. In an adjunctive treatment strategy, a second treatment can be added to a first one to positively impact one or more additional outcome domains. For example, an SSRI can be added to CBT to address comorbid depression.

As our understanding of both mental disorders in youth and adolescent development increases, treatment innovations inevitably will accrue, including knowledge about when and how to combine treatments (see Table 10.1). The good news is that the National Institute of Mental Health (NIMH)-funded comparative treatment trials that include a combination cell as well as CBT and medication monotherapy conditions are currently under way. Unfortunately, adolescent cases play too small a role and appear in too small a number in these ongoing trials to allow for specific examination of the effects of CBT, medication, and their combination on adolescents with anxiety disorders. The clear mandate is for similar programmatic research with adolescent cases. Before such work is undertaken, however, we offer a review of what is known to date. Because the state of knowledge varies by disorder, our review will consider each of the anxiety disorders separately (i.e., social phobia, generalized anxiety disorder, separation anxiety disorder, specific phobia, panic disorder, obsessive-compulsive disorder, and posttraumatic stress disorder). The information will be provided within the categories of (a) acute treatment, (b) maintenance treatment, and (c) management of partial response and nonresponse. In each category we very briefly summarize what is known about the treatment of adults and then provide more detailed coverage of treatments for youth. As noted above, there are very few studies of combined treatments of any kind in child or adolescent samples. Moreover, with few exceptions (e.g., Barlow, Gorman, Shear, & Woods, 2000), most of the combined-treatment studies in adults have not included a CBT plus pill placebo condition, which leaves an important mechanism question essentially unanswered by the extant literature.

Table 10.1 Summary of Literature on Pediatric Treatment Outcome by Anxiety Disorder

Anxiety Disorder

Standards of Evidence

Summary of Key Type 1 Studies

Social anxiety disorder

Psychosocial Treatment

Three Type 1 studies, several Type 3 studies

A few dismantling studies (e.g., Spence et al., 2000; CBT + family therapy failed to separate from CBT delivered individually)

Multiple Type 1 CBT studies that included SAD patients but did not analyze separately (e.g., Flannery-Schroeder & Kendall, 2000)

Pharmacotherapy

Multiple Type 3 studies

Type 1 study: RUPP study of fluoxetine vs. placebo, SAD patients included

Beidel, Turner, & Morris (2000): Social effectiveness therapy > nonspecific treatment (Testbusters)

Hayward et al. (2000): Group CBT > assessment only

Spence et al. (2000): CBT, CBT + family therapy > WL

RUPP (2001, 2003): Fluvoxamine > placebo overall, but SAD diagnosis identified as a moderator of treatment outcome in that those with social anxiety disorder did not fare as well as those with GAD or separation anxiety

Selective mutism

Psychosocial Treatment

Type 6 case studies provide preliminary support for various behavioral techniques (e.g., contingency management, exposure, self-modeling)

No Type 1 or Type 2 studies for any behavioral or cognitive-behavioral therapy

Pharmacotherapy

Only one Type 1 study: fluoxetine vs. placebo

Black & Uhde (1994): Fluoxetine > placebo in a small randomized, double blind trial that also included a single-blind placebo lead-in

Generalized anxiety disorder (GAD)

Psychosocial Treatment

Five Type 1 studies support the efficacy of CBT packages for anxious youth; many, but not all, of subjects were diagnosed with GAD

Pharmacotherapy

Several Type 3 studies provide preliminary support for use of several classes of medication, including benzodiazepines

Some negative findings in Type 3 studies of benzodiazepines, plus concerns about dependency and withdrawal (e.g., Rickels et al., 1990)

Some Type 1 studies of TCAs for youth with “school refusal,” some of whom may have had GAD

Concerns about cardiac risks with TCAs

Some preliminary evidence for the SSRIs, plus two Type 1 studies (1 for sertraline, 1 for fluvoxamine)

Kendall (1994): CBT package (“Coping Cat”) > WL

Kendall et al. (1997): Coping Cat > WL

Barrett (1998): Group CBT, group family-based CBT > WL; family-based treatment afforded advantages over CBT alone on some measures

Rynn et al. (2001): Sertraline > placebo

RUPP (2001, 2003): Fluvoxamine > placebo; unlike SAD, GAD not found to be a predictor of nonresponse

Separation anxiety disorder (SAD; including school refusal behavior)

Psychosocial Treatment

Several Type 1 studies of school refusal, which included many individuals with separation anxiety (e.g., Bernstein et al., 2000)

Several Type 1 studies of anxious children and adolescents that included separation-anxious participants (e.g., Kendall et al., 1999, Silverman et al., 1999a)

Family and teacher involvement in CBT was found initially superior to CBT alone for school refusal behavior, which presumably included separation anxious participants (Heyne et al., 2002)

Pharmacotherapy

Several Type 1 studies, with mixed results: imipramine was first efficacious but then a later study found no difference (Gittleman-Klein & Klein, 1971; Klein, Koplewicz, et al., 1992); benzodiazepines did not separate from placebo (Graae et al., 1994)

SSRIs have had efficacy (RUPP, 2001, 2003) and are generally considered first-line option

King et al. (1998): CBT > WL for school refusal behavior

Last et al. (1998): CBT = educational support for school refusal behavior, with children and parents' ratings of improvement generally higher than that found by study investigators

Gittleman-Klein & Klein (1971): Imipramine > placebo

Klein, Kopelwicz, et al. (1992): Failed to replicate earlier positive findings for imipramine

Graae et al., 1994: Benzodiazepine did not separate from placebo

RUPP (2001, 2003): Fluvoxamine > placebo; unlike SAD, separation anxiety not found to be a predictor of nonresponse

Specific phobia

Psychosocial Treatment

Participant modeling and reinforced practice are well established; other behavioral methods are “probably efficacious” in children (Ollendick & King, 1998, 2000)

Two completed Type 1 studies, one large study still in progress

Type 3 study suggested that one-session CBT is comparable if not superior to longer treatments (Muris et al., 1998)

Pharmacotherapy

No Type 1 studies of any medication have been conducted; Type 3 study of fluoxetine suggested efficacy

Silverman et al. (1999b): Contingency management, self-control > educational support in terms of clinically significant improvement, but all three groups improved functioning

Öst et al. (2001): One-session CBT > WL

Ollendick & Öst (in progress): One-session CBT compared with educational support and WL

Panic disorder

Psychosocial Treatment

Preliminary evidence for CBT packages based on Barlow's panic control treatment was found in Type 3 studies (Barlow & Seidner, 1983; Ollendick, 1995)

Pharmacotherapy

Type 3 evidence for SSRIs (e.g., Renaud et al., 1999)

No Type 1 studies of any class of medication

Mattis et al. (2001): Panic control treatment for adolescents (PCT-A) compared with self-monitoring; preliminary evidence from this trial is encouraging: PCT-A > self-monitoring in reducing panic attack severity and other symptoms of panic disorder

Obsessive compulsive disorder (OCD)

Psychosocial Treatment

Multiple Type 3 studies provide preliminary evidence for efficacy of CBT involving EX/RP for children and adolescents (e.g., Piacentini et al., 2002)

Preliminary evidence from Type 3 studies shows that EX/RP augments SRI pharmacotherapy (e.g., March et al., 1994; Wever & Rey, 1997)

Preliminary evidence from Type 3 study shows that intensive EX/RP and weekly EX/RP are comparable (Franklin et al., 1998)

One completed Type 1 study directly comparing EX/RP with pharmacotherapy suggested an advantage for EX/RP (DeHaan et al., 1998)

Two large-scale Type 1 studies of EX/RP are underway, one of which examines EX/RP + SSRI (sertraline)

Pharmacotherapy

Several Type 1 studies of clomipramine (e.g., Leonard et al., 1989), including a multicenter study (DeVeaugh-Geiss et al., 1992)

Multiple large-scale, multicenter Type 1 studies of SSRIs (e.g., March, Biederman, et al., 1998)

Type 3 studies examining augmentation of SSRIs with atypical neuroleptics

Investigational Treatments

Two Type 1 studies examining treatments for children and adolescents diagnosed with PANDAS

De Haan et al. (1998): EX/RP > clomipramine, both yielded significant reductions

Pediatric OCD Collaborative Study Group: Compared combined treatment with CBT and sertraline, and all with placebo

Piacentini (1999): Describes a soon-to-be-completed study comparing EX/RP + family therapy with relaxation control

DeVeaugh-Geiss et al. (1992): Clomipramine > placebo

March, Biederman, et al. (1998): Sertraline > placebo

Riddle et al. (2001): Fluvoxamine > placebo

Geller et al. (2001): Fluoxetine > placebo

Garvey et al. (1999): Oral penicillin = placebo in children diagnosed with PANDAS, but penicillin administration may have been ineffective in preventing reinfection with GABHS

Perlmutter et al. (1999): Plasma exchange = IV immunoglobulin > IV placebo for PANDAS

Posttraumatic stress disorder

Psychosocial Treatment

Several Type 3 studies provide preliminary evidence for individual + group CBT (Goenjian et al., 1997) or group CBT (e.g., Layne, Pynoos, Saltzman, et al., 2001; March, Amaya-Jackson, et al., 1998); one study for a form of EMDR (Chemtob et al., 2002)

Four Type 1 studies of CBT for PTSD associated with child sexual abuse

No other Type 1 studies of CBT for other forms of trauma

Pharmacotherapy

Limited to Type 3 studies

Deblinger et al. (1996, 1999): CBT > community treatment as usual

King et al. (2000): CBT = CBT + family involvement

Cohen & Mannarino (1996a, 1996b): CBT > supportive therapy

Cohen & Mannarino (1998): CBT > supportive therapy

CBT, cognitive-behavioral therapy; EMDR, eye movement desensitization and reprocessing; EX/RP, exposure and response prevention; GABHS, group A β‎-hemolytic streptococcal infection; IV, intravenous; PANDAS, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection; SRI, serotonin reuptake inhibitor; RUPP, Research Units on Pediatric Psychopharmacology; SSRI, selective serotonin reuptake inhibitor; TCA, tricyclic antidepressant; WL, wait list.

ACUTE TREATMENT

Social Anxiety Disorder

Treatment of Social Anxiety Disorder in Adults

With respect to psychosocial interventions, behavioral, cognitive, and combined cognitive-behavioral interventions have each been found to be efficacious in the acute treatment of social phobia in adults, delivered either in groups or individually. Direct comparisons of behavioral and cognitive-behavioral treatments have been mixed, and it is unclear as yet whether there is a strong advantage for one over the other. As with pharmacotherapy, residual impairment remains an issue (for a comprehensive review see Hambrick, Turk, Heimberg, Schneier, & Liebowitz, 2003).

A variety of medications have been found use ful for social anxiety disorder. There are no controlled trials of patients with nongeneralized social anxiety disorder, and studies containing both generalized and nongeneralized patients include too few of the latter to be definitive. Placebo-controlled trials of patients with the generalized subtype suggest efficacy for phenelzine, clonazepam, paroxetine, sertraline, fluvoxamine, venlafaxine, gabapentin, and pregabelin. The average responder rate in these trials is 40%–55%, defining response as a 1 or 2 on the Clinical Global Impression (CGI) Improvement scale. A majority of the patients classified as responders in these trials still have clinically significant symptoms. Patients with comorbid major depressive disorder (MDD) or significant substance abuse have usually been excluded. Drugs such as phenelzine or sertraline have shown greater acute efficacy than CBT in trials comparing the two modalities. Phenelzine plus CBT, and sertraline plus CBT, showed modestly greater efficacy than the respective drug monotherapies alone in controlled trials. Remission has not been assessed in any trials, and there is also no agreement on the criteria to define remission in social anxiety disorder. Negative findings from controlled trials exist for buspirone, atenolol, moclobemide, and fluoxetine in generalized social anx iety disorder (for a review see Roy-Byrne & Cowley, 2002).

Social Anxiety Disorder in Children and Adolescents

Increased self-consciousness and preoccupation with social matters are extremely common during late childhood and early adolescence, a developmental stage in which the importance of peers is typically heightened. Accordingly, adult epidemiological studies have also consistently indicated that onset of social phobia is common during late childhood, with onset typically occurring between ages 11 and 12 (Albano, 2003). Differentiating normative adolescent social concerns from the clinical social anxiety disorder poses difficulties for clinicians, parents, teachers, and adolescents alike, and perhaps the best way to parse the two is to examine functional impairment and concomitant symptoms: compared to non-anxious counterparts, youth with social anxiety disorder more often report depressed mood, high trait anxiety, and perceived social incompetence (Albano, Chorpita, & Barlow, 2003), higher levels of loneliness and fewer friends (Beidel, Turner, & Morris, 1999), a wide range of social avoidance (Albano, Detweiler, Logsdon-Conradsen, Walker, & Ollendick, 1999), and, in at least some cases, social anxiety is associated with school refusal (Kearney & Drake, 2002). Given the potentially serious consequences of social anxiety disorder and its sequalae for the life trajectory of adolescents, detection and treatment are especially important.

Psychosocial Treatment for Social Anxiety Disorder in Children and Adolescents

There is an increasing body of evidence demonstrating the efficacy of CBT approaches for children and adolescents with anxiety disorders, which has included those with social phobia (or with the previous diagnostic term, avoidant disorder). A number of controlled trials targeting anxious children have included those diagnosed with social phobia (Barrett, Dadds, & Rapee, 1996; Barrett, 1998; Cobham, Dadds, & Spence, 1998; Dadds et al., 1999; Dadds, Spence, Holland, Barrett, & Laurens, 1997; Flannery-Schroeder & Kendall, 2000; Ginsburg & Schlossberg, 2002; Kendall, 1994; Kendall et al., 1997; Last, Hansen, & Franco, 1998; Lumpkin, Silverman, Weems, Markham, & Kurtines, 2002; Silverman et al., 1999a, 1999b).

