Obsessive-compulsive disorder (OCD) is characterized by the presence of recurrent obsessions or compulsions that are distressing, time consuming, or debilitating.1 Obsessions are characterized as persistent and intrusive thoughts, ideas, impulses, or images that result in anxiety. Compulsions are repetitive or ritualistic behaviors or mental acts that reduce or prevent anxiety in response to the obsessive thought.
Although all obsessions are mental events, compulsions may be either behavioral or mental actions that serve to reduce distress elicited by obsessions or according to rigid personal rules.2 Unlike adult patients, children are not required to recognize the OCD symptoms as bizarre and unrealistic. Additionally, the perception that obsessions and compulsions must be ego-dystonic (or unpleasant) to the child is highly variable.3
The most common obsessive themes among pediatric patients include fears of contamination (dirt, germs, toxin); worries about harm to self or others; the need for symmetry, exactness and order; and religious or moralistic concerns or scrupulosity (eg, worrying they have sinned).4 Obsessions also may manifest as excessive guilt, self-doubt, forbidden thoughts (eg, sexual or aggressive), or a need to seek reassurance (asking or confessing to others). Common compulsions include cleaning or decontamination rituals (excessive washing, showering, or bathing); checking, counting, repeating, straightening, and routinized behaviors (eg, doors, locks, homework, appliances); confessing, praying, and seeking reassurance; touching, tapping and rubbing; and avoidance. In early-onset cases (prepubertal), presentation with compulsions in the absence of obsessions is common.5
Although many of the symptoms of pediatric OCD are similar to those in adults, children may be less likely to view their symptoms as nonsensical.6 Likewise, there is a wide range of severity and impairment within pediatric OCD with functional impairments (eg, psychosocial difficulties at school, home, or socially) being frequently endorsed by both children and their caregivers.7
Recent epidemiological studies estimate the prevalence of pediatric OCD to be much higher than believed as recently as 10 years ago. While estimates vary, recent estimates place the lifetime prevalence rates, by late adolescence, between 1% and 4%.8,9 It is currently believed that as many as 80% of adult OCD cases have an initial onset during childhood.10,11 Modal age of onset varies by gender with a male preponderance in cases of prepubertal onset5 with the initial peak of incidence around puberty and subsequently in young adulthood. The gender distribution becomes equal during adolescence;4 the modal age of onset in females is between 20 and 29 years.
The occurrence of pediatric OCD may be somewhat higher given secrecy in reporting embarrassing thoughts and behaviors.12 Additionally, limited insight, parental inability to recognize OCD symptoms, and the lack of awareness about the availability of efficacious treatment may contribute to underdiagnosis. Therefore, it is reasonable to assume that many cases of OCD remain undetected.
Although the cause of OCD remains unknown, there are multiple bio-etiological theories. The neurochemical explanation hypothesizes that abnormal serotonin metabolism is implicated in the expression of obsessive and compulsive symptoms. This hypothesis is supported by data from successful treatment-outcome studies with serotonin-enhancing agents (ie, serotonin reuptake inhibitors or SRIs).13–16 Others cite genetic, neuroimaging, and neuroendocrine evidence in support of the neurochemical etiological model of pediatric OCD.17 Positron emission tomography studies suggest that abnormal metabolism in the globus pallidus, orbitofrontal cortex, neostriatum, thalamus is associated with OCD symptoms.18 Further, functional magnetic resonance imaging identified hyperactivity in the anterior cingulatecortex in patients with OCD.19 These data suggest that a functional disturbance in the frontal-limbic-basal ganglia system may mediate OCD symptoms in children.20 Another contemporary explanation of OCD implicates cortical and subcortical neuro-structural abnormalities. Specifically, subtle structural abnormalities in the caudate nucleus as well as possible functional dysregulation of the neural cortical striatal pathway involving the orbitofrontal cortex, cingulate cortex, and the caudate are linked to OCD symptomology.14
A recent investigation using magnetic resonance imaging found both smaller globus pallidus volume and gray matter volumetric abnormalities in the anterior cingulate gyrus in pediatric patients with OCD, compared with healthy controls.21 Additionally, investigations support a relationship between pediatric OCD and cases group A beta-hemolytic streptococcal infections (GABHS) similar to OCD symptoms observed in Sydenham's chorea. More specifically, these cases are believed to result from autoimmune responses misdirected towards regions of the basal ganglia.22–24 The model suggests that the acquired basal ganglia dysfunction may result in chorea, tics, obsessions, compulsions, and hyperactivity. This condition, characterized by abrupt childhood onset and episodic course of neurological abnormalities (including OCD or tic disorder symptoms), is referred to as pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).3
Evaluations of family genetic factors contributing to OCD suggest an autosomal dominant model of inheritance with incomplete penetrance.14,25 In other words, the phenotypic expression varies in manifestation from OCD-symptoms to other obsessive-compulsive (OC) spectrum disorders (eg, Tourette's disorders, tic disorders). Variations may be dependant on other genetic or environmental factors.
