Clinical Description

The child may have either obsessions (worries) or compulsions (rituals), although most patients have both. Recognition by the affected individual that the obsession or compulsion is excessive or unreasonable is no longer required. In DSM-5 (American Psychiatric Association 2013), there are three revised specifiers for insight: good or fair, poor, and absent insight/delusional beliefs.

Epidemiology

OCD is underrecognized and underdiagnosed and is more common than clinical populations would suggest. Symptoms are poorly understood by and embarrassing to children and therefore often concealed, which delays assessment and diagnosis. The prevalence of OCD in children and adolescents is thought to be 1%–2%, although rates as high as 4% have been reported. Mild or transient rituals, obsessions, or compulsions are common in the general population. At various stages of development, ritualistic behaviors and compulsions are normal. Examples are rigid bedtime routines; collecting, arranging, and storing of objects; and concerns about dirt and germs in preschool and early-school-age children (Leckman and Bloch 2008). Onset of OCD peaks in preadolescence and again in early adulthood (Geller et al. 1998). Boys tend to have earlier onset than girls; however, by adolescence gender distribution is likely equal (Swedo et al. 1989). Neither gender nor age at onset influences the number, specific type, or severity of OCD symptoms. Childhood OCD generally has a more favorable outcome than adult-onset OCD.

Etiology

OCD is a model neuropsychiatric disorder. The “serotonin hypothesis” for the etiology of the disorder was initially developed following the success of selective serotonin reuptake inhibitors (SSRIs) in the treatment of OCD. Family studies indicate a genetic diathesis, with greater genetic loading in pediatric OCD compared with adult-onset OCD. Neuroimaging suggests abnormalities in connections between the basal ganglia and the cortex. A cortico-striatal-thalamic circuitry mechanism has been implicated, involving the neurotransmitters glutamate, dopamine, and serotonin (Rosenberg and Keshavan 1998). The scarcity of a known family history of OCD in many cases raises speculation about environmental influences. Perinatal events among children with OCD are associated with earlier age at onset; increased symptom severity; and comorbidity with attention-deficit/hyperactivity disorder (ADHD), persistent tic disorder, anxiety disorder, and major depressive disorder (Geller et al. 2008). Both comorbid anxiety and externalizing psychopathology are associated with increased symptom severity and impairment (Langley et al. 2010).

Although the existence of pediatric autoimmune neuropsychiatric disorders associated with streptococcus infections (PANDAS) is controversial, there is some evidence supporting the hypothesis that group A beta-hemolytic streptococcus (GABHS) infection is linked to disease onset and clinical exacerbations in a subset of youth with OCD and/or tic disorders (Kurlan et al. 2008). On the other hand, a prospective study found that documented streptococcal infections were not associated with exacerbations of tic or obsessive-compulsive symptoms in children whose symptoms met strict criteria for PANDAS, compared with children with Tourette’s disorder and/or OCD who did not have a PANDAS history (Leckman et al. 2011). The current consensus is that a subset of children with OCD may have onset or exacerbation linked to GABHS. However, in a blinded randomized controlled trial (RCT) with patients strictly diagnosed with PANDAS and OCD, intravenous immunoglobulin was not superior to intravenous saline (Williams et al. 2016). More recently, there has been a decoupling of the specific pathogen, GABHS, from the dramatic onset of OCD symptoms, now described as pediatric acute-onset neuropsychiatric syndrome (PANS) (Murphy et al. 2015). These cases may have other, not yet identified, causes. Traumatic experiences, such as being a victim of assault or witnessing harm/violence, are occasionally associated with onset of OCD (Lafleur et al. 2011).

Course and Prognosis

OCD in children (as in adults) appears to be a chronic condition, following a waxing and waning course. A follow-up study found that 41% of youth with OCD continued to have OCD 9 years later and that 40% of the participants had an additional psychiatric diagnosis at follow-up (Micali et al. 2010). However, many youth will experience partial or full remission. The most commonly reported obsessions include contamination, sexual or somatic thoughts, and overly moralistic worries, and the most commonly reported compulsions are washing, repeating, checking, and ordering (Geller et al. 1998).