Three Type 1 randomized, controlled cognitive-behavioral treatment studies specifically for children and adolescents with social phobia have reported positive clinical response. Hayward et al. (2000) randomly assigned 35 female adolescents with social phobia to cognitive-behavioral group therapy (CBGT) (N = 12) or no treatment (N = 23). Eleven of the 12 cases completed the active treatment. After 16 weeks of treatment, significantly fewer treated patients met criteria for social phobia. At 1-year follow-up, however, there was no difference between the two groups, suggesting that the CBGT may result in a moderate short-term effect. Spence, Donovan, and Brechman-Toussaint (2000) randomly assigned 50 children with social phobia, ages 7–14 years, to either child-focused CBT, CBT plus parent involvement, or a wait-list control. The integrated CBT program involved intensive social skills training with graded exposure and cognitive challenging. After treatment, children in both CBT groups had a greater decrease in social and general anxiety and a greater increase in parental ratings of child social skills than did those in the wait-list control group. At 12-month follow-up, both CBT groups had retained their improvement. Beidel, Turner, and Morris (2000) demonstrated the efficacy of social effectiveness therapy for children (SET-C) in comparison to an active but nonspecific intervention (Testbusters): children ages 8–12 treated with SET-C had enhanced social skill, reduced social anxiety, decreased associated psychopathology, and increased social interaction both at posttreatment and at 6-month follow-up.

Researchers have also examined whether the treatment should be delivered individually, with family, or with peers. In the Spence et al. (2000) study described above, superior results seemed to have emerged when parents were involved in CBT treatment, but this effect was not statistically significant. In a Type 3 study, Masia, Klein, Storch, and Corda (2001) piloted a school-based behavioral treatment for adolescents and con cluded that the school setting is a logical place to deliver the treatment because it is where the individuals with social anxiety endure the most distress.

Current research is attempting to identify the necessary or sufficient components in the psychosocial treatment of social phobia, as well as the optimal context. Based on meta-analyses of adult studies, exposure in some form may be a key ingredient (Beidel et al., 2000). Treatment of the adolescent with social phobia may require different treatment interventions from those used in the younger ages (Beidel et al., 2000; Spence et al., 2000).

Pharmacotherapy of Social Anxiety Disorder in Children and Adolescents

As recently as 1999, no definitive data existed on the efficacy of psychopharmacology in the treatment of anxiety disorders in youth (excluding OCD) (Labellarte, Ginsburg, Walkup, & Riddle, 1999). In 2001, fluvoxamine, an SSRI, was studied in children and adolescents 6 to 17 years of age with either social phobia, SAD, or generalized anxiety disorder (GAD; Walkup et al., 2001). Youth (N = 153) were evaluated and enrolled in a 3-week open treatment trial with supportive psychoeducational therapy. Only five children improved with brief psychoeducation and did not go on to medication therapy. One hundred and twenty-eight children were assigned to either fluvoxamine or placebo for 8 weeks. The fluvoxamine dose was increased every week by 50 mg to a maximum of 300 mg/day for adolescents and 250 mg/day for children less than 12 years of age. The average dose of fluvoxamine was 2.9 + 1.3 mg/kg, and the average last dose was 4.0 + 2.2 mg/kg. The medication was generally well tolerated; five children in the fluvoxamine group and one in the placebo group discontinued because of adverse effects. Adverse effects were more common in the medication group; abdominal discomfort was significantly greater in the fluvoxamine group than in the placebo group, and there was a trend toward a greater frequency of increased motor activity in the fluvoxamine group. The youth in the fluvoxamine group had significantly greater reductions in symptoms of anxiety and higher rates of clinical response than did the children in the placebo group. On the CGI scale, 48 of 63 (76%) of children had a response to treatment, in comparison to only 19 of 65 children (29%; p < .001). The study led to the conclusion that fluvoxamine is an effective treatment for children and adolescents with social phobia, SAD, or generalized anxiety.

In follow-up analyses, Walkup and colleagues (RUPP, 2003) examined the data for moderators and mediators of pharmacologic response in these 128 youths. Interestingly, no significant moderators of efficacy were identified, except for lower baseline depression scores, based on “parent” (but not “child”) report, which were associated with greater improvement. Patients with social phobia and greater severity of illness, irrespective of medical assignment, were less likely to improve. Further study will be needed to determine why the diagnosis of social phobia predicted a less favorable outcome in this specific study.

Although there have been few studies examining the effects of treatments that combine CBT and medication in adults, no systematic studies of combined treatment for children and adolescents with social phobia exist. Given the lack of information about adolescents with anxiety disorders, efficacy studies on both CBT and pharmacotherapy and on the relative efficacy of each treatment alone and in combination are very much needed.

Selective Mutism: Is It a Form of Social Phobia?

Over the last 10 years, the literature has focused on the relationship between selective mutism and social phobia across developmental phases, in particular as to whether selective mutism is a childhood form of later social phobia. Selective mutism is currently classified under “disorders usually first diagnosed in infancy, childhood or adolescence,” in DSM-IV (American Psychiatric Association, 1994). There is an emerging consensus that it is most consistent with an anxiety disorder. Although still somewhat debated, selective mutism may represent a childhood form of social phobia (Black & Uhde, 1992, 1995; Dummit et al., 1997; Steinhausen & Juzi, 1996). Some have argued that selective mutism should not continue to be a separate diagnostic category but rather be considered a symptom, or subtype, of social phobia (Anstendig, 1999; Black & Uhde, 1995; Dummit et al., 1997).

Psychosocial (Behavioral) Treatment for Selective Mutism

Behavioral treatment of selective mutism has generally been the initial and the primary intervention in clinical practice, but there are no randomized controlled trials (RCTs) evaluating behavioral treatment. On the basis of Type 6 case reports and single case designs, contingency management, exposure-based techniques, and self-modeling are the most frequently used behavioral interventions (Anstendig, 1998; Cunningham, Cataldo, Mallion, & Keyes, 1984; Holmbeck & Lavigne, 1992; Kehle, Owens, & Cressy, 1990).

Pharmacological Treatment of Selective Mutism

Despite the paucity of controlled trials on the efficacy of medications for the treatment of selective mutism, pharmacotherapy is often used in clinical practice. In one Type 1 report, Black and Uhde (1994) treated 16 children with selective mutism with single-blind placebo for 2 weeks. The 15 placebo nonresponders were then randomly assigned to double-blind treatment with fluoxetine (N = 6) or placebo (N = 9) for 12 weeks. The mean maximum dose of fluoxetine was 21.4 mg/day (range 12–27 mg/day, 0.60 to 0.62 mg/kg/day). Side effects were minimal, and all double-blind patients completed the 12 weeks. Patients on fluoxetine (N = 6) were significantly better than those on placebo (N = 9) on parent's rating of mutism change and global change. However, clinician and teacher ratings did not show any significant differences between those receiving medication and those on placebo. The authors suggested that this could in part be due to the small number of patients or the more severe baseline symptoms of the medication group. Nevertheless, the authors cautioned that despite improvement for some, patients in both groups remained very symptomatic at the end of the study.

Generalized Anxiety Disorder

Treatment of Generalized Anxiety Disorder in Adults

Several CBT programs have been developed and empitacally evaluated for GAD. As might be expected given the nature of GAD, some of these protocols place less emphasis on exposure to specific fear cues and instead focus primarily on the development of effective coping strategies, of which exposure-based procedures (e.g., worry time) are among several techniques used. The outcome data for CBT are generally encouraging, with several meta-analytic reports indicating very large within-subjects effects and moderate to large effects in comparison to psychosocial control treatments and to low-dose diazepam treatment (Borkovec & Ruscio, 2001; Gould, Buckminster, Pollack, Otto, & Yap, 1997). Although the efficacy of several CBT programs has been established, outcome studies also suggest that there is significant room for improvement, especially with respect to the percentage of patients who achieve high end-state functioning (Orsillo, Roehmer, & Barlow, 2003). This observation has prompted recent innovations in GAD treatment, including the addition of interpersonal elements into the existing CBT programs (Borkovec, Newman, & Castonguay, 2003).

Several medications have been found effective for acute treatment of GAD. Benzodiazepines, such as alprazolam, have demonstrated short-term efficacy for reducing GAD symptoms, with response rates (usually defined as a 40%–50% improvement in symptoms on the Hamilton Anxiety Scale or a CGI improvement rating of “moderately” or “much” improved) as high as 75%. Benzodiazepines have the advantage of being faster acting than alternative medications. Despite concerns about side effects (e.g., sedation, memory loss, physiologic dependence, withdrawal syndromes), benzodiazepines are still among the most widely used medications for treatment of GAD. Buspirone has also been found effective in controlled trials and its side- effect profile (e.g., not sedating) may be better tolerated by some patients than that of benzodiazepines.

Antidepressant medications have shown efficacy for GAD in controlled trials. Because of very high rates of comorbidity of GAD with depressive disorders and symptoms, antidepressant medications may provide additional benefits for GAD patients. However, most antidepressants are slower acting than benzodiazepines, often taking 3–4 weeks for benefits to become obvious. Tricyclic antidepressants (TCAs) such as imipramine demonstrated benefit over placebo in early controlled trials, yet recent controlled trials have shown benefits for newer antidepressants such as the SSRI paroxetine and the dual serotonin–norepinephrine reuptake inhibitor (SNRI) venlafaxine-XR. The latter is the first antidepressant to receive a U.S. Food and Drug Administration (FDA) indication for treatment of GAD. These antidepressants are well tolerated and lend to long-term treatment, and not surprisingly have quickly become commonplace for treatment of GAD. For a detailed review of pharmacotherapy for adult GAD see the report by Roy-Byrne and Cowley (2002).

In examining the relative and combined efficacy of CBT and medication, Power et al. (1990) randomly assigned 113 patients to one of five treatment conditions: CBT + diazepam (DZ), CBT + placebo (PBO), CBT alone, DZ alone, and PBO. Percent responders, defined as reduction of >2 standard deviations from pretreatment, at posttreatment were 90.5% for CBT + DZ, 83% for CBT + PBO, 86% for CBT, 68% for DZ, and 37% for PBO. All active treatments were superior to PBO, but did not differ from one another. Percent responders at 6-month follow-up were 71% for CBT + DZ, 67% for CBT + PBO, 71% for CBT, and 41% for DZ; chi-squared analysis revealed the superiority of treatments that included CBT treatments over medication (DZ) alone.

Generalized Anxiety Disorder in Children and Adolescents

Generalized Anxiety Disorder is primarily excessive worry in one or more areas of one's life. Youth with GAD are often viewed by others as “little adults” because their worries may focus on keeping schedules, family finances, the environment, health issues, relationships, and perfectionism—themes that are more typically concerns for adults. Youth with GAD may not be disruptive or acting-out in their behavior, so their difficulties may go unnoticed by parents, family, and teachers. Nevertheless, their internal distress interferes with their overall functioning.

Preliminary data evidences developmental differences in symptom report between older and younger children with GAD (formerly overanxious disorder [OAD]), and it seems that with age, children's manifestation of GAD changes in both content and in symptom number (Kendall & Pimentel, 2003; Strauss, Lease, Last, & Francis, 1988). There also appear to be differences across GAD symptoms with respect to their efficiency in yielding a DSM-IV diagnosis (Pina, Silverman, Alfano, & Saavedra, 2002). In addition, older children, over the age of 12, present with a higher number of overall symptoms, as well as more anxiety about past events. This increase in symptom report may be somewhat GAD-specific, rather than a mere function of increased age, as findings with youth with SAD often reveal that younger children report more symptoms than do older children (Francis, Last, & Strauss, 1987).

Psychosocial Treatment of Generalized Anxiety Disorder in Children and Adolescents

Historically, a wide range of treatments has been used to treat youth with GAD, including various psychological approaches (e.g., behavioral, cognitive-behavioral, psychodynamic, family, play) as well as medications. Only a very small number of treatments have met the criteria for and have been assigned the label of “empirically supported.” With regard to GAD, much of this research has been with children, not with adolescents. Our descriptions here of the treatment of GAD in youth will place an emphasis on the treatments that have received empirical support.

The results of several Type 1 randomized clinical trials using CBT, conducted by different research groups, support the application of this ap proach (Barrett, Rapee, Dadds, & Ryan, 1996; Flannery-Schroeder & Kendall, 2000; Kendall, 1994; Kendall et al., 1997; Mendlowitz et al., 1999). Evidence to date suggests that CBT for children and adolescents is effective compared to no-treatment control conditions (e.g., Barrett, Dadds, & Rapee, 1996; Kendall, 1994; Kendall et al., 1997) and that CBT for youth with anxiety is a “probably efficacious” treatment (Chambless & Hollon, 1998).

An initial Type 1 randomized clinical trial evaluated a CBT protocol with 8-to 13-year-old children (Kendall, 1994). The manual-based CBT intervention (called the “Coping Cat”) targets one or more of the following disorders; SAD, social phobia, and GAD. A large percentage of the cases in the report were highly comorbid and many had GAD as the primary disorder. Cognitive-behavioral therapy addresses the cognitive biases associated with anxiety through psychoeducation, cognitive restructuring to change self-talk, relaxation training, guided imagery, problem solving, and numerous graded exposure tasks. In this RCT, 47 children ages 8 to 13 years were randomized to either CBT or a wait-list condition. Children in the CBT condition demonstrated significant improvement from pre-to posttreatment on self-reported distress, parent-reported distress of child, and, importantly, diagnostic status. Specifically, 66% of treated children no longer met criteria for their principal anxiety diagnosis following treatment.

In a second Type 1 randomized clinical trial (Kendall et al., 1997), 94 children aged 9 to 13 years were randomized to the CBT protocol or a wait-list condition. Over 50% of treated youth were free of their principal diagnosis at posttreatment, with significant reductions in disorder severity even for the youth remaining symptomatic. Other controlled trials (e.g., Barrett, 1998) support the efficacy of CBT in childhood anxiety (for review see Kazdin & Weisz, 1998; Ollendick & King, 2000) and CBT protocols have also been adapted to the group format (Flannery-Schroeder & Kendall, 2000; Manassis et al., 2002; Silverman et al., 1999a).

When considering the treatment of adolescents with GAD, one must take into account that the literature on the treatment of “child and ad-olescent” anxiety is based primarily on studies that have evaluated treatments for youth ages 7 to 14, with a mean age around 10.6 (e.g., Barrett, Dadds et al., 1996; Kendall, 1994; Kendall et al., 1997). Moreover, in one of these studies (Barrett, Dadds, et al., 1996), the treatment effects were not the same across age ranges, showing that a combined CBT and family intervention was significantly more effective than CBT alone for 7-to 10-year-old children, but not for 11-to 14-year-old children. This finding suggests that older children might respond differently than younger children to the same treatment. More research on this important topic is sorely needed.