Franklin and Foa2 reviewed several ancillary accounts of the etiology (and maintenance) of OCD, including behavioral conditioning (through negative reinforcement of distress-reducing behaviors) and cognitive theories. By classical conditioning, a neutral stimulus (or event) becomes conditioned to elicit distress due to its association with another feared situation. Fear can be conditioned to both mental events (eg, blasphemous or sexual thoughts) and physical stimuli, activities, or behaviors (eg, contaminated objects, items perceived as dangerous, showering, driving).2 Subsequent to the acquisition of the conditioned fear, rituals develop to reduce or avoid distress. These compulsive behaviors persist and become excessive because they temporarily ameliorate the distress associated with obsessive thoughts by operant conditioning (negative reinforcement). In other words, the decreased anxiety associated with performing a compulsive behavior results in an increase in compulsive behaviors.
Salkovskis explains the acquisition of OCD from a cognitive perspective.26 This perspective poses that OCD results from the interpretation of intrusive thoughts rather than the frequency or content of these cognitions. If intrusive thoughts are interpreted such that an individual perceives responsibility for causing or failing to prevent harm, obsessional patterns develop. Attempts to neutralize intrusive thoughts (obsessions) via motor or cognitive rituals, avoidance, and reassurance seeking behavior prevents the disconfirmation of the patient's fears and facilitates proliferation of the anxiety.
Differential Diagnosis, Comorbidity, and Assessment
A thorough diagnostic assessment of children with suspected OCD symptoms is crucial given the frequency and multitude of co-occurring psychiatric conditions. Mood, tic, disruptive behavior, attentional, developmental, and other anxiety disorders are common in pediatric OCD. For example, in a study of 70 youth with OCD, just 26% had OCD listed as the only psychiatric diagnosis.4 The comorbidity breakdown was as follows: tic disorders (30%), major depression (26%), specific developmental disorders (24%), oppositional defiant disorder (11%), and attention deficit hyperactivity disorder (10%). The presentation of obsessive-compulsive spectrum disorders (eg, trichotillomania and body dysmorphic disorder) along with OCD is not uncommon. A comprehensive clinical evaluation, differential diagnosis, and subsequent treatment of these conditions has significant clinical implications as co-occurring disorders may exacerbate symptoms and impede optimal treatment.3 For example, children with disruptive behavior disorders will likely require a behavior modification plan (with deliberate, consistent contingencies for on- and off-task behavior) to elicit the child's cooperation. On the other hand, a child with significant depression may require ancillary cognitive-behavior or pharmacologic interventions.25
A detailed review of family history of psychiatric illness as well as child developmental, medical, and psychosocial history should be conducted.3 For example, early onset of OCD has a strong familial aggregation.5 Children with OCD have high rates of OCD and other anxiety disorders in their first degree relatives.27 Additionally, past medical history of possible streptococcal infections, rheumatic fever, and other evidence of PANDAS should be ascertained.24
Given the neurobiological abnormalities associated with these autoimmune conditions (which may result in dramatic onset of personality changes, hyperactivity, and other symptoms), pharmacologic and behavioral treatment modifications for OCD symptoms likely are necessary,28 highlighting the significance of proper diagnostics. Also during assessment, a child's developmental level must be taken into consideration, as most children exhibit transient, age-appropriate obsessive and compulsive behaviors that wax and wane with normal development (eg, bedtime rituals, superstitions, and concerns about sameness).17 Pathological obsessive-compulsive phenomena can be distinguished from periods of normative development by virtue of persistence, excessive distress, and impediment of adaptive functioning.
