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Integrated treatment of pediatric ocd.doc
JOHN S. MARCH, MD, MPH
Program in Child and Adolescent Anxiety Disorders DUMC Box 3527 Durham, NC 27710 (919)-416-2400 InterNet: email@example.com
OBSESSIVE-COMPULSIVE DISORDER IN CHILDREN AND ADOLESCENTS
Approximately 1 in 200 children suffers from Obsessive-Compulsive Disorder (OCD). Children and adolescents with OCD experience unwanted intrusive thoughts, urges, or images (termed obsessions) and associated dysphoria-reducing behaviors or rituals (termed compulsions). Common obsessions include the fear of dirt or germs, fear of harm to oneself or someone else, or a persistent need to complete something “just so”; corresponding compulsions include hand washing, checking, and repeating or arranging.
Despite a distinctive symptom picture, presenting complaints are commonly shaped by comorbidity on Axis I, accounting for many missed cases. Comorbidity on Axis II can also be problematic. Subjects with OCD not uncommonly present with undiagnosed learning disorders often reflecting impairments in right hemisphere mediated visual-spatial-organizational functions. While obsessive-compulsive personality traits not uncommonly remit with successful treatment for OCD—suggesting that OCP may be an adaptation to OCD in some patients—learning impairments require separate interventions that often have an important effect on long-term outcome.
Children and less commonly adolescents may fail to view their obsessions as senseless and their compulsions as excessive. More commonly, despite intact insight, young persons with OCD are secretive about their symptoms out of embarrassment or fear of punishment. Unless a comorbid psychotic disorder is present, loss of insight is not an indication for initial treatment with neuroleptics; aggressive treatment for OCD is the treatment of choice.
OCD is remarkably resistant to traditional insight-oriented psychotherapy; in contrast, the benefits of behavioral psychotherapy, in the form of exposure and response prevention, are well established. Key elements include: (1) Keeping the focus on OCD as a neurobehavioral disorder; (2) graded exposure and response prevention guided by the child’s selection of targets from a carefully constructed stimulus hierarchy; (3) a “tool kit” for managing dysphoric affects and faulty thinking habits; and (4) liberal psychoeducation for family members and school personnel who then become allies on a treatment team. Predictors of a successful response to behavior therapy include the presence of overt rituals, the desire to eliminate symptoms, ability to monitor and report symptoms, and willingness to cooperate with treatment.
More specifically, hierarchy based exposure and response prevention is the central element in psychosocial treatment. Exposure relies upon the fact that anxiety usually attenuates after sufficient duration of contact with a feared stimulus. Thus a child with fear of germs must confront relevant feared situations until his or her anxiety decreases. Repeated exposure is associated with decreased anxiety across exposure trials, with anxiety reduction largely specific to the domain of exposure, until the child no longer fears contact with specifically targeted phobic stimuli [March, 1994 #5318]. Exposure is typically implemented in a gradual fashion (sometimes termed graded exposure), with exposure targets under patient or, less desirably, therapist control. Adequate exposure depends on blocking rituals or avoidance behavior, a process termed response prevention. For example, a child with germ worries must not only touch “germy things,” but must refrain from ritualized washing until his or her anxiety diminishes substantially. Selection of E/RP tasks by the child from those items where the child is already successfully resisting OCD maximizes the probability that E/RP will be successful .
While family dysfunction does not cause OCD, clinicians universally recognize that families affect and are affected by OCD. Control struggles surrounding rituals, difficulty dealing with sexual or aggressive obsessions, and differences of opinion about how to cope with OCD symptoms are not uncommon. It is important to address these issues early in treatment, since helping family members struggle against the disorder rather than each other is crucial to designing an effective treatment program. Conversely, apart from psychoeducation, family based treatment is only necessary when OCD tangles up family members or family dysfunction constrains the implementation of CBT.
Until the mid-1980s, psychopharmacological interventions in OCD were thought to be largely ineffective. Positive effects were attributed to relief of depressive symptoms or to a reduction in overall anxiety. However, it is now clear that drug treatment can benefit the majority of pediatric patients with OCD.