Most of the CBT treatments that have been empirically supported for children have substantial room for improvement when applied to adolescents. First, we cannot assume that previous findings from children ages 7 to 14 automatically apply to all adolescents. Second, adolescence is a transitional period, characterized by more biological, physical, psychological, and social role changes than any other stage except infancy (Kendall & Williams, 1986). However, these developmental differences among children and adolescents have been largely ignored in treatment outcome studies of anxious youth. Holmbeck and colleagues (2000) note, “although many authors advocate for adaptations of treatment manuals in ways that take development into account, few provide methods for doing so” (Holmbeck et al., 2000, p. 339). Similarly, Weisz and Hawley (2002) assert that one of the long-term goals for the field of treatment outcome research should be to “develop an array of developmentally tailored treatments that are effective with clinically referred teens” (p. 21). Because treatments have not fully addressed the developmental changes of adolescence, one could argue that the impact of the treatment on the adolescent's anxiety disorder has not yet been examined empirically.

To date, no controlled studies have investigated CBT for adolescent GAD. It is important for such studies to be conducted because GAD is prevalent in adolescents (see Merikangas & Avenevoli, 2002).

Pharmacotherapy of Generalized Anxiety Disorder in Children and Adolescents

There are limited data on pharmacotherapy of GAD, and anxiety disorders in youth in general, with the exception of OCD (March, Biederman, et al., 1998). This situation exists despite the fact that there has been an increase in the use of psychotropic medications in child and adolescent samples (Pincus et al., 1998; Zito et al., 2000). There are few adequately designed studies available that establish the safety and efficacy of any class of medication for childhood GAD (Allen, Leonard, & Swedo, 1995; Bernstein, Borchardt, & Perwein, 1996). Medication options for the treatment of GAD in children and adolescents would appear to include the benzodiazepines, the nonbenzodiazepine anxiolytic buspirone, the SSRIs, and the TCAs. These medications have efficacy in adult GAD (Rickels, Downing, Schweizer, & Hassman, 1993) and venlafaxine has also been shown to be effective for adult GAD (Derivan, Entsuah, Haskins, Rudolph, & Aguiar, 1997; Rickels, Pollack, Sheehan, & Haskins, 2000). However, at this juncture there are not adequate data with regard to the use of medications with adolescents.

Although there exists a literature on the effectiveness of benzodiazepines in adult anxiety disorders (Rickels et al., 1983; Rickels, Schweizer, Case, & Greenblatt, 1990), there have been only a few studies, with small sample sizes, to examine the use of benzodiazepines in childhood anxiety disorders (Biederman, 1987; Graae, Milner, Rizzotto, & Klein, 1994; Simeon et al., 1992). Most of the studies involve children and adolescents with additional comorbidities such as major depression, panic disorder, and school refusal (Bernstein, Garfinkel, & Borchardt, 1990; Kutcher & Mackenzie, 1988). The results of these studies are mixed, with some finding positive results and others finding limited efficacy for benzodiazepines. Because of the inconsistency in results, reports of potentially serious side effects (Rickels et al., 1990, 1993), and risk of dependency and withdrawal, the benzodiazepines cannot be considered a front-line treatment.

Although buspirone has been shown to have both anxiolytic and antidepressants affects in adults (Rickels et al., 1990, 1991), it does not appear to be a highly effective or broad-spectrum anxiolytic in youth (Pohl, Balon, Yergani, & Gershon, 1989; Sheehan, Raj, Sheehan, & Soto, 1990).

Most of the clinical trials in which TCAs were used did not have children and adolescents with GAD only, but rather the much more complicated comorbid group of “school-refusing” children. The several Type 1 placebo-controlled studies of TCAs for children with anxiety-based school refusal provide conflicting results (Berney et al., 1991; Bernstein et al., 1990; Gittelman-Klein & Klein, 1973; Klein, Manuzza, Chapman, & Fyer, 1992). None of these studies were designed to examine children with the primary diagnosis of GAD, so no conclusions can be drawn as to the efficacy of TCAs for this anxiety disorder. Another issue of concern with TCA use in children is associated with a growing recognition of cardiac risk (Popper & Ziminitzky, 1995; Riddle, Geller, & Ryan, 1993; Riddle, Nelson, et al., 1991; Varley & McClellan, 1997). Given the uncertain clinical efficacy of TCAs for anxiety-disordered children (including GAD) plus the significant side effects, this class of medication is not a first choice.

The SSRI antidepressants are potential candidates for the treatment of childhood GAD. The safety of the SSRIs recommends them, as does their effectiveness in treating depression, which may be comorbid with childhood GAD. The SSRIs have shown preliminary efficacy in the treatment of adult GAD (Pohl, Wolkow, & Clary, 1998) and there is some evidence to suggest the use of SSRIs to treat childhood GAD. Unfortunately, the majority of studies include patients with GAD, SAD, social phobia, selective mutism, and anxiety disorder not otherwise specified. In Type 3 open trials, fluoxetine has shown some preliminary benefit for overanxious disorder, SAD, and social phobia (Birmaher et al., 1994; Fairbanks et al., 1997; Manassis & Bradley, 1994). In a Type 1 study, Rynn, Siqueland, and Rickels (2001) randomized (n = 22) children meeting the diagnosis of GAD to receive either placebo or 50 mg (maximum dose) of sertraline for 9 weeks, with positive results. The main side effects of the sertraline-treated children, as compared to the placebo-treated children, were dry mouth, drowsiness, leg spasms, and restlessness. The RUPP study (2001), mentioned earlier, also provides supportive evidence.

There have been previous reports of activation or agitation with the SSRIs, and it appears to be dose related (Apter et al., 1994; Riddle, Harin, & King, 1990; Riddle, King, et al., 1991). With these recent positive studies, it appears that SSRIs are emerging as the first line medication treatment for childhood anxiety disorders. Because of withdrawal symptoms being reported with the discontinuation of SSRIs, including nausea, headache, dizziness, and agitation (Labellarte, Walkup, & Riddle, 1998), these medications should not be abruptly discontinued.

The combination of medications and CBT for the treatment of GAD has several potential merits and a few potential enigmas. First, the GAD youth who is nonresponsive to one of the approaches may be responsive to the other or to their combination. Second, on the optimistic side, it may be that the combined treatment effect is additive—medications reduce initial distress and prepare the client for a more active and involved participation in CBT treatment. A less optimistic view of the combined treatment is that a medication may detract from the efficacy of CBT. That is, if exposure to the situation and the facing of the unwanted emotional distress in that situation contribute to the efficacy of CBT, then it is possible that the medication-produced nonanxious condition will prevent the CBT participant from experiencing the anxiety during exposure to in vivo tasks. The effectiveness of the medications could undermine one of the thought-to-be-active aspects of CBT (habituation to anxiety in the situation). Clearly, research on this question is very much needed.

Separation Anxiety Disorder

Distress upon separation from home or caretakers is a normal developmental feature. However, it can become so intense as to cause marked interference with ordinary function. In the extreme, children or adolescents are limited in their independent activities, unable to venture out alone, and may resist going to school. In young children fear of going to school (school phobia) is almost invariably due to separation anxiety, whereas in adolescence, social anxiety or depression may be involved. Likewise, childhood school refusal behavior is often associated with SAD, whereas school refusal behavior in adolescents may be more strongly linked to social anxiety disorder.

Psychosocial Treatment of Separation Anxiety Disorder in Children and Adolescents

Indirect information on psychosocial treatment comes from a Type 1 controlled study of behavior therapy combined with either imipramine or a placebo in 45 6-to 14-year-olds with school refusal specifically due to separation anxiety (Gittelman-Klein & Klein, 1971, 1973). To enter the drug study, children had to fail 4 weeks of vigorous behavioral therapy (Gittelman-Klein, 1975)—half (50%) of the children responded. With another 6 weeks of behavior therapy, now combined with a placebo, another 20% improved; thus 70% of severely separation-anxious children derived marked benefit from 10 weeks of behavior therapy. The comprehensive behavioral treatment in the Gittelman-Klein report had beneficial impact, but its precise efficacy is unknown because there were no comparison conditions. A Type 3 naturalistic study of school refusers reported superior efficacy of behavior therapy compared to inpatient care and to home schooling (Blagg & Yule, 1984). The lack of randomization weakens the conclusions.

Type 1 studies of CBT for children with school refusal behavior have also been conducted (King, Leonard, & March, 1998; Last, Hansen, & Franco, 1998). King et al. (1998) found that 4 weeks of CBT was superior to a wait-list control. School attendance was higher in the treated children than in the untreated children (89% vs. 60%), and ratings of anxiety also showed meaningful differences. In contrast, Last et al. (1998) found no significant difference in the improvement rate between CBT and standardized educational support treatment: mean percentages of school attendance were 67% and 60%, respectively. The more stringent criterion of 95% school attendance was met by 22% of the CBT group and 21% of those receiving educational support. In both treatments, a high rate of children judged themselves to be improved, as did parents and clinicians (90% to 100%), but considerably less were considered well by independent raters.

Other studies of CBT have not focused solely on SAD but have included youth with this disorder in addition to other anxiety disorders. These studies have reported efficacy in treating SAD (e.g., Kendall, 1994; Kendall et al., 1997). Another Type 1 study (Silverman et al., 1999a) focused mostly on specific fears, the majority (67%) consisting of anxiety at bedtime requiring the presence of a parent, a cardinal symptom of separation anxiety. Following 10 weeks, children showed similar patterns of improvement with CBT, behavior therapy focusing on training parents in contingency management, or educational support.

Some investigators have examined whether parental involvement in treatment contributes to childrens' improvement. Of all the childhood anxiety disorders, SAD can be said to have the most direct impact on the family. Consequently, there is a strong rationale for parental involvement in treatment. A study of anxious school refusers reported significant superiority for the condition involving parents and teachers in the children's treatment, compared to treatment without this component (Heyne et al., 2002), but the advantage was not sustained over a 5-month follow-up. In a recent Type 1 study, group CBT was compared to a group family anxiety management program and to a wait-list control for youth with mixed anxiety disorders, 43% of whom had separation anxiety (Barrett, 1998). The treatments were superior to the wait-list condition, but did not differ from each other on most outcome measures.

Pharmacotherapy of Separation Anxiety Disorder in Children and Adolescents

The first use of a pharmacological agent, imipramine, in SAD derived from a postulated relationship between this childhood condition and adult panic disorder (Klein, 1964; Klein & Fink, 1962). Marked clinical benefit for imipramine (mean 125 mg/day) versus a placebo was reported in a Type 1 study of 45 children with school phobia and separation anxiety (Gittelman-Klein & Klein, 1971). A smaller study (N = 20) failed to replicate earlier positive findings (Klein, Koplewicz, & Kanner, 1992). These two treatment studies targeted SAD specifically. Another study failed to observe a significant advantage in school-phobic children treated with relatively low doses of clomipramine (75 mg/day) (Berney et al., 1981). More recently, a Type 1 controlled trial in adolescent school refusers reported efficacy for imipramine (Bernstein et al., 2000), but interpretation is complicated by the comorbidity of major depression. The well-documented cardiotoxic effects of high doses of TCAs have limited their usefulness, especially since SSRIs do not present such a risk.

Clinical reports have claimed benefit from high-potency benzodiazepines (i.e., clonazepam) in mixed anxiety, but the only Type 1 controlled trial did not confirm these clinical observations (Graae et al., 1994). The design of this trial was less than rigorous, however. Benzodiazepines can induce behavioral disinhibition in children, which limits their application.

As noted earlier, a Type 1 multisite, placebo-controlled study (N = 128) of fluvoxamine (up to 300 mg/day) in children with separation anxiety, social anxiety, and generalized anxiety disorders reported a marked advantage for the medication (RUPP, 2001) with an overall improvement rate of 78% for fluvoxamine vs. 29% for placebo. There were no interactions for diagnosis and treatment outcome, except for the lesser response rate among patients with social phobia than that among those with other diagnoses (RUPP, 2003). Therefore, it may be surmised that SAD responded to fluvoxamine.

At this time, SSRIs may be the first-line pharmacological treatment for childhood SAD, but we are in need of information specifically regarding adolescents. On the whole, the SSRIs are well tolerated and have a favorable side effect profile, and some have demonstrated efficacy.

Specific Phobia

Treatment of Specific Phobia in Adults

Although it is relatively uncommon for adults with only a specific phobia to seek treatment, it is also one of the most effectively treated disorders. The primary treatment for specific phobias is CBT. Several controlled studies have found that up to 90% of participants experienced significant symptom reduction within 2 to 3 hr of therapy (Öst, 1989; Öst, Ferbee, & Furmark, 1997; Öst, Salkovskis, & Hellstroem, 1991). The effectiveness of CBT is likely the result of exposing the patient to feared stimuli in a supportive environment. This is commonly done systematically, with the therapist using a hierarchy to address the patient's fears. Research has also shown that although exposures tend to be more effective when therapists model the treatment tasks for the patient, direct observation in and of itself is generally not sufficient (e.g., Öst et al., 1997). With the exception of dental phobias (e.g., Jerremalm, Jaansson, & Öst, 1986), cognitive therapy alone has not been examined in the treatment of specific phobias.

Researchers have examined the effectiveness of benzodiazepines, beta-blockers, and SSRIs in treating specific phobias. Some controlled studies have found benzodiazepines to be helpful for patients who are averse to initial exposures to feared stimuli, or who simply need acute symptom relief (e.g., Schmidt, Koselka, & Woolaway-Bickel, 2001). However, both controlled and uncontrolled studies have found long-term use of benzodiazepines to be associated with unsatisfactory outcome and a myriad of other complications (Sanderson & Wetzler, 1993; Westra & Stewart, 1998). These unwanted effects include depression, a higher rate of symptom relapse once drugs are discontinued, and a risk of drug tolerance, dependence, and abuse (Spiegel & Bruce, 1997).