Factors associated with a more severe course include very early age at onset, psychiatric comorbidities, poor initial treatment response, longer illness duration, and having a first-degree relative with OCD. Complications of OCD can include impairment in peer relations, adult intimacy, and employment, as well as physical sequelae such as dermatitis secondary to washing rituals. OCD does not appear to negatively affect educational achievement (Geller et al. 1998).

OCD in children is usually accompanied by other psychiatric disorders, which may include anxiety and mood disorders; tics or Tourette’s disorder; speech and developmental disorders; ADHD; and disruptive, impulse-control, and conduct disorders.

Evaluation and Differential Diagnosis

Children and adolescents are often secretive about obsessions and compulsions. Temper outbursts, academic struggles, or changes in eating may be the presenting concerns until obsessions and compulsions are carefully elicited with specific questions to the child, parents, and teachers. Pathological rituals need to be distinguished from normal developmental childhood routines and careful assessment of impairment is critical. The clinician-rated Children’s Yale-Brown Obsessive Compulsive Scale (C-YBOCS; Scahill et al. 1997) is the gold standard assessment tool for use at initial diagnosis and in symptom monitoring during treatment. It provides a standardized inventory of symptoms and aids in assessing severity, subjective distress, impairment, internal resistance, and degree of control.

Alternative diagnoses include phobic disorder, Tourette’s disorder (which may be comorbid), anorexia and bulimia nervosa, and schizophrenia. Neurological conditions can precipitate OCD symptoms. The usefulness of throat culture and streptococcal antibody titers in the absence of sore throat is highly controversial. Complex tics may be hard to distinguish from compulsions. Patients with autism spectrum disorder (ASD) can exhibit obsessive-compulsive symptoms. Stimulant medication can induce over-focused or perseverative behaviors, especially at higher doses.

Treatment

Cognitive-behavioral therapy (CBT) is the first-line treatment for mild to moderate OCD in youth. Medication should be considered when OCD symptoms are severe, in the presence of comorbid disorder or family dysfunction, when the patient or family resists engaging in CBT, or when a skilled CBT clinician is not available. In the Pediatric OCD Treatment Study (POTS; March et al. 2004), CBT and medication treatment with sertraline were equally effective, and each was better than placebo treatment, although subsequent data analysis examining OCD with or without tics revealed somewhat different outcomes. Combining CBT and medication yielded the greatest treatment response. Specific CBT techniques used in the POTS included psychoeducation, cognitive training (cognitive restructuring), mapping OCD, exposure and response prevention (ERP), and relapse prevention/generalization training. CBT has been extended to group therapy and family-based approaches. Family-based CBT was shown to be superior to family-based relaxation treatment in OCD treatment for younger children ages 5–8 years (Freeman et al. 2014). Acceptance and commitment therapy (ACT) has shown some effect in reducing anxiety. The goal of ACT is for patients to accept their thoughts as just thoughts (instead of reality) while avoiding specific experiences that do not support acceptance (Park and Geller 2014). However, empirical evidence for ACT in pediatric OCD is lacking.

In addition to sertraline, the SSRIs paroxetine, fluoxetine, and fluvoxamine, and the tricyclic antidepressant clomipramine, have been shown to be effective in childhood OCD (Geller et al. 2003), although clomipramine is typically reserved for treatment-resistant cases because of its side-effect profile and interactions with other medications, and paroxetine is very rarely used in children. Because there are no comparative efficacy data, clinical factors determine which SSRI to select (including citalopram and escitalopram, which have not been studied in OCD trials). Clomipramine, fluoxetine, fluvoxamine, and sertraline have U.S. Food and Drug Administration (FDA) labeling for pediatric OCD. If medication augmentation is required, the most common addition (extrapolating from research with adults) is an atypical antipsychotic, particularly if there are concurrent tic disorders, ASD symptoms, or mood dysregulation.