Clomipramine (Anafranil, manufactured by CIBA-Geigy) was the first medication to be studied in treating OCD in children and adolescents. Clomipramine differs from imipramine in structure only by the addition of a chloro-substituent to the fused-ring system. This change confers markedly increases the potency of serotonin reuptake inhibition. Following completion of multicenter placebo-controlled double-blind trials, the FDA approved clomipramine for the treatment of OCD in patients age eight and older in 1989. Besides clomipramine, which is a non-selective tricyclic compound, the selective serotonin reuptake inhibitors (SSRIs) fluvoxamine (Luvox, manufactured by Solvay), sertraline (Zoloft, manufactured by Pfizer), paroxetine (Paxil, manufactured by GlaxoSmithKline), fluoxetine (Prozac, manufactured by Lilly) and citalopram (Cilexia, manufactured by Forrest also are likely effective treatments for OCD in youth. Controlled studies now support the efficacy of all but citalopram in the treatment of pediatric OCD. Based on large multicenter trials fluvoxamine (age 8-18) and sertraline (age 6-18) recently received FDA approval for pediatric OCD.
Clinically relevant lessons originating from the multicenter trials, include: (1) In contrast to depressed patients treated with medications, there is little or no placebo effect in patients with OCD; (2) clinical effects begin at three weeks and plateau at ten weeks; (3) SRIs produce about a thirty percent reduction in OCD symptoms, corresponding to a rating of moderately to markedly improved on a measure of patient satisfaction; and (4), given that subjects on average remained in the mildly to moderately ill range at the conclusion of the trial, the SRIs are not a panacea for all patients. Side effects and magnitude of improvement in pediatric trials are comparable to those seen in adult trials. The absence of typical tricyclic side effects, including cardiac toxicity, give the SSRIs significant advantages over clomipramine, which is usually given only after two or three failed SSRI trials.
Although many patients will respond early to one of the serotonin uptake inhibitors, a substantial minority will not respond until eight or even twelve weeks of treatment at therapeutic doses. Thus it is important to wait at least eight weeks at therapeutic doses before changing agents or undertaking augmentation regimes.
Approximately one third of patients will fail to be helped by monotherapy with a serotonin uptake inhibitor. Some of these patients will benefit from combination therapy, for example with a neuroleptic, such as risperidone, especially when comorbid schizotypal personality disorder or a tic-spectrum disorder is present. Clonazepam and L-tryptophan have also been used as augmenting agents, while lithium and buspirone seem not to be effective in controlled studies in adults. Clinical evidence suggests that a successful augmenting response may depend in part on comorbidity. For example, augmentation with clonazepam may be particularly helpful when comorbid panic symptoms are present. When augmenting an SRI, adding 25-50mg of clomipramine to an SSRI may be the best choice. However, it is important to watch for p450 2D6 inhibition of CMI by fluoxetine or paroxetine; sertraline and fluvoxamine are less likely to cause high CMI levels. Fluvoxamine may be the best choice to augment with CMI because it inhibits p450 1A2, which is the enzyme that demethylates CMI to its inactive desmethyl metabolite, thereby keeping more of the active parent compound available.
Evidence-based clinical practice guidelines that employ a stages-of-treatment model are assuming increasing importance in pediatric psychiatry. Most discussions of practice guidelines focus only on selection of initial treatment or management of treatment refractory patients. However, maximum clinical utility requires a stages-of-treatment model that addresses selection of initial treatment, the management of partial response, maintenance treatment, treatment resistance and comorbidity. We were instrumental in developing the only two practice guidelines that so far have been published for the treatment of OCD in youth: The Expert Consensus Guidelines and the AACAP Practice Parameters for OCD. Both recommend starting with CBT or CBT plus an SSRI, depending on severity and pattern of comorbidity; both recommend that patients started on SSRI monotherapy who are partial responders be augmented with CBT. Thus, experts generally consider CBT a first-line augmentation strategy and medication augmentation a second-line option.