The use of benzodiazepines in conjunction with exposure therapy was found to interfere with the treatment efficacy of exposure (e.g., Marks et al., 1993; Wilhelm & Roth, 1997). Studies have shown benzodiazepines to interfere with both the acquisition and retention of new information (Barbee, Black, & Tordorov, 1992) and to affect the way new information is stored in memory (Gray, 1987). This interference can cause state-dependent learning, whereby information encoded in the presence of the drug may not be properly retrieved in a drug-free state. In addition, uncontrolled studies have reported that the use of benzodiazepines can interfere with the development of tolerance to anxiogenic stimuli on a neurochemical level (Gray, 1987). It has been speculated that these medications interfere with the central nervous system's ability to adapt to persistently elevated levels of neurotransmitters involved in the stress response (Anisman & Zacharko, 1992). More research is needed to further examine these potentially important findings.

Specific Phobia in Children and Adolescents

Fear is a normal response to active or imagined threat that is characterized by affective, behavioral, and cognitive components. As discussed elsewhere (King et al., 1988; Ollendick, King, & Muris, 2002), nearly all children and adolescents experience some degree of fear. For the most part, these fears are adaptive—they appear to emanate from day-to-day experiences of children and they reflect their emerging cognitive and representational capabilities. Moreover, most of these fears do not involve intense or persistent reactions, and they are short-lived. This is not so with specific phobias.

Psychosocial Treatment of Specific Phobia in Children and Adolescents

Using criteria established for empirically supported treatments (see Chambless & Hollon, 1998; Chambless & Ollendick, 2000), Ollendick and King (1998, 2000) have indicated that two psychosocial treatments have attained “well-established” status (participant modeling, reinforced practice) and five treatments have achieved “probably efficacious” status (imaginal desensitization, in vivo desensitization, live modeling, filmed modeling, and verbal self-instruction) in the treatment of phobic disorders in children. The well-established treatments have been shown to be more effective than credible placebo controls in at least two RCTs, whereas probably efficacious treatments have been shown to be more effective than wait-list control conditions in at least two RCTs or to be more effective than a credible placebo control in at least one RCT. Support for these interventions has come solely from intervention studies with children 12 or 13 years of age and younger. None of the studies treated specific phobia in adolescents. More research is needed with adolescents to determine the efficacy of behavioral treatments for them. Two recent studies conducted have examined cognitive-behavioral interventions in samples that included adolescents.

In the first Type 1 study examining the treatment of both children and adolescents, Silverman et al. (1999b) examined the relative benefits of an operant-based contingency management treatment and a cognitive-based self-control treatment, in comparison to an education-support control group. Graduated in vivo exposure was used in both the self-control and the contingency management conditions but not in the education-support condition. Phobic children (N = 81) between 6 and 16 years of age along with their parents were evaluated using child, parent, and clinician measures. The children were assigned randomly to one of the three 10-week manualized treatment conditions (i.e., self-control, contingency management, or education support). Although all three conditions were found to impart improvement in the child's functioning as measured by the reports of children, parents, and clinicians, clinically significant improvements were noted only in the two cognitive-behavioral treatment conditions. Specifically, on a measure of clinical distress at posttreatment, 80% of the participants in the self-control and 80% of the participants in the contingency management conditions reported very little or no distress, compared to only 25% in the education-support condition. Notably, 88% of the participants in the self-control condition no longer met diagnostic criteria at posttreatment compared to 55% in the contingency management and 56% in the education-support condition.

In the second Type 1 study, Öst, Svensson, Hellström, and Lindwall (2001) evaluated the effects of a cognitive-behavioral procedure referred to as “one-session treatment” on phobic children and adolescents 7 to 17 years old. The hallmark of this one-session treatment is a graduated, systematic, prolonged exposure to the phobic stimulus combined with the active dissuading and repair of faulty cognition. As such, it involves a combination of strategies including cognitive restructuring, in vivo graduated exposure, participant modeling, and social reinforcement. Notably, this treatment has been designed to be maximally effective in one session, and therefore lasts 3 or more hours in length. Results indicated that the treatment was superior to wait-list and produced significant gains both immediately posttreatment and at 1-year follow-up (Öst et al., 2001). Also, in a Type 3 study, one-session treatment has been found to be comparable to other, longer treatments with more sessions (see Muris, Merckelbach, Holdrinet, & Sijsenaar, 1998). Presently, Ollendick and Öst are completing a larger Type 1 study examining the effectiveness of one-session treatment in comparison to educational support and wait-list conditions. Approximately 200 youth with specific phobias are participating in this trial, which is being conducted in the United States and Sweden.

Pharmacotherapy of Specific Phobia in Children and Adolescents

At present, no randomized pharmacological treatment studies of specific phobia in children and adolescents have been completed (Ginsburg & Walkup, 2004). The lack of such studies appears to be related to the common misconception that specific fears are a part of normal experience and not a condition associated with impairment. On the basis of the findings obtained with adults, however, SSRIs may be effective among children and adolescents with specific phobia (in contrast to the benzodiazepines and TCAs). A recent Type 3 open trial suggests their utility. Fairbanks et al. (1997) completed a 9-week trial of fluoxetine in children ages 9 to 18 years with mixed anxiety disorders (N = 16). After not responding to brief psychotherapy, patients were started on low-dose fluoxetine (5 mg/day), which was then increased weekly until side effects or improvement occurred to a maximum of 40 mg/day (children) and 80 mg/day (adolescents). Of the 16 patients enrolled, 6 had specific phobia and 4 of the 6 responded to fluoxetine. The medication was also generally well tolerated.

To date, no randomized clinical trials have examined the joint efficacy of psychosocial and pharmacologic treatments with children or adolescents. Given the promise of several treatments, however, there is reason to believe that beneficial effects of combined treatment may occur. Research into their combinatorial effects is needed before any conclusions can be drawn.

Panic Disorder

Treatment of Panic Disorder in Adults

The efficacy of cognitive, behavioral, and cognitive-behavioral treatment programs has been examined and is now well established for panic disorder. Under a broad theoretical umbrella, the emphasis in treatment has been on disconfirming mistaken beliefs about the meaning of physical sensations (Clark, 1986, 1996) and on exposing the patient to the feared physical sensations (Barlow, 1988). Cognitive-behavioral therapy has proven efficacious even when cognitive therapy is condensed (Clark et al., 1999). A commonly used protocol, panic control treatment, has been found to be efficacious in several studies (e.g., Zarate, Craske, & Barlow, 1990), and in the largest combined treatment study published to date, it was superior to pill placebo at the end of acute treatment but not superior to imipramine alone (Barlow et al., 2000). Notably, although panic control treatment typically includes breathing retraining, a procedure designed to minimize panic sensations, a recent controlled study indicated that the inclusion of breathing retraining did not provide incremental benefit above and beyond CBT alone, and on some outcome measures actually yielded less favorable outcome (Schmidt et al., 2000).

A wide range of medications have demonstrable efficacy for panic in the initial phase of treatment, including TCAs, low-and high-potency benzodiazepines, monoamine oxidase inhibitors (MAOIs), and SSRIs. Because of the comparable efficacy to that of older medications, yet a vastly superior side-effect profile, SSRIs are now considered first-line medications for treating panic. Paroxetine was the first SSRI approved by the FDA for panic disorder and its antipanic effects have been demonstrated in placebo-controlled studies. A 12-week double-blind, placebo-controlled study of 367 panic patients found that both paroxetine and clomipramine were superior to placebo (Lecrubier, Bakker, Dunbar, & Judge, 1997). Compared to clomipramine, paroxetine acted more quickly to block spontaneous panic attacks, overall was associated with less adverse effects, and for 9 months after the 12-week acute phase demonstrated improvement. In a double-blind, placebo-controlled study, Ballenger, Davidson, Wheadon, and colleagues (1998) compared different doses of paroxetine and concluded that 40 mg daily was the most effective dosage. Sertraline (now also FDA approved), fluvoxamine, and fluoxetine have all shown significant ability to block panic compared to placebo. The general pattern of treatment response is as follows. First, spontaneous panic attacks are blocked, usually within the first 6 to 8 weeks. This is followed by a gradual reduction in anticipatory anxiety and agoraphobic avoidance behavior. A critical issue that has emerged from virtually all studies of SSRI treatment for panic is the vulnerability of these patients to jitteriness, restlessness, and increased anxiety during initial dosing. Starting with low doses is thus recommended (e.g., paroxetine 10 mg/day, sertraline 25 mg/day, fluvoxamine 50 mg/day, fluoxetine 10 mg/day) with gradual increases to the optimal target dose.

High-potency benzodiazepines are also effective for panic disorder. Alprazolam and clonazepam have been the most widely studied. In Phase 1 of the Cross-National Collaborative Panic study of 481 panic patients, alprazolam at a mean dose of 5.7 mg/day was more effective than placebo with a 55% response rate (compared to 32% placebo rate) at the 8-week end point (Ballenger, Davidson, Lecrbier, et al., 1998). Rosenbaum, Moroz, and Bowden (1997) conducted a multicenter, parallel group, placebo-controlled, fixed-dose study of clonazepam in 413 patients. Patients were randomly assigned to one of five fixed doses. The results indicated significant improvement at all doses but a differentiation of the four higher doses from the 0.5-mg dose and placebo. The mini mum effective dose was 1 mg; beyond this dose all doses were equally efficacious. Reticence to prescribe benzodiazepines for panic has been based on the (unwarranted) assumption that patients will gradually escalate the dose to achieve therapeutic effect in a pattern similar to that seen in substance abusers. However, controlled studies have shown that panic disorder patients are not likely to increase dosages and actually found such increases to be uncomfortable and associated with unwanted effects (Salzman, 1993).

With respect to TCAs, imipramine has been the most studied antipanic agent, with several studies demonstrating superiority over placebo. The serotonergic-acting clomipramine also has strong antipanic effects and in one placebo-controlled trial was actually superior to imipramine and placebo (Modigh, Westberg, & Eriksson, 1992). However, the majority of studies point to equivalent efficacy for TCAs and SSRIs yet a superior side-effect profile with SSRIs (Bakker, Spinhoven, van der Does, van Balkom, & van Dyck, 2002). Although venlafaxine, nefazodone, and mirtazapine have not been studied in a controlled fashion, they have all been shown to exhibit antipanic action, particularly in patients with comorbid depression. For a detailed review of the literature on panic disorder treatment outcome see Roy-Byrne and Cowley (2002).

Panic Disorder in Children and Adolescents

Panic disorder can be a disabling condition accompanied by psychosocial, family, peer, and academic difficulties (Birmaher & Ollendick, 2004; Moreau & Weissman, 1992; Ollendick, Mattis, & King, 1994). In addition, panic disorder is associated with increased risk for other anxiety disorders, major depressive disorder (MDD), and substance abuse (Birmaher & Ollendick, 2004; Moreau & Weissman, 1992). Moreover, such adverse outcomes are more prevalent in adults whose panic disorder starts early in life (before 17 years of age; see Weissman et al., 1997). Despite this, it takes on average 12.7 years from the onset of reported symptoms for adults to initiate and seek treatment (Moreau & Follet, 1993). Unfortunately, it appears that very few youngsters with panic disorder seek help at all (Essau, Condradt, & Petermann, 1999).

Psychosocial Treatment of Panic Disorder in Children and Adolescents

Psychosocial treatments for panic disorder have been based largely on cognitive and cognitive-behavioral theories (Chambless & Ollendick, 2000), and the few studies of cognitive-behavioral treatment of panic disorder in children and adolescents have used a protocol based largely on panic control treatment (Barlow, 1988). This treatment consists of three primary strategies: relaxation training and breathing retraining to address neurobiological sensitivities to stress, interoceptive exposure to address heightened somatic symptoms, and cognitive restructuring to address faulty misinterpretations associated with the somatic symptoms. Adolescent treatment studies based on Barlow's model have been sparse; however, two Type 3 case series studies lend initial support to its use and one randomized, large-scale, Type 1 treatment outcome study appears promising. In the first of the Type 3 studies, Barlow and Seidner (1983) treated three adolescents who had panic disorder with agoraphobia using an early version of panic control treatment. The patients were treated in a 10-session group-therapy format and were accompanied by their mothers, who were enlisted to facilitate behavior change. Following treatment, two of the three adolescents showed considerable improvement in their symptoms; the third did not show significant change. In the second of the Type 3 studies, Ollendick (1995) used a multiple baseline design to illustrate the effects of an adapted version of panic control treatment with four adolescents who had panic disorder with agoraphobia. The adolescents ranged in age from 13 to 17 years; however, their panic attacks began when they were between 9 and 13 years of age, nearly 4 years on average prior to the beginning of treatment. The patients were treated individually but, as in Barlow and Seidner's (1983) study, their mothers were enlisted to facilitate behavior change. Treatment varied in duration but lasted between 10 and 12 sessions for the four adolescents. Treatment was effective for all the patients eliminating panic attacks, reduc ing agoraphobic avoidance, decreasing accompanying negative mood states, and increasing self-efficacy for coping with previously avoided situations and panic attacks should they occur in the future.

Presently, Mattis and colleagues are in the final stages of a Type 1 RCT of a developmental adaptation of panic control treatment for adolescents (PCT-A) and a self-monitoring control condition in the treatment of panic disorder. Three aspects of panic disorder are addressed in this 11-session, manualized intervention: (1) the cognitive aspect of panic disorder or the tendency to misinterpret physical sensations as catastrophic; (2) the tendency to hyperventilate or overbreathe, thus creating and/or intensifying physical sensations of panic; and (3) conditioned fear reactions to the physical sensations. Although the trial is still under way, initial findings suggest a reduction in severity of panic attacks and panic disorder in patients receiving PCT-A relative to those in the monitoring control group (Mattis et al., 2001).

Pharmacotherapy of Panic Disorder in Children and Adolescents

No RCTs for the pharmacological treatment of panic disorder in children and adolescents have yet been completed (Birmaher & Ollendick, 2004). In children and adolescents, anecdotal case reports suggest that benzodiazepines and the SSRIs (Birmaher & Ollendick, 2004) may be efficacious for panic disorder. For example, in a prospective Type 3 open trial, Renaud, Birmaher, Wassick, and Bridge (1999) treated 12 children and adolescents with panic disorder with SSRIs for a period of 6 to 8 weeks. Nearly 75% of the youth showed much to very much improvement with SSRIs without experiencing significant side effects. At the end of the trial, eight (67%) no longer fulfilled criteria for panic disorder whereas four (33%) continued to have significant and lasting effects.