As discussed, patient secrecy may obfuscate proper differential diagnosis of OCD. Parental complaints during clinical care appointments may relate to behaviors secondary to OCD. For example, inadvertent diagnosis may result from visits to health professionals for symptoms secondary to unrecognized OCD behaviors (eg, temper tantrums, declines in school performance, dermatitis due to skin picking, food restriction, dental visits due to excessive teeth-cleaning rituals, eczematous damage due to repetitive hand-washing, secondary enuresis or encopresis due to bathroom avoidance, or co-occurring depression or anxiety).25
In addition to a thorough clinical interview, rating scales and structured interviews may be useful in pinpointing a diagnosis and monitoring treatment progress. The Anxiety Disorders Interview Schedule for Children (ADIS)29 or the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children – Present and Lifetime Version (K-SADPL)30 are diagnostic instruments for OCD and other psychiatric disorders. Once an OCD diagnosis has been established, the severity and topography of symptoms can be assessed using the Children's Yale-Brown Obsessive Compulsive Scale (CYBOCS)31 or the National Institute of Mental Health Global Obsessive Compulsive Scale (NIMH-OC).32
Two treatment modalities for OCD have been supported empirically for children and adolescents: cognitive-behavior therapy (CBT) with exposure and response prevention (E/RP), and pharmacotherapy (SRIs and selective serotonin reuptake inhibitors, or SSRIs). CBT or CBT with concurrent pharmacotherapy is considered the first-line treatment for pediatric OCD.2,14,33–36
For example, a review of controlled trials of CBT versus SRIs in adults suggests that CBT with E/RP is as effective as or superior to pharmacotherapy2,33 and should be considered a viable first-line treatment.14 While there is a paucity of controlled comparisons between CBT, medication, and combined therapies, CBT was found to be superior to clomipramine in a randomized trial of children ages 8 to 18.35
More recently, a large-scale, multisite, randomized placebo-controlled trial of CBT, sertraline, and concomitant CBT and sertraline in 112 children ages 7 to 17 was completed.36 Results indicate that CBT alone or sertraline alone was superior to placebo. However, OCD symptoms were more likely to diminish in patients receiving CBT alone or in combination with sertraline. Accordingly, the authors concluded that beginning treatment for children and adolescents with OCD should be either CBT alone or CBT with an SSRI.36
CBT with ER/P for OCD is distinguished from other “talk-therapies.” Play-based, supportive, insight-oriented, relaxation, psychoanalytic, and psychodynamic therapies have generally been demonstrated as not effective for the treatment of pediatric OCD.2,3,17,33 In contrast, the efficacy of CBT in children has been demonstrated in numerous open trials34,37–40 and three controlled trials35,36,41 with generally low rates of relapse during follow-up analyses (9 to 24 months post-treatment). Further, unlike pharmacotherapies (for which relapse is not uncommon when medication is discontinued), treatment gains from CBT commonly endure after therapy is completed.3 While there are several manualized CBT protocols for adults and children, each consist of similar components.
The three central aspects of CBT therapy for pediatric OCD are: exposure (placing the patient in situations that elicit anxiety related to their obsessions); response prevention (deterring the ritualistic or compulsive behaviors that may serve to reduce or avoid anxiety); and cognitive therapy (training the child to identify and reframe anxiety-provoking cognitions). Before treatment, education about OCD is provided to both the patient (often in framework of a story for young children) and parents. During this phase, a “fear-hierarchy” is developed. The hierarchy consists of situations the patient avoids or for which the patient would find it difficult to inhibit compensatory overt or mental rituals.