OCD/tic symptoms arising or exacerbating in the context of Group A beta hemolytic Streptococcal infection (GABHS), which the NIMH group has labeled “pediatric autoimmune neuropsychiatric disorder associated with strep (PANDAS), may define a singular subgroup of children with OCD or tic disorders. Obsessive-compulsive symptoms are not uncommon in pediatric patients with Sydenham’s chorea, which is a neurological variant of
rheumatic fever (RF). Moreover, when compared with non-choreic rheumatic fever patients, OCD is far more common when chorea is present than when absent. LIke rheumatic carditis, Sydenham’s is believed to represent an autoimmune inflammation of the basal ganglia triggered by anti-streptococcal antibodies. Thus Swedo and colleagues have theorized that OCD in the context of Sydenham’s chorea may provide a medical model for the etiopathogenesis of OCD and tic disorders. In this model, antineuronal antibodies formed against group A beta-hemolytic strep cell wall antigens are seen to cross react with caudate neural tissue, with consequent initiation of OC symptom. In turn, this would suggest that acute onset or dramatic exacerbation of OCD or tic symptoms should prompt investigation of GABHS infection, especially since immunomodulatory treatments, including antibiotic therapies, plasmapheresis or IV IGG, may be of benefit some patients.
In summary, children and adolescents with OCD should receive behavioral psychotherapy and, if not rapidly responsive, a serotonin uptake inhibitor should be added. Some physicians and patients will choose medication first, trying to avoid the time, effort, and anxiety associated with behavior therapy, especially with younger children. Others will choose behavior therapy in preference to medication and the chance of aversive side effects. Most will prefer to combine the two approaches. In some children, immunomodulatory treatments may play an important role. Although these treatments are not curative, their skillful application will provide relief for the majority of patients with OCD.
March, J., Frances, A., Kahn, D., & Carpenter, D. (1997). Expert Consensus Guidelines: Treatment of
Obsessive-Compulsive Disorder. J Clin Psychiatry, 58(Suppl. 4), 1-72.
March, J., & Mulle, K. (1998). OCD in Children and Adolescents: A Cognitive-Behavioral Treatment Manual.
March, J., & Wells, K. (in press). Combining Medication and Psychotherapy. In J. F. Leckman & A. Martin &
L. Scahill & D. S. Charney (Eds.), Textbook of Child and Adolescent Psycopharmacology. London: Oxford University Press.
March, J. S., & Leonard, H. L. (1998). OCD in Children: Research and Treatment. In R. Swinson & J.
Rachman & M. Antony & M. Richter (Eds.), Obsessive-compulsive disorder: Theory, research, and treatment. (pp. 367-394). New York: Guilford.
To understand the differential diagnosis of Obsessive-Compulsive Disorder in children and
adolescents, including the influence of comorbidity and development on the symptom picture.
To understand the rationale and application of cognitive-behavioral and pharmacotherapy to children
and adolescents with Obsessive-Compulsive Disorder.
MULTIPLE CHOICE QUESTIONS
Question I: The major determinants of anxiety in children are:
Question II: Appropriate treatments for children with OCD include:
Revised Fall, 2001
Obsessive-Compulsive Disorder Executive Summary
A. Consensus Recommendations for First Line Treatments by Clinical Situation
indicate treatments of choice)
Selecting the Initial Treatment Strategy and the Sequence of Treatments
• Prepubescent children: CBT first for milder or more severe OCD
• Adolescents: CBT first for milder OCD; CBT + SRI for more severe OCD
• Adults: CBT first for milder OCD; CBT + SRI or SRI alone first for more severe OCD
Considerations Based on Overall Efficacy, Speed, and Durability of Treatment
Considerations Based on Tolerability and Patient Acceptability
• More severe OCD: CBT + SRI; or SRI alone
Selecting CBT Strategy
Obsessions and Compulsions
Tailoring treatment for specific symptoms
counting/repeating, hoarding, aggressive urges
Scrupulosity and m oral guilt, pathological doubt
Intensity of CBT
• Gradual (i.e., weekly): recommended for most patients (usually 13–20 sessions)
• Intensive (i.e., daily): recommended when speed is of the essence; or for patients who have not responded
to gradual CBT or who have extremely severe symptoms
Selecting a specific medication: use a serotonin reuptake inhibitors (SRI)
• Inadequate response to average SRI dose: push to maximum dose in 4–9
• Inadequate response after 4–6 additional weeks at maximum dose:
If no response or p artial response to CBT alone
Add an SRI; add more CBT with changes in
If no response or partial response to SRI alone
If partial response to combined CBT and SRI
After failing trials of 2–3 SSRIs + CBT
If no response or partial response to combined CBT
and 3 SRI trials (one of which was clomipramine)
Augment with another medication (select agent based on associated features) Add more CBT with changes in approach
After 3–4 mild/moderate relapses or 2 –4 severe relapses despite
Gradually taper meds after 1 –2 years while continuing monthly CBT
(Decrease meds by 25% and wait 2 months before next decrease)
Weekly to monthly for the next 3–6 months
Note: CBT = cognitive behavioral therapy. SRI (serotonin reuptake inhibitor) refers to the five compounds clomipramine, fluoxetine, fluvoxamine, paroxetine, and sertraline; SSRI (selective SRI) refers to all but clomipramine.