Panic disorder is accompanied frequently by a variety of other mental health disorders (Biederman, Faraone, et al., 2001; Mattis & Ollendick, 2002). Treatment of these comorbid conditions may be needed to improve the youngster's overall functioning. Fortunately, two of the common comorbid disorders, depression and other anxiety disorders, also respond to CBT and/or SSRIs (Birmaher et al., 1994; Brent et al., 1997; Emslie et al. 1997; Kendall et al., 1997; Ollendick & King, 1998; RUPP, 2001).

To date, no randomly controlled clinical trials have examined the joint efficacy of psychosocial and pharmacologic treatments with children or adolescents with panic disorder. Given the independent promise of both treatments, however, there is reason to believe that synergistic effects could occur. Nevertheless, research into their separate and combined effects, such as that pursued in adult populations (e.g., Barlow et al., 2000), is needed.

Obsessive-Compulsive Disorder

Treatment of Obsessive-Compulsive Disorder in Adults

Among the psychosocial treatments for OCD, exposure and response (or ritual) prevention (EX/RP) is the most well-established treatment for adults, having been found superior to a variety of active and control treatments (for a review see Franklin & Foa, 2002). In this treatment patients gradually confront situations that evoke their obsessional fears (e.g., sitting on the floor, where they feel contaminated by germs) and at the same time are refrained from reducing their discomfort by performing ritualistic behaviors (e.g., excessive washing and cleaning).

The only medications studied in randomized clinical trials and reported to be efficacious for OCD are serotonin reuptate inhibitors (e.g., clomipramine) and the SSRIs (e.g., fluoxetine, fluvoxamine, sertraline, paroxetine, citalopram). The data suggest a 20% to 40% reduction in symptoms, but many patients classified as responders in these trials still have clinically significant symptoms. Moreover, patients with severe comorbid MDD or significant substance abuse have usually been excluded (for a review see Dougherty, Rauch, & Jenike, 2002).

Several RCTs examining the efficacy of combined treatment have been conducted in OCD (Cottreaux et al., 1990; Foa, Rothbaum, & Furr, 2003; Hohagen et al., 1998; Marks et al., 1988; van Balkom et al., 1998), and their collective re sults suggest that combined treatment, at least as applied simultaneously, has not proven to be a panacea (Foa, Franklin, & Moser, 2002; Franklin & Foa, 2002). In trials directly comparing serotonin reuptake inhibitors (SRIs) and CBT (including EX/RP), outcome has been influenced by the design of the study, the SRI dosage, and the quality and the quantity of the EX/RP delivered. When intensive EX/RP (e.g., 15 sessions delivered five times per week for 3 weeks) was compared to adequately dosed clomipramine over 12 weeks, arguably the two most efficacious OCD treatments, the two treatments were both superior to placebo and EX/RP was superior in most analyses (Foa et al., 2005). Further, when results from this study using an intensive CBT approach are compared with a study employing weekly CBT with and without concomitant medication (Cottraux et al., 1990), intensive CBT alone appears to fare better than weekly CBT alone, with no differences evident in the combined treatment groups (Foa, Franklin, & Moser, 2002). It is important to note that response prevention in the study by Foa et al. (2005) appears to have been more strictly applied than that in the Cottraux et al. study (1990), and thus the effects of the visit schedule cannot be isolated in this comparison. Nevertheless, perhaps the addition of medication may enhance outcome when EX/RP is not implemented intensively or when variations are made to the EX/RP protocol.

Obsessive-Compulsive Disorder in Children and Adolescents

Children and adolescents with OCD typically present with both obsessions and compulsions, although the youngest sufferers may have difficulty articulating their obsessions. As is the case with adults, the cardinal feature of OCD in youth is neutralizing: when the patient describes anxiety-inducing thoughts or images and attempts to relieve this anxiety or reduce the chances that feared consequences would occur by performing some overt or covert neutralizing behavior, the OCD diagnosis should be considered. Functional impairment is required for diagnosis as well, as subclinical obsessions and compulsions are probably ubiquitous. Insight into the senselessness of obsessional concerns is not required for diagnosis in children and adolescents, and, as with adults, probably exists along a continuum from complete awareness of their senselessness to no insight (Foa, Hearst-Ikeda, & Perry, 1995). In general pediatric OCD is formally similar to OCD in adults, yet the content of obsessions and compulsions is likely to be influenced by developmental factors. For example, younger children are generally more “magical” in their thinking and thus may have more superstitious OCD symptoms (e.g., “If I don't retrace my steps then something really bad will happen to my little sister”). As with adults, some pediatric OCD patients are able to identify feared consequences of not ritualizing (e.g., books will be stolen if the locker is not checked), whereas others experience anxiety and distress in the absence of articulated consequences. Further, although the logic of some patients' feared consequences is shared by many in their culture (e.g., contracting disease via direct contact with a public toilet seat), other patients' fears are extremely unusual (e.g., losing their essence by discarding trash that has touched them). It is important to recognize that bizarre content does not necessarily preclude a diagnosis of OCD and that patients with such unusual fears may also be responsive to CBT (Franklin, Tolin, March, & Foa, 2001).

A subgroup of children with pediatric onset of either OCD or a tic disorder has been described by the term PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infection). These children have an abrupt onset of symptoms after a group A β‎-hemolytic streptococcal infection (GABHS), and their course of illness is characterized by dramatic acute worsening of symptoms with periods of remission (Swedo 1994, Swedo et al., 1998). The PANDAS subgroup is defined by five clinical characteristics: (1) presence of OCD and/or a tic disorder; (2) prepubertal symptom onset; (3) dramatic onset and acute exacerbations with an episodic course of symptom severity; (4) temporal association between symptom exacerbations and GABHS infections; and (5) associated neurological abnormalities (e.g., choreiform movements) (Swedo et al., 1998). Identification of this subtype is important because the symp toms may require a different assessment and treatment. In a child who has an acute onset of OCD and/or tics or has had a dramatic deterioration, medical illnesses (including seemingly benign upper respiratory infections) in the prior months should be carefully considered. A throat culture, antistreptolysin O (ASO) titer, and anti-DNaseB streptococcal titer may help to diagnose such an infection, even in the absence of clinical symptoms of pharyngitis (Murphy & Pichichero, 2002; Swedo et al., 1998).

Psychosocial Treatments of Obsessive-Compulsive Disorder in Children and Adolescents

Expert Consensus Guidelines (March, Francis, Kahn, & Carpenter, 1997) and the American Academy of Child and Adolescent Psychiatry (AACAP) Practice Parameters for OCD (King et al., 1998) consider CBT, specifically the features of EX/RP, an important intervention, and recommend starting with CBT or CBT plus an SSRI, depending on severity and comorbidity. Exposure and response prevention involves therapist-assisted in vivo exposure to feared situations, imaginal exposure to feared “disasters,” and instructions to refrain from rituals and avoidance behaviors. In the treatment of OCD, cognitive therapy procedures are sometimes used to identify faulty cognition, engage in cognitive restructuring and, with behavioral experiments, have the patient be exposed to situations that are designed to “disconfirm” the faulty cognition. Notably, exposure exercises provide the patient with the information that is needed to “correct” their distorted thinking without formal cognitive therapy.

Although CBT (specifically EX/RP) is recommended for children by Expert Concensus Guidelines and AACAP Practice Parameters (King et al., 1998; March, Frances, et al., 1997), there are no published large RCTs of CBT with children or adolescents. Uncontrolled CBT treatment trials reported to date suggest that most of the patients were responders, with a mean symptom decrease from 50% to 67%. March, Mulle, and Herbel (1994) reported on the outcome of a Type 3 study of a manualized and structured CBT protocol with 15 youth ages 8 to 18 years. There were significant differences between pre-and posttreatment, with a mean reduction in symptom severity of about 50%. Sixty-seven percent of the patients had better than 50% symptom improvement (which was maintained at follow-up). Only 20% were nonresponders. At the end of treatment, 40% were rated as asymptomatic, and at follow-up 60% were rated as such. Forty percent of the sample was able to discontinue medication with booster sessions. This work has led to a manual for children and adolescents with OCD (8 to 17 years) (March & Mulle, 1998), and an RCT comparing the relative efficacy of this CBT manual, sertraline, combined treatment, and placebo has just been completed (Franklin, Foa, & March, 2003); a second RCT comparing EX/RP plus family therapy to relaxation is also nearing completion (J. Piacentini, personal communication).

Franklin and colleagues (1998) conducted a Type 3 study and reported that 14 youth (ages 10 to 17 years) had a 67% improvement at posttreatment, and found no difference in response between those who received CBT alone and those with CBT in combination with an SRI. Others have also reported generally positive results for CBT in Type 3 open studies (Piacentini et al., 1994; Wever & Rey, 1997). Most of the studies used a weekly therapy regimen, generally over 3 months. Wever and Rey (1997) used a more intensive CBT protocol of 10 daily sessions over 2 weeks and found generally similar results. Franklin and colleagues (1998) reported that there was no difference in results, regardless of whether the treatment was delivered in 14 weekly sessions over 14 weeks or in 18 sessions over 4 weeks, although there was no random assignment.

In the only published direct Type 1 comparison of CBT and pharmacotherapy for pediatric OCD, de Haan, Hoogduin, Buitelaar, and Keijsers (1998) reported that whereas CBT and clomipramine both appeared to reduce OCD symptoms, CBT was superior to clomipramine. Until the systematic comparisons of single and combined treatments are completed, the relative efficacy cannot be directly compared, although the existing data suggest that CBT may provide more durability than medication.

The family context may play an important role in treating OCD. Freeman, Garcia, and Leonard (2003) proposed that the family is a vehicle for treatment of OCD in youth and in the treatment of childhood anxiety disorders more broadly (Barrett, Dadds, et al., 1996; Howard & Kendall, 1996; Sanders, 1996; Siqueland & Diamond, 1998). Cognitive-behavioral therapy with family intervention can and often does involve parents and significant others as “behavior change agents.” Because the affective and cognitive aspects of the parent–child relationship, as well as the anxiety targets of intervention, are dealt with, the approach has been called cognitive-behavioral family therapy. Freeman and colleagues (2003) have manualized a treatment for children and their families with OCD, and initial pilot results are promising.

Pharmacotherapy of Obsessive-Compulsive Disorder in Children and Adolescents

The systematic efficacy studies of the SRIs for the treatment of pediatric OCD form the largest body of work in the pharmacotherapy of the childhood psychiatric disorders, other than that of ADHD. An increasing literature supports the acute efficacy of clomipramine and the SSRIs in the treatment of children and adolescents with OCD.

The TCA clomipramine (an SRI) was the first medication systematically studied in children and adolescents with OCD. Three studies supported the efficacy of clomipramine for pediatric OCD (DeVeaugh-Geiss et al., 1992; Flament et al., 1985; Leonard et al., 1989). Flament and colleagues (1985) reported in a Type 1 study that in 23 youth in a 10-week double-blind, placebo-controlled, crossover study, clomipramine (in doses of 3 mg/kg) was significantly more effective than placebo in decreasing OCD symptomatology at week 5. For some patients, a reduction in symptoms was seen by 3 weeks. Of the 19 children who completed the trial, 75% had a moderate to marked improvement, and only 16% of the patients were unchanged. Extending this finding in an 8-week multicenter double-blind, parallel Type 1 study, DeVeaugh-Geiss and colleagues (1992) reported that clomipramine was superior to placebo for the treatment of OCD in youth. The 31 patients on clomipramine had a mean reduction in OCD severity scores of 37%, compared to 8% in the 29 patients on placebo. This study led to FDA approval for an SRI in pediatric OCD (children 10 years and older). The studies reported that clomipramine was generally well tolerated and had an anticholinergic adverse-effects profile. Periodic electrocardiograms (EKGs) are obtained during ongoing clinical care because of concerns about tachycardia and prolongation of the QTc interval.

To address whether the serotonergic specificity of clomipramine was critical, a double-blind crossover Type 1 study of clomipramine and desipramine (a selective noradrenergic reuptake inhibitor without serotonergic activity) was completed in 48 children and adolescents with OCD (Leonard et al., 1989). In this 12-week double-blind design, a patient received two weeks of placebo, then 5 weeks of clomipramine and 5 weeks of desipramine in a crossover. Clomipramine (targeting 3 mg/kg/day and not exceeding 5 mg/kg/day) was significantly better than desipramine in decreasing the OCD symptoms at week 5. Desipramine was no more effective in reducing OCD symptoms than placebo was in the Flament et al. (1985) study. The study noted that some of the patients who had received clomipramine in the first phase and desipramine in the second phase had a return of their symptoms when transferred to desipramine in the last phase, which suggests that the serotonergic reuptake inhibition may be critical.

With the development of the SSRIs, there is considerable discussion as to whether clomipramine is more effective than the SSRIs and at what point it should be chosen over the SSRIs. Initial meta-analysis (Griest, Jefferson, Kobak, & Katzelnick, 1995) indicated that clomipramine might be somewhat more effective than an SSRI for OCD in adults, but small head-to-head comparisons of clomipramine and fluvoxamine (Freeman, Trimble, Deakin, Stokes, & Ashford, 1994) and of fluvoxamine, paroxetine, and citalopram (Mundo, Bareggi, Pirola, & Bellodi, 1997) suggest that they have equivalent efficacy. The Expert Consensus Guidelines (March, Frances, et al., 1997) suggest that clomipramine be used when a patient has failed two or three adequate trials of an SSRI in combination with CBT.

The SSRIs have now emerged as the first-line pharmacotherapeutic agent for OCD. They have the advantage over clomipramine of having a generally more tolerable side-effect profile with few anticholinergic effects, safer profile in overdoses, and no required EKG monitoring. Large multicenter Type 1 efficacy studies have shown that fluoxetine, fluvoxamine, and sertraline were each superior to placebo for children and adolescents with OCD (Geller et al., 2001; March, Biederman, et al., 1998; Riddle et al., 2001). Type 3 open studies support the use of citalopram and paroxetine (Rosenberg, Stewart, Fitzgerald, Tawile, & Carroll, 1999; Thomsen, 1997). The FDA has approved sertraline for the treatment of OCD in children ages 6 years and older, fluvoxamine for children ages 8 years and older, and fluoxetine for 8 years and older.