Next, the therapist and child (often together with a parent) begin hierarchy-based E/RP based on a patient's identified fear-hierarchy (typically starting at the least-distressing situation and progressing up the hierarchy during subsequent sessions). E/RP is based on the assumption that obsessions and compulsions are functionally related (ie, compulsions are performed to reduce/avoid anxiety associated with obsessions).2 Exposure during E/RP exercises relies on the gradual attenuation of anxiety after sufficient duration or contact with a feared stimulus.33 Successive exposures with the feared stimulus result in both decreased elevations in anxiety and more rapid attenuation of distress. Response prevention is based on the assumption that compensatory behaviors (eg, overt or covert rituals or compulsions) serve as short-term reducers of anxiety via negative reinforcement (escape and/or avoidance of distress). Therefore, individuals with OCD do not habituate to anxiety and instead rely on compulsions or rituals to mitigate distress. Accordingly, response-prevention requires the individual to avoid the negative-reinforcement-producing behavior (ie, the compulsion) so that anxiety can be reduced via habituation instead of by rituals. The child must be convinced to accept the short-term distress for the long-term gain (ie, learning to habituate to anxiety without compulsions). The child's willingness to tolerate the procedure depends on his or her developmental level, motivation, and understanding of the procedure. However, the therapist and parents can often mitigate these difficulties in two ways: by minimizing the negative reinforcement-seeking behaviors (by not allowing the ritual to result in escape, avoidance, or decreased anxiety; ie, behavioral extinction) and through differential reinforcement of non-OCD behaviors (eg, providing tangible rewards for RP). In addition to ER/P, cognitive strategies are also used (eg, cognitive restructuring of obsessive thoughts) depending on the child's developmental level. Cognitive exercises such as restructuring teach the patient to challenge anxiogenic thought processes (related to obsessions) and the necessity of performing compulsive behaviors.
As discussed above, family involvement is often central to the success of CBT for pediatric OCD. This is particularly important because family members may accommodate the child's symptoms by facilitating avoidance, assisting with ritualistic behaviors, or inadvertently facilitating the development of the disorder by participating in rituals (eg, providing reassurance when a child expresses excessive doubt, allowing compulsive avoidance of feared stimuli, and tolerating delays associated with ritual completion) that would otherwise be debilitating without adult assistance.25 In addition to extinction and differential reinforcement procedures (see above), parents and families can provide substantial support as a child's “allies” in the “fight” against OCD.17,40 Also, the efficacy of parental participation in treatment (as co-therapists) has been demonstrated in the treatment of pediatric OCD.41,42
Although CBT for OCD is typically conducted via weekly 1-hour sessions,36,39–41 an alternative CBT format has been utilized for the treatment of refractory pediatric OCD.43 Preliminary research suggests that Intensive CBT, which involves 90-minute therapy sessions held daily for approximately two to four weeks, is indicated in cases of difficult-to-treat pediatric OCD.44 Another adjunctive CBT approach includes group family-based therapy. In a recent controlled trial, the efficacy of group-based CBT for multiple families of youth with OCD was empirically supported.41
Prognostic indicators of a positive response to CBT for pediatric OCD include the willingness to cooperate with treatment, the presence of overt rituals, motivation to eliminate rituals and symptoms, and the ability to monitor and report symptoms.33 Conversely, there are several putative factors associated with a poor response to CBT, including: extensive psychiatric comorbidity (eg, mood and disruptive behavior disorders, psychosis, substantial family turmoil), and developmental factors (eg, developmental delay, mental retardation, and very young children).3 Additionally, individuals with poor insight into the senselessness of their obsessions and compulsions may be less responsive to E/RP.2