B. Consensus Recommendations for First Line Psychosocial Treatments Cognitive Behavioral Therapy
• When available, CBT is likely to be used for every patient with OCD except those
who have very severe symptoms or who are unwilling to participate in CBT
• Add when patient has been a nonresponder or partial responder to SRI alone
• Use alone if patient is intolerant to side effects of medication or is pregnant or
has a medical condition that contraindicates medication
• Comorbidity with other psychiatric disorders for which CBT may be helpful,
especially i f modified for the comorbid disorder
Exposure plus response
• Especially helpful for contamination or other fears, symmetry rituals,
counting/repeating, hoarding, aggressive urges
• Especially helpful for scrupulosity, moral guilt, and pathological doubt
Treatment Format and Intensity
• Individual weekly therapy sessions combined with homework or therapist-
assisted out-of-office (in vivo) techniques.
Consider adding family therapy when appropriate
• 13–20 sessions typically required to treat an uncomplicated OCD patient
• Gradual, i.e., weekly: recommended for most patients
Intensive, i.e., daily: recommended when speed is of the essence or patients
have not responded to gradual CBT or have very severe symptoms
• Schedule: monthly booster sessions for 3-6 months
C. Consensus Recommendations for First Line Somatic Treatments Selective Serotonin
Combine with CBT or use alone in adults with moderate to severe sym ptoms
Reuptake Inhibitors (SSRIs)
Add when no response or partial response to CBT alone
Rather than clomipramine when anticholinergic, cardiovascular, sexual,
sedative, or weight gain side effects are a concern
Comorbidity with other psychiatric disorders for which an SSRI may be helpful
Augment SSRI in partially responsive or nonresponsive patient
Less likely than SSRIs to cause insomnia, akathisia, nausea, or diarrhea
Comorbidity with other psychiatric disorders for which a TCA may be helpful
Note: SRI (serotonin reuptake inhibitor) refers to the five compounds clomipramine, fluoxetine, fluvoxamine, paroxetine, and sertraline; SSRI (selective SRI) refers to all but clomipramine.
D. Consensus Recommendations for OCD Complicated by Comorbid Illness
Attention-Deficit Hyperactivity Disorder
CBT + SRI (start SRI first for severe symptoms)
CBT + mood stabilizer alone; or CBT + mood stabilizer + SRI
Overall Strategies for Acute Phase Treatment of OCD
Selection of initial treatment based on severity and age
Change CBT approach; Switch to another SRI; Augment with another
Use clomipramine after 2–3 failed trials of SSRIs‡ + CBT
Still poor response?
Consider 3rd line medication.
‡ SSRI = selective serotonin reuptake inhibitor
Tactics for Duration and Intensity of Treatment During Acute and Maintenance Phases
Initial approach to CBT based on predominant symptoms
Change approach and consider intensive program (e.g., daily for 3 weeks)
Initial acute phase approach with medication
Fluoxetine Clomipramine Sertraline Paroxetine
Adjust dose based on response:
achieve average dose in 4–5 weeks
Continue trial for a total of 8–12 weeks
Push to maximum dose
Duration of medication treatment based on
Good response after initial or subsequent trials:
long term medication if CBT does not work
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