March, Biederman, and colleagues (1998) reported on 187 children and adolescents (ages 6 to 17 years of age) with OCD in a randomized double-blind, placebo-controlled, 8-week trial of sertraline (forced titration to 200 mg/day) versus placebo. Patients on sertraline, in comparison to those on placebo, showed significantly greater improvement on the several scales. Significant differences (with intent-to-treat analyses) between the two groups were seen as early as week 3 and continued for the entire study.

Riddle and colleagues (2001) reported the safety and efficacy of fluvoxamine for 120 youth (ages 8 to 17 years) with OCD in an RCT in which youth received either fluvoxamine (50–200 mg/day) or placebo for 10 weeks. Patients in the fluvoxamine group had a significant improvement (as measured on the Children's Yale-Brown Obsessive-Compulsive Scale, CY-BOCS) in comparison to the placebo group, and a difference could be measured as early as the first week. In the fluvoxamine group, 42% were responders (defined as a 25% decrease in measure of OCD symptom severity, CY-BOCS) in comparison to 26% in the placebo group, which was significantly different.

Geller and colleagues (2001) randomized 103 youth with OCD to either fluoxetine (starting at 10 mg/day) or placebo (in a 2:1 ratio) for 8 weeks. Intent-to-treat analyses reported that those in the fluoxetine group had significantly better improvement on CY-BOCs than did the placebo group. The authors concluded that fluoxetine at 20 to 60 mg daily was effective and well tolerated in the pediatric group. In contrast, Liebowitz and colleagues (2002) randomized 43 patients to either fluoxetine or placebo for 8 weeks. Responders then went into an 8-week maintenance phase. Fluoxetine dosage was fixed at 60 mg/day for 6 weeks and then could be increased to 80 mg/day. At week 8, fluoxetine was not significantly better than placebo on the CY-BOCs or CGI-Improvement scale; authors attributed this to either low power or short duration of treatment. The fluoxetine group continued to improve during the maintenance phase such that at week 16, 57% of the fluoxetine patients, as compared to 27% of the placebo patients (using data at week 8), were much or very much improved. The authors concluded that fluoxetine's effect took more than 8 weeks to develop.

Review of adverse effects of the SSRIs suggests that dropouts from blinded active medication assignment are usually less than 13%, and in many studies there are no significant differences between the dropouts receiving medication or placebo (March, 1999). Generally, the most common side effects seen with the SSRIs include sedation, nausea, diarrhea, insomnia, anorexia, tremor, sexual dysfunction, and hyperstimulation (March, Biederman, et al., 1998; Riddle et al., 2001). Children and adolescents may be more vulnerable to agitation or activation while on SSRIs than are adults, but this is not well studied. Rare adverse reactions include apathy syndrome, serotonin syndrome, and extrapyramidal symptoms. Pharmacokinetic studies of sertraline (Alderman, Wolkow, Chung, & Johnston, 1998) and of paroxetine (Findling et al., 1999) reported wide intra-and between-individual pharmacokinetic variability but generally similar results to those reported in adults.

How large is the treatment response on an SSRI? The pediatric treatment response is similar to that reported in adults. In general, a 30%–40% reduction in OCD symptoms, which corresponds to an average 6-to 8-point decrease on the CY-BOCS (Scahill et al., 1997), is reported in the medication treatment group in the SSRI controlled studies (March, 1999). Unlike some of the other disorders, there is little or no placebo effect reported. Clinical benefits may begin as early as 3 weeks and typically plateau at about 10 weeks (March, 1999).

The Expert Consensus Guidelines (March, Frances, et al., 1997) and the AACAP Practice Parameters for OCD (King et al., 1998) both recommend starting treatment in children with CBT or CBT plus an SSRI, depending on severity and comorbidity. Both guidelines recommend that patients started on SSRI alone who are partial responders should have a trial of CBT. The study of the relative efficacy of medication, of CBT, and their combination has just been completed using a Type 1 randomized controlled trial (Franklin et al., 2003; Pediatric OCD Collaborative Study Group, 2004; Foa & March, personal observations).

Investigational Treatments

Hypotheses concerning whether Sydenham's chorea and PANDAS might share similarities in their pathophysiology have led to the question of whether penicillin prophylaxis would reduce neuropsychiatric symptom exacerbation in children with PANDAS by preventing streptococcal infection. An 8-month, Type 1 double-blind, placebo-controlled, crossover trial of oral penicillin V (250 mg twice daily) and placebo was conducted in 37 children (Garvey et al., 1999). There was no significant difference between phases in either the OCD or tic symptom severity; however, penicillin administration failed to provide adequate prophylaxis against GABHS (as evidenced by the fact that 14 of 35 GABHS infections occurred during the penicillin phase). A number of children received antibiotic treatment multiple times during the placebo phase. The authors concluded that because of the failure to achieve an acceptable level of streptococcal prophylaxis, no conclusions could be drawn regarding the efficacy of penicillin prophylaxis in preventing tic or OCD symptom exacerbation. Further studies are needed that use a more effective prophylactic agent and include a larger sample size. Clinical experience would recommend workup for GABHS infection in children with abrupt and sudden onset of OCD or tics and dramatic exacerbations (Murphy & Pichichero, 2002; Swedo et al., 1998).

If post-streptococcal autoimmunity is the cause of the exacerbations in this subgroup, then children with PANDAS might benefit from immunomodulatory therapies that have been shown in preliminary findings to treat symptoms of Sydenham's chorea. In a Type 1 study, children with severe, infection triggered exacerbations of OCD or tic disorders were randomly assigned to plasma exchange (five single-volume exchanges over 2 weeks), intravenous immunoglobulin (IVIG;1 g/kg daily on 2 consecutive days), or placebo (saline solution given in the same manner as IVIG). Plasma exchange and IVIG were both effective in lessening of symptom severity for this group of children. Ratings were completed at 1 month and symptom gains were maintained at 1 year (Perlmutter et al., 1999). It should be noted that these children were more much significantly impaired than the average child with OCD or tics, and thus these invasive interventions were considered. These interventions are investigational and should only be considered in the context of research approved by a human investigations committee and not in the context of routine clinical care (Leonard & Swedo, 2001).

Posttraumatic Stress Disorder

Treatment of Posttraumatic Stress Disorder in Adults

With respect to psychotherapy for addressing posttraumatic stress disorder (PTSD), treatments derived from behavioral and cognitive theoretical models have been most carefully examined. In RCTs, the efficacy of several CBT treatments has been evaluated, including prolonged exposure (PE), anxiety management, eye movement desensitization and reprocessing (EMDR), cognitive therapy, and treatment packages that combine approaches.

Summaries of the studies of PE with veterans (e.g., Cooper & Clum, 1989; Glynn et al., 1999; Keane, Fairbank, Caddell, & Zimmering, 1989a) have consistently indicated that although exposure therapy is superior to various control conditions, the magnitude of the improvement has been somewhat limited. Because of the extent and chronicity of their problems and the presence of incentives for the veterans to minimize acknowledging treatment gains (e.g., losing service-connected disability compensation), evaluating the efficacy of a treatment within a veteran population is a very strict and difficult test. Indeed, in contrast to the exposure therapy findings with veterans, RCTs examining the efficacy of PE and other CBT interventions in civilian populations have generally yielded very positive results. Among the comparative outcome studies conducted using civilian samples, exposure therapy has been found to be as or more effective than relaxation, self-instructional training (SIT), and cognitive therapy (e.g., Devilly & Spence, 1999; Echeburua, Corral, Zubizarreta, & Sarasua, 1997; Foa et al., 1999; Marks, Lovell, Noshirvani, Livanou, & Thrasher, 1998; Resick, Nishith, & Griffin, 2003). Moreover, the addition of CBT procedures to exposure therapy alone does not augment its efficacy (Foa et al., 2003).

Multiple medications and classes of medications have been found to be effective in treating PTSD (Albucher & Liberzon, 2002). But there are relatively few placebo-controlled trials of medications outside the class of SSRIs (Albucher & Liberzon, 2002). Sertraline (Davidson, Rothbaum, van der Kolk, Sikes, & Farfel, 2001), paroxetine (Marshall, Beebe, Oldhau, & Zaninelli, 2001; Tucker et al., 2001), and fluoxetine (Martenyi et al., 2002a, 2002b) were found to be significantly more efficacious than placebo for symptom reduction and have few side effects (Albucher & Liberzon, 2002). Both have received FDA indication for PTSD. The SSRIs are considered the first-line pharmacotherapy for PTSD related to both interpersonal and wartime trauma as well as acute and chronic PTSD (Marshall et al., 2001; Smajkic et al., 2001; Tucker et al., 2001). A clinician-administered PTSD scale evidenced a 25%–30% reduction, but most of the patients classified as responders still have clinically significant symptoms despite significant reductions in number and severity of symptoms after an average of 12 weeks of medication (Marshall et al., 2001).

Other classes of medications shown to be effective for symptom reduction in double-blind, placebo-controlled trials include reversible and irreversible MAOIs, TCAs, and the anticonvulsant lamotrigine (Hageman, Andersen, & Jorgensen, 2001). However, these medications all have higher rates of side effects than the SSRIs (Albucher & Liberzon, 2002; for a review see Hembree & Foa, 2003).

Posttraumatic Stress Disorder in Children and Adolescents

Adolescence represents a developmental transition in the maturation of self-efficacy in the face of danger. There is increasing reliance on the peer group for appraisal of danger and estimation of needed protective actions along with greater engagement of the peer group in dangerous and protective behavior. Developmental epidemiology suggests that adolescence carries a high risk of exposure to a spectrum of traumatic situations, subsequent PTSD, comorbid psychopathology, and age-related impairments. Included among the salient types of exposure are adolescent physical and sexual abuse (Kaplan et al., 1998; Pelcovitz, Kaplan, DeRosa, Mandel, & Salzinger, 2000); interpersonal and community violence (Berman, Kurtines, Silverman, & Serafini, 1996; Kilpatrick, Acierno, Resnick, Saunders, & Best, 1997; Wolfe, Scott, Wekerlee, & Pittman, 2001); serious accidental injury, especially traffic accidents; traumatic losses, including those by homicide, suicide, and fatal automobile accidents; and life-threatening medical illness accompanied by life-endangering medical procedures (e.g., kidney and liver transplant) (Shemesh et al., 2001). For example, juveniles are two times more likely than adults to be victims of serious violent crime and three times more likely to be victims of simple assault. There are differential rates of exposure, with boys more likely to experience criminal assault and girls, dating violence and rape. A national survey of adolescents found that 23% reported having been both a victim of assault and a witness to violence, and that over 20% met lifetime criteria for PTSD (Kilpatrick, Saunders, Resnick, & Smith, 1995). In addition to general rates of exposure to war and disasters, international studies indicate that adolescents in these situations are often engaged in resistance and rescue efforts (Nader et al., 1989) that expose them to many stressful experiences. Studies among adolescents suggest that there may be multiple forms of exposure, with comorbid admixtures of PTSD, depression, and SAD (Pelcovitz, Kaplan, DeRosa, et al., 2000; Warner & Weist, 1996). Finally, adolescent exposures may be superimposed on prior trauma histories and untreated chronic posttraumatic stress symptoms.

Considerable evidence indicates that traumatized adolescents are at increased risk for a spectrum of adverse psychosocial difficulties and functional impairments. These include reduced academic achievement; aggressive, delinquent, or high-risk sexual behavior; substance abuse and dependence (Cavaiola & Schiff, 1988; Collins & Bailey, 1990; Farrell & Bruce, 1997; Kilpatrick et al., 2000; Saigh, Mroueh, & Bremner, 1997; Saltzman, Pynoos, Layne, Steinberg, & Aisenberg, 2001); and nonadherence to prescribed posttransplant medical treatment (Shemesh et al., 2001). Further, trauma in adolescence has been linked with long-term developmental disturbances, including disrupted moral development, missed developmental opportunities, delayed preparation for professional and family life, and disruptions in close relationships (Goenjian et al., 1999; Layne, Pynoos, & Cardenas, 2001; Malinkosky-Rummell & Hansen, 1993; Pynoos, Steinberg, & Piacentini, 1999). Ongoing reactive behavior to trauma reminders in adolescence carries the bimodal risk of reckless behavior or extreme avoidant behavior that can derail the adolescent's life.

Psychosocial Treatment of Posttraumatic Stress Disorder in Children and Adolescents

Given the high rates of trauma and serious adverse consequences, the treatment of PTSD in adolescence is emerging as an important area for the identification of evidence-based interventions. Advances are being made and the field of child and adolescent PTSD is at the cusp of placing the treatment of PTSD on an evidence-based foundation.

Beginning in the early 1980s, school-age children and adolescents were found to be able to describe their posttraumatic stress symptoms and to engage in the work needed to address their acute traumatic experiences. Pilot studies suggested clinical improvement in posttraumatic stress symptoms after (1) exploration of the complexity of the experience; (2) identification of the most traumatic moments; (3) repeated attention to the subjective and objective features of these moments, especially experiences of helplessness, fear, and ineffectualness; (4) clarification of distortions, misattributions, and confusions; and (5) identification of current trauma reminders and an increase in cognitive, emotional, physiological and behavioral management. At the same time, features of traumatic bereavement were distinguished from primary PTSD (Cohen et al., 2002; Pynoos, 1992). Similar to the treatment of adults, school-age children and adolescents were found to be capable of being helped to contend with their anticipatory anxieties about addressing their traumatic experience and were capable of mustering the needed courage to participate in treatment.