Randomized, placebo-controlled trials have demonstrated the efficacy of pharmacotherapy for OCD in pediatric populations. Clinically significant reductions in OCD symptomology have been documented in children and adolescents using SRIs including clomipramine, sertraline, fluoxetine, paroxetine, and fluvoxamine.13,18,36,45–50 A recent meta-analysis of pharmacotherapy trials in children identified the SRI clomipramine (a tricyclic antidepressant, or TCA) to be significantly superior over SSRIs in reducing OCD symptoms.13 However, the effectiveness of several SSRIs (sertraline, fluoxetine, paroxetine, and fluvoxamine) has also been demonstrated in pediatric populations. Further, because of the risk profile, adverse effects, and required EKG and blood-level monitoring associated with TCAs (eg, antiadrenergic, anticholinergic, and antihistaminergic adverse effects), SSRIs (with a relatively minimal side effect profile) are the consensus first-line medication for pediatric OCD.13,45,49 Recent research suggests that the SSRIs are equally efficacious and the specific choice should be based on the patient's medical history, concomitant medications, and the adverse events profile.13,25 It is noteworthy that a clinical response is unlikely within the first several weeks of treatment with an SSRI. Generally, 10 to 12 weeks at adequate dosage is necessary to evaluate the efficacy of the medication; also, poor clinical response to one SSRI is not necessarily predictive of failure with other SSRIs, suggesting adequate trials of multiple SSRIs may be indicated before augmentation.3
In pediatric cases that are unresponsive to CBT and trials with multiple SSRIs, second-line pharmacological treatments include SRI augmentation.14,15 To our knowledge, there is a paucity of data regarding augmentation strategies for pediatric OCD. Two pediatric case-series suggest that SSRI augmentation with clomipramine resulted in marked improvement; it is notable that this combination requires diligent blood, EKG, and side effect monitoring.51,52 However, in the adult OCD treatment literature, numerous agents have been used in combination with SRIs for patients whose symptoms have not been reduced in monotherapy. A limited number of controlled trials and case series in adults support the augmentation of SRI pharmacotherapy with use of low doses of dopamine antagonists (eg, typical neuroleptics such as haloperidol and pimozide, atypical neuroleptics such as risperidone, olanzapine) and a benzodiazepine (clonazepam).14
Preliminary data support that some patients with comorbid OCD and tic disorders may require combined therapy of serotonin-reuptake inhibitors plus neuroleptics or other augmentation strategies.53 However, significant undesirable side effects should be considered prior to prescribing neuroleptics and benzodiazepines in children. Ameliorations in OCD symptoms using SRI augmentation with lithium, clonidine, and buspirone have not been supported in the treatment of adults.15
Based on recent concerns regarding the safety of prescribing antidepressants to children younger than 8, it is important to note the medications currently approved by the United States Food and Drug Administration (FDA) for pediatric patients with OCD. These include sertraline (not for children younger than 6), fluoxetine (not for children younger than 7), fluvoxamine/paroxetine (not for children younger than 8), and clomipramine (for children younger than 10). Of particular relevance is that, on October 15, 2004, the FDA issued a “Black Box Warning” to alert healthcare providers of an increased risk of suicidality (suicidal thinking and agitation) in children and adolescents being treated with antidepressants. In light of this warning, increased attention to symptoms of depression among pediatric patients being treated with antidepressant medication appears warranted. This should include formal assessment of suicidal ideation prior to and throughout the course of pharmacological treatment. One implication of this warning may be to attempt an adequate trial of cognitive-behavior therapy prior to pharmacologic intervention.
Pediatric OCD, a chronic and impairing condition, is not uncommon. Diagnosis is often difficult given the secrecy of many patients and co-occurring psychopathology. CBT alone or CBT with concurrent SSRI therapy are considered the first-line treatment.36 Nevertheless, relatively few mental health professionals are adequately trained in CBT for OCD.3 For example, in a national survey of 79 clinicians treating pediatric OCD in Norway, less than 33% of clinicians reported using exposure/response prevention (or similar techniques) despite rating CBT as a favorable approach to treatment.54 Limited access to professionals proficient in CBT may result in the prescription of pharmacotherapy alone or pharmacotherapy with other concurrent psychotherapies (that are not demonstrated as efficacious).
Clearly, improving the referral network to experts trained in CBT for OCD is necessary to provide efficacious treatment, associated with reduced rates of relapse. Intensive CBT may extend resources to families without access to trained professionals in their area, given the potential for effective therapy in a succinct time period. Accordingly, in addition to the controlled trial evaluating CBT, pharmacotherapy, and combined treatment,36 initial investigations of intensive CBT for pediatric patients appear necessary. Additionally, intervention studies for children with significant comorbid psychopathology should be pursued.
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