In the past decade, there have been continuous advances in treating PTSD in youth. The approaches have included individual, group, and family therapy modalities and psychopharmacology. Studies among school-age children, adolescents and young adults have provided preliminary evidence about the effectiveness of different interventions for adolescent PTSD. Key Type 1 randomized studies among school-age children have primarily examined CBT approaches for sexually abused children, using both symptoms and sexually inappropriate behavior as outcome measures. In a study of 100 sexually abused children Deblinger and colleagues (Deblinger & Heflin, 1996; Deblinger, Steer, & Lippman, 1999) provided evidence for the effectiveness of a 12-week CBT treatment that emphasizes gradual confrontation of traumatic thoughts, feelings, and memories, using response to even subtle trauma reminders to more fully explore their traumatogenic origins and ongoing cognitive, emotional, and physiological reactions. The CBT treatment included exposure components and cognitive therapy. Children treated alone or with their parents were significantly improved in PTSD symptoms, depression, and externalizing behavior, compared with treatment for the mothers only and with treatment as usual in community-based clinics. Studies of child sexual abuse treatment will benefit from follow-up into adolescence to measure treatment effects on later psychosexual developmental challenges and new sets of reminders. Pertinent to adolescent treatment strategies, when the age range of subjects extended from school age through late adolescence, a randomized clinical trial on treatment of child sexual abuse found no effect of parent involvement in treatment (King, Gaines, Lambert, Summerfelt, & Bickman, 2000). Cohen and Mannarino (1996a, 1996b, 1998) provided evidence for CBT effectiveness in comparison to supportive therapy for preschool and early adolescent subjects. Their CBT emphasizes developmental skills in emotional labeling and regulation. The effect size among adolescents was considerably greater than that for younger children. Each of these three treatment protocols includes a section devoted to promoting safety behaviors both currently and in the future.

Using a staggered start comparison group, March, Amaya-Jackson, Murry, and Schulte (1998) reported a robust beneficial effect of an 18-week CBT for school-age children and adolescents who experienced a single-incident traumatic experience. In this small size study (14 of 17 completers), there was significant improvement in PTSD, symptoms, depression, anxiety, and anger. The treatment was modeled on prolonged exposure (Foa & Rothbaum, 1998). Treatment began with anxiety management techniques and included a preparatory individual break-out session to establish a trauma hierarchy and initial trauma narrative before group exposure work. The treatment then moved toward a focus on “worst moments,” augmented by homework that addressed avoidant behavior, then promoted anger management skills, restructured future expectations, and finished with attention to relapse prevention. The study confirmed that adolescents can engage in this extended, demanding treatment with acceptance, safety, and effectiveness.

Two comparison studies reported the effectiveness of delayed, intermediate school-based trauma-focused interventions for school-age children and adolescents after large-scale disasters. One and one-half years after the catastrophic 1988 earthquake in Armenia, Goenjian et al. (1997) employed a five-foci approach (trauma reminders, traumatic experience[s], traumatic bereavement, secondary adversities, developmental progression) over six 90-min combined classroom and individual sessions for adolescents with severe chronic PTSD. When treated and untreated adolescents were compared 3 years after the earthquake, treatment was associated with significant improvement in PTSD and stable depressive symptoms, whereas untreated adolescents suffered a worsening of PTSD and exacerbation of depressive symptoms that reached clinical diagnostic levels. In this extremely traumatized population with persistent and pervasive postearthquake adversities, treat-ment gains were maintained for 1 and 1 2 years posttreatment and, even without specific strategies to ameliorate depression, this intervention appeared to have protected against adolescent depression.

Three and one-half years after Hurricane Iniki, Chemtob, Nakashima, and Carlson (2002) used a lagged group design to treat a group of school-aged children who continued to experience moderate levels of PTSD after being unresponsive to an earlier psychoeducational intervention. With a form of EMDR, this intermediate intervention sequentially addressed in four sessions positive cognition, worst memories, worst reminders, and fears about future hurricanes. Both treatment groups demonstrated pre-to posttreatment reductions in PTSD symptoms and moderate reductions in anxiety and depression. These gains were maintained at 6-month follow-up. These studies demonstrated the potential usefulness of school-based interventions across disasters of different magnitudes and ranges of PTSD outcomes, even if delayed by postdisaster circumstances.

More recently, manualized school-based, trauma-focused, adolescent group therapy has been studied among adolescents exposed to multiple traumatic experiences during war or urban community violence. The same five foci of treatment used by Goenjian et al. (1997) were employed, and specific adolescent measures were used to evaluate the targeted outcome improvement for each module. Layne, Pynoos, Saltzman, and colleagues (2001) reported on the treatment of 55 war-traumatized students from schools in Bosnia-Hercegovina 3 years after the Dayton Accords ended the war. The treatment resulted in significant reduction in PTSD, depression, and traumatic grief reactions. Saltzman, Pynoos, Layne, Steinberg, and Aisenberg (2001) reported on the treatment of chronic PTSD and academic impairment among urban adolescents living in a high-crime area. Similar results were achieved as in the Layne et al. study, with additional evidence for significant improvement in grade point average (GPA), especially reflected in reduced number of failed classes. As the study authors point out, the improvement in GPA to a “C” range carries significant developmental im-portance, as these adolescents were able to participate once again in many school interpersonal and enrichment activities that promote adolescent developmental progression. The group intervention was preceded by an individual session in which the adolescent formed a hierarchy of prior traumatic experiences, identified salient features and developmental impact, and selected one to focus on in treatment. As a prelude to core trauma-specific group and homework exposure exercises, the use of beginning strategies to inventory and enhance management of current trauma and loss reminders served as a useful introduction for adolescents to make the work immediately relevant, understandable, and acceptable. Since many adolescent exposures entail traumatic deaths, a specific module directed at traumatic bereavement was included. Beyond a focus on PTSD-related avoidant behavior, the last module focused on resumption of adolescent activities in response to missed developmental opportunities, restoration of investment in the social contract, and engagement in prosocial activities. These programs indicate the advantage of school-based interventions, with each study reporting nearly 100% completion rates. They also suggest that group formats may be powerful among adolescents, providing the opportunity to engage the peer group in reexamination of appraisal of danger and protective action. School-based group interventions also provide a potentially cost-efficient method of delivering mental health services to the underserved population of youth with unaddressed PTSD.

Pharmacotherapy of Posttraumatic Stress Disorder in Children and Adolescents

Pharmacotherapy of PTSD for children and adolescents is limited, with open trial reports and only one RCT (Cohen, 2001). The strategies include targeting specific symptoms, for example, sleep disturbance, that carry significant functional consequence, as well as overall symptom remission. The earliest report documented overall clinical improvement in a small sample of sexually and/or physically abused young children treated with propanolol (Famularo, Spivak, Bunshaft, & Berkson, 1988). Isolated clinical reports also suggest effective treatment of significant sleep disturbance in young children with clonidine or guanfacine (e.g., Harmon, Morse, & Morse, 1996). A clinical report on the use of carbamazepine in treatment of PTSD among a series of 28 children and adolescents suggested remission of PTSD, although children with comorbid conditions (half of the sample) required additional medications. With evidence for the efficacy of SSRIs in the treatment of adult PTSD discussed above, there is interest in conducting RCTs with children and adolescents.

Table 10.2 provides some tentative recommendations of acute treatment strategies for use with adolescents suffering from anxiety disorders. It is important to emphasize that the outcome literature remains underdeveloped and thus our suggestions should be viewed as just that, rather than as specific recommendations that have been rigorously tested with large samples.

Table 10.2 Recommendations for Acute Treatment Strategies

Anxiety Disorder

Psychosocial Treatment

Pharmacotherapy

Social anxiety disorder, selective mutism

CBT involving some form of exposure; needs to be adjusted to address specific fears in selective mutism (e.g., hearing own voice)

SRIs

Generalized anxiety disorder

CBT; development of problem-focused coping strategies to handle frequently changing themes

SRIs; possibly also TCAs, benzodiazepines, buspirone

Separation anxiety disorder

CBT; graded exposure rather than flooding

SRIs

Specific phobias

Exposure for most fears, possibly 3-hr sessions

If CBT is not available and problem is severe, possibly SRIs

Panic disorder

CBT, exposure to interoceptive cues

SRIs, possibly imipramine or benzodiazepines

Obsessive-compulsive disorder

CBT involving both exposure and response prevention

SRIs

Posttraumatic stress disorder

CBT involving exposure to traumatic memories and to objectively safe yet fear-evoking trauma-related situations

SRIs

CBT, cognitive-behavioral therapy; SRI, serotonin reuptake inhibitor; TCA, tricyclic antidepressant.

MAINTENANCE OF GAINS AFTER ACUTE TREATMENT

There is a paucity of knowledge about what happens after the acute phase of treatment with adults, children, and adolescents. Studies of CBT have commonly reported uncontrolled follow-up data, but did not control the treatments that patients received during the naturalistic follow- up period. These data suggest that on the average, a meaningful degree of maintenance of the gains that accrues from CBT, with few studies reporting only mild overall relapse. Although more data are needed, one study reported favorable maintenance of gains at a 7.4-year follow-up of cases treated with CBT (Kendall, Saf-ford, Flannery-Schroeder, & Webb, 2004). Traditionally, the vast majority of psychopharmacological trials have focused entirely on efficacy during acute, short-term treatment. More recently, studies have examined the effects of treatment during a longer, maintenance phase and after medication discontinuation. Even less is known about these effects in children and adolescents. Below we discuss what we know about maintenance of treatment gains and discontinuation of treatment in each disorder, for adults, children, and adolescents.

Social Anxiety Disorder

Maintenance trials with phenelzine, paroxetine, and sertraline in adults suggest that responders maintain their gains with continued medication (Liebowitz et al., 1992; Stein et al., 1996; Walker et al., 2000). However, discontinuation trials with phenelzine (after 9 months treatment), sertraline (after 20 weeks treatment), and paroxetine (after 13 weeks treatment) suggest that relapse rates are high when medication is discontinued. Use of CBT showed good continuation of gains during maintenance and after discontinuation in a comparative trial with phenelzine, and in another study in comparison with a psychoeducational condition. Knowledge about optimal lengths of treatment to minimize relapse and about predictors of who can discontinue when without relapsing are lacking, as are studies of maintenance of gains and treatment discontinuation in treated children and adolescents.

Separation Anxiety Disorder and Selective Mutism

No adult studies have examined these conditions that almost invariably occur exclusively during childhood and adolescence. Studies of CBT that have included separation-anxious children in the samples have generally shown maintenance of gains following treatment discontinuation (e.g., Barrett, Rapee, et al., 1996; Kendall et al., 1997) and SAD diagnosis has not been a predictor of poor outcome in these studies. Thus it can be surmised that CBT provides lasting benefits for these children. As mentioned above, SAD may be more common in young children, and its treatment and maintenance of gains have not been studied in adolescent samples. The treatment of selective mutism has also received little attention in the acute treatment literature, thus even less is known about maintenance of gains, especially in adolescents. In general, the available data indicate partial response to acute treatment, which suggests continued impairment. What is unknown is whether the posttreatment gains are maintained over time.

Generalized Anxiety Disorder

Relapse rates following discontinuation of acute benzodiazepine treatment in adults are as high as 80%, indicating the absence of maintenance of medication-produced gains (Rickels, Case, & Diamond, 1980; Rickels, Case, Downing, & Fridman, 1986). A few studies demonstrate lasting benefit for GAD patients treated for 6 months or more with benzodiazepines and buspirone. However, concern over physiologic dependence and potential for abuse make long-term treatment with benzodiazepines controversial. A recent placebo-controlled trial of venlaflaxine XR showed that benefits from this medication continued following 6 months of treatment and that it was well tolerated over the long term. Several CBT studies involving GAD in youth have indicated maintenance of gains up to 12 months after CBT discontinuation. In addition, there are supportive data for 3.5-year (Kendall & Southam-Gerow, 1996), 6-year (Barrett, 1998), and 7.4-year (Kendall et al., 2004) follow-ups. Although not all of these treated cases had GAD as the principal diagnosis and not all evidenced complete initial benefit from CBT, those individuals who do benefit seem to be able to maintain their gains for several years, even without continued treatment.

Specific Phobia

The adult literature on maintenance of gains following treatment of specific phobias generally suggests that benefits associated with CBT are lasting even when the treatment is delivered in a single 3-hour long session (Öst, 1989; Öst et al., 1991, 1997). Studies of children and adolescents have indicated that CBT produces significant gains immediately after treatment up to and at 1-year follow-up (Öst et al., 2001; Silverman et al., 1999a). The pharmacotherapy literature on this topic is underdeveloped and thus no conclusions can be drawn about maintenance of gain over time using this approach.

Panic Disorder

Mavissakalian and Perel (1992) compared patients who responded to 6 months of acute treatment with adult patients who had a similar response to a 6-month acute treatment period and then additionally received 1 year of half-dose maintenance imipramine treatment. Both groups entered a double-blind discontinuation study for 3 months, followed by a 3-month drug-free period. The group who had acute and maintenance treatment did significantly better during this 6-month period than the group that had only acute treatment. Maintenance treatment with antidepressants may have a significant prophylactic effect and reduce the rate of relapse after treatment discontinuation (Mavissakalian & Perel, 1992). A follow-up study found prophylactic efficacy for maintenance treatment continued beyond 1 year of maintenance and into a second year. However, the persistence of difficult side effects, particularly weight gain, was noted with imipramine over long-term treatment (Mavissakalian & Perel, 2001). A recent naturalistic study (Simon et al., 2002) involving 78 patients who achieved remission in an 8-week acute phase (with benzodiazepine alone, antidepressant alone, or both) and then received maintenance pharmacotherapy for 2 years found that 46% of these patients relapsed over the maintenance phase and that combination therapy did not confer any added advantage.

As briefly noted earlier, a multicenter trial studied the efficacy of medication therapy and CBT and explored whether combined therapy (medication plus CBT) is more effective than either therapy alone in a randomized, double-blind placebo study (Barlow et al., 2000). In terms of acute response, combined treatment did not differ from medication or CBT alone, but was better than placebo. The 6-month maintenance response rate of the combination therapy was high (approximately 57% for the Panic Disorder Severity Scale [PDSS] and 60% for the CGI) and significantly different from medication alone or CBT alone but not significantly different from CBT plus placebo. After the 6-month maintenance phase, patients had treatment discontinued and were followed for 6 months. Improvement in CGI was highest for CBT plus placebo (41%), 32% for CBT alone, 20% for imipramine alone, and 26% for combined treatment. This study and another large-scale RCT using alprazolam (Marks et al., 1993) indicate that combined treatment for panic disorder may be advantageous at posttreatment and during maintenance but may attenuate the benefits of CBT following medication discontinuation (for a review see Foa, Franklin, & Moser, 2002). Ollendick's (1995) small multiple-baseline study included follow-up over a 6-month interval, and these results affirmed the lasting effects of a similar treatment for a pediatric sample. Much more research employing controlled designs needs to be done using pediatric samples.

Obsessive-Compulsive Disorder

Little is known about how long SRI medication should be continued in OCD. In practice, many adult patients continue taking their medication for at least one year; some seem to require indefinite treatment. There are only three published double-blind SRI discontinuation studies (Koran, Hackett, Rubin, Wokow & Robinson, 2002; Pato, Zohar-Kadouch, Zohar, & Murphy, 1988; Romano, Goodman, Tamura, Gonzales, & the Collaborative Research Group, 2001) in adults with OCD. Each uses a different SRI (clomipramine, fluoxetine, sertraline) and comes to a different conclusion regarding the effects of discontinuing the SRI (substantial [89%] recurrence over 12 weeks for clomipramine, moderate relapse [32%] after one year and not different from staying on SRI [21%] for fluoxetine, low rate of recurrence [24%] after 28 weeks but significantly more than staying on SRI [9%] for sertraline). Given the paucity of blind studies and the methodological differences between them (e.g., relapse definition, length of follow-up, procedure for placebo substitution), the posttreatment effects of SRIs in OCD remain unclear.

A recent comparative trial of clomipramine and EX/RP in adults suggested that the relapse rate with clomipramine may not be as high (i.e., 45%) as previously thought. However, even with this lower relapse rate, EX/RP showed superior maintenance of gains 12 weeks after treatment discontinuation (Simpson et al., 2004). Optimal lengths of SRI treatment to minimize relapse, and predictors of who can discontinue without relapsing are lacking. Moreover, there is no agreement on the criteria to define relapse. The few open studies of CBT in pediatric OCD that have included follow-up data suggest good maintenance of gains following treatment discontinuation (Franklin et al., 1998; March et al., 1994; Wever & Rey, 1997), and the one study of pharmacotherapy discontinuation in pediatric OCD suggests that relapse is common (e.g., Leonard et al., 1991). A systematic follow-up study (done when clomipramine was available only investigationally and access to CBT was limited) of 54 children and adolescents with OCD treated acutely with clomipramine was completed (Leonard et al., 1993). Of the 54 subjects, 38 (70%) were taking psychoactive medication at follow-up; 23 of 54 (43%) patients still met diagnostic criteria for OCD, and 43 (80%) were improved from baseline. Of the six patients (11%) who were totally asymptomatic, three were taking medication at the time of reevaluation; thus, only three could be considered to be in true remission. This finding suggested that patients were improved at follow-up, but most were on medication maintenance, and only 3 of 54 were asymptomatic and not on medication. Although not every patient had attempted discontinuation of medication, this study for patients treated with an SRI indicates that they may require long-term maintenance therapy.

Posttraumatic Stress Disorder

Deblinger and colleagues' (Deblinger and Heflin, 1996; Deblinger et al., 1999) work with sexually abused children provided evidence for the long-term effectiveness of a 12-week CBT treatment. March, Amaya-Jackson, et al. (1998) reported a robust beneficial effect and maintenance of gains up to 6 months in a small study of CBT for school-age children and adolescents who experienced a single incident traumatic experience. Pharmacological studies in adolescents need to take into account the two adult randomized studies of SSRIs in the treatment of PTSD that indicate relapse with discontinuation of medication (Martenyi, et al., 2002a). These adult studies raise the same issue as that in the treatment of other anxiety disorders—whether a combination of medication and trauma-focused CBT would provide greater resistance to relapse.

A Comment on Relapse Prevention in Children and Adolescents

It is important to note that there has been no research specifically addressing maintenance treatment and relapse prevention for anxiety disorders in youth and adolescents. In general, the ultimate goal of most psychosocial treatment programs for anxiety disorders is to equip children with skills that will help them manage anxious distress after treatment discontinues; a “cure” for anxiety is not the goal (see Kendall, 1989). Because some degree of anxious arousal is likely to persist after treatment, modifying dysfunctional expectations and distorted processing styles can help to enable more adaptive functioning. The use of in vivo exposure tasks in treatment provides performance-based experiences of coping that bolster a child's confidence for future situations. Therapeutic intervention may be only a first step, but it is a step that helps to alter the maladaptive developmental trajectories of these children so that they are better able to address the inevitable challenges emerging in their lives. Upon completion of a treatment program, the guiding principle (and hope) is for the child to continue to practice the skills learned.

There are several clinical strategies to help guide youth toward consolidation of treatment-produced gains. First, the therapist should shape and encourage “effort” attributions regarding the management of anxiety. Youth should be encouraged to reward their hard work and coping efforts, even if the successes are only partial. A second principle for continued posttreatment functioning includes introducing children to the concept of “lapses in efforts,” rather than “relapses” (see also Brownell, Marlatt, Lichtenstein, & Wilson, 1986; Marlatt & Gordon, 1985). Mistakes and partial successes are not viewed as incompetence or inability; rather, they can be constructively framed as vital and inextricably linked to the learning process. Within this framework, children can label and accept inevitable setbacks as temporary and then proceed to work on forward-looking problem solving. Mistakes are viewed as an acceptable part of the learning process and not as excuses for giving up or confirming anxious cognition.

Maintenance treatment may require combinations of CBT and medications, booster sessions, or a return and reexperience of the initial therapy. Alternate approaches, or even as-yet undeveloped treatments may be needed, especially for cases that are refractory to the otherwise reasonably successful program. To date, the field is lacking information about how best to maintain treatments, prevent relapses, and integrate psychological and pharmacological approaches to maximize long-term gains.

MANAGEMENT OF PARTIAL RESPONSE AND NONRESPONSE

Social Anxiety Disorder

There are no controlled studies in any age group on how to address partial responders and nonresponders with social anxiety disorder. Cognitive-behavioral therapy is a logical candidate to augment partial drug response, and Liebowitz and colleagues have recently found CBT to be helpful in augmenting partial SSRI responders in an open trial (unpublished data). Gabapentin and clonazepam are also considered possible augmenting agents for partial SSRI re sponders. Complicating this research is the fact that there is no accepted definition of partial response.

Generalized Anxiety Disorder

Most adult GAD patients who improve with acute treatment do not reach full remission of symptoms. In early trials, full remission occurred in as few as one-third of GAD patients. Unfortunately, there are no systematic studies of treatment options for patients with partial medication response in GAD. Partial response and a nonresponder rate also characterize CBT outcomes for GAD. Unfortunately, there are no systematic trials assessing nonresponders to initial treatment.

Specific Phobia

There are no controlled data on how to address or augment partial responders and there are no controlled data on how to treat nonresponders to an initial drug or CBT trial.

Panic Disorder

A recent double-blind, placebo-controlled trial with adults found that pindolol had a beneficial augmentation effect on fluoxetine-treated panic patients (Hirschmann et al., 2000). Patients with panic disorder (N = 25) who had not responded to 8 weeks of fluoxetine (and prior to that, two other trials of antidepressants) were randomly assigned to pindolol or placebo for 4 weeks. The pindolol group achieved significant improvement on ratings compared to the placebo group. However, since the augmentation period studied was so brief, it is difficult to determine if these effects would be sustained and whether they would actually lead to remission. Three studies have examined the effects of benzodiazepine treatment combined with antidepressant treatment. Imipramine plus alprazolam was compared to imipramine plus placebo. The combination group responded with therapeutic effect more quickly. Clonazepam augmentation of paroxetine was shown to be superior to paroxetine alone (Mathew, Coplan, & Gorman, 2001). Goddard et al. (2001) studied 50 panic patients and randomized them to either .5 mg of clonazepam three times per day plus sertraline or placebo clonazepam plus sertraline for the first 4 weeks. At week 1, 41% of the combination group evidenced improvement compared to 4% of the placebo group. At 3 weeks, there was a significantly higher (63%) response rate in the combination group than that in the placebo group (32%), but this difference did not emerge at any other point in the trial. This study suggests that benzodiazepine augmentation of SSRIs at the beginning of treatment can lead to earlier improvement. Recently, Kampman, Keijsers, Hoogduin, and Hendriks (2002) found that paroxetine augmentation of 43 nonresponders to an acute phase of CBT significantly reduced overall anxiety and agoraphobic behaviors. Nonresponders pose a special challenge, yet there is a paucity of systematic investigation in this area.

Obsessive-Compulsive Disorder

In considering medication augmentation, a benzodiazepine, such as clonazepam, is occasionally added, but disinhibition, dependence, and tolerance to the medication have limited the enthusiasm for this choice in the long run (Leonard et al., 1994). Adult studies support a trial of neuroleptic augmentation in SRI non-or partial responders (McDougle et al., 1995). In a Type 1 controlled risperidone versus placebo SRI augmentation study, risperidone addition was superior in reducing OCD symptoms (McDougle et al., 2000). Neuroleptic augmentation has not been systematically studied in children; a case series of children who were refractory to SRI therapy improved significantly after risperidone was added (Fitzgerald, 1999). T. Owley, S. Owley, Leventhal, and Cook (2002) reported four cases of 8-to 25-year-olds who were partial responders to an SSRI and subsequently responded after mixed salts of dextroamphetamine (Adderall) was added. The authors speculated that the “del icate” balance of serotonergic and dopaminergic systems may be affected by both neuroleptic or Adderall augmentation, resulting in increased serotonergic transmission.

There is no accepted definition of a nonresponder. Sometimes nonresponders have meant patients who have had a suboptimal response to one therapy, but such a definition would include both partial responders and nonresponders. If a nonresponder is defined as someone who has had absolutely no improvement from an initial treatment, there are no published controlled data on how to treat such patients.

Posttraumatic Stress Disorder

There is only one placebo-controlled study on augmentation for partial responders: combat veterans with PTSD who were minimally responsive on an SSRI (sertraline) were given augmentation with the atypical antipsychotic medication olanzepine (Stein, Westenberg, & Liebowitz, 2002). Olanzapine augmentation was associated with statistically significantly greater reduction than that with placebo in specific measures of posttraumatic stress, depressive, and sleep disorder symptoms (Petty et al., 2001). One recently completed study found an augmentation effect for PE compared to sertraline continuation in patients who evidenced at least a 20% symptom reduction following 10 weeks of open label sertraline (Foa, Franklin, & Moser, 2002). In a subgroup analysis of these data, patients who experienced only a marginal response to 10 weeks of open label sertraline benefited substantially when PE was added, compared to those who continued on sertraline for an additional 5 weeks.

There are no controlled data on how to treat nonresponders to pharmacologic or CBT treatment for PTSD in adults. Given the high rates of comorbidity with PTSD, it is recommended that patients be given evidence-based treatments for their comorbid conditions and that thereafter the patient's PTSD symptoms be reassessed.

A Comment on Management of Partial Response and Nonresponse in Children and Adolescents

There is little to no research on the management of partial response and nonresponse in the treatment of adolescent anxiety disorders. This area is one that sorely needs to be addressed in future research. Although the literature has yet to provide the data needed to guide evidence-based treatments for partial responders and nonresponders, several issues still warrant our consideration.

The evidence accrued to date informs us about the choice of an initial treatment to be undertaken for anxious children and, at least to some extent, anxious adolescents. There is a noted absence of studies specifically about adolescents and what to do for them at the various other stages of treatment. Studies reviewed above have evaluated the efficacy of various treatments for children identified with anxiety disorders and these data guide our treatment choices. However, it is likely that some of the cases treated in these studies had prior experience with one or another treatment, and may or may not have been partially refractory to those earlier treatments. More detailed analyses of initial treatment response may reveal useful information about the moderating role of prior treatment experiences in the efficacy of the treatment being evaluated. The field has nevertheless made meaningful progress in identifying at least a few initial treatments that are quite promising for anxious youth.

We know little about what to do when the youthful patient's response to treatment is not favorable. Even when approximately two-thirds of patients respond favorably to CBT, for example, there are still one-third of the patients who did not respond well and may need something additional. One might speculate that within the CBT approach, a combination of more practice, increased exposure tasks, and help with the use of new skills in new, challenging situations would be worthwhile. One might also speculate that a combination of approaches may be valuable. Treatment of a nonresponsive client can be complicated by the fact that a nonresponder to one treatment approach (psychosocial, medication) may then seek another approach as a way to rectify the less-than-preferred previous outcomes. Again, more information is needed about prior treatment history and its effect on the evaluation of a current intervention, and there is a real need for studies of the preferred treatment for patients whose response to treatments are less than satisfactory.

Insufficient research on adults and almost none on youth regarding the continuation and maintenance treatment phases for specific phobia have been carried out. In adults with anxiety disorders, it may be recommended that medications be continued for at least 12–18 months and, thereafter, if the person is judged to be stable, that the medications be reduced very slowly to avoid withdrawal side effects. It is conceivable that at least some children and adolescents will require treatment for years, consistent with findings from the adult literature. As in other psychiatric and medical illnesses, after achieving a therapeutic response it is important to continue the same treatment (CBT and/or medications) to prevent relapses. During these phases, depending on the youngster's clinical status, she or he may need to be seen less frequently.

It is important that an adequate trial be conducted (dose and duration of an SSRI; expertise and number of sessions of CBT) prior to concluding that a patient is a partial responder. For example, the Expert Consensus Guidelines for OCD recommend clomipramine after two or three failed SSRI trials (March, Frances, et al., 1997). Cognitive-behavioral therapy would be a first choice for an augmentation strategy after a partial response or nonresponse to adequate pharmacotherapy with an agent of known efficacy, although availability of trained therapists is sometimes limited, and some children are not motivated to participate. Systematic study of CBT dissemination strategies is sorely needed, as is the development of CBT techniques designed specifically to enhance motivation to engage fully in treatment. Such study is well under way in adult anxiety disorders, and clearly needs to be addressed next in children and adolescents. Much more needs to be done to establish the efficacy and safety of such augmentation for adolescents with anxiety disorders. Clinically we know that many are treated with this strategy, but the literature supporting this approach has yet to be developed.