Pediatric Obsessive-Compulsive Disorder

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Obsessive-compulsive disorder (OCD) is a significant neurobiologic disorder that severely can disrupt academic, social, and vocational functioning. [1, 2, 3] The major features of this disorder are the presence of recurring obsessions (recurrent unwanted thoughts) and compulsions (repetitive excessive actions that interfere with a person’s life). (See Etiology, History.)

Once believed to be relatively rare in children and adolescents, OCD now is thought to affect as many as 2–3% of children. Among adolescents with OCD, the literature indicates that very few receive an appropriate and correct diagnosis, and even fewer receive proper treatment. This finding is unfortunate, because effective cognitive, behavioral, and pharmacologic treatments are now available. If obsessive-compulsive disorder (OCD) is suspected, referral to a mental health professional is indicated. (See Epidemiology.)

In the history of treatment, insight-oriented psychotherapy did not appear to improve OCD, and psychodynamic understanding was not helpful. (See Treatment.)

Go to Pediatric Generalized Anxiety Disorder and Pediatric Panic Disorder for complete information on these topics.

Obsessions are defined as recurrent and persistent thoughts, images, or impulses that are ego-dystonic, intrusive, and, for the most part, acknowledged as senseless. [4]  Obsessions usually are accompanied by dysphoric affect, such as fear, doubts, and disgust.

Children and adolescents with OCD typically first try to ignore, suppress, or deny obsessive thoughts and may not report the symptoms as ego-dystonic or senseless. However, by trying to neutralize excessive thoughts, individuals with OCD very quickly change their behaviors by performing some type of compulsive actions, which are repetitive, purposeful behaviors carried out in response to the obsession. Usually, these repetitive actions follow certain rules or are quite stereotyped.

Some compulsions observed include behaviors such as washing, counting, or lining up of objects. Other compulsions are covert mental acts, such as counting or reading a passage again and again. Thus compulsions as mental rituals may not be apparent to those around the patient; patients may hide their compulsions from others. These compulsions serve to reduce the anxiety produced by the obsessive thoughts. If something interferes with or blocks the compulsive behavior, the child feels heightened anxiety or fear and can become quite upset and oppositional. (See History.)

Not confusing OCD with normal ritualistic behavior of childhood is important. Most children exhibit typical, age-dependent, compulsive behaviors. Frequently, young children prefer that events occur in a particular way, they insist on specific bedtime or mealtime rituals, and they become distressed if these rituals are disrupted.

Cross-sectional research of ritualistic behavior in children demonstrates that these behaviors appear when the individual is aged approximately 18 months, peak when the individual is aged approximately 2–3 years, and decline afterward. Presence of these behaviors appears to be related to mental age; thus, children who are mentally retarded and have cognitive levels at a developmental age of 2–3 years may have higher rates of compulsive behaviors, which are appropriate to their cognitive levels of development. These behaviors are best understood by acknowledging that they involve mastery and control of their environment, and, usually, they decrease to low levels by middle childhood. As a child ages, compulsive behaviors are replaced by hobbies or focused interests.

Normative compulsive behaviors can be discriminated from OCD on the basis of content, timing, and severity. Normative compulsive behaviors do not interfere with daily functioning.

One of the leading causes of death of patients with OCD is suicide. A population study in Sweden demonstrated that patients with OCD have a markedly increased risk of suicide. [5]

For patient education information, see the Anxiety Center, as well as Anxiety, Panic Attacks, and Hyperventilation.

Obsessive-compulsive disorder (OCD) is considered a neuropsychiatric disorder. OCD symptoms do not appear to represent intrapsychic conflicts within individuals. Indeed, relatively few OCD behaviors exist, and they are experienced in much the same manner by patients, regardless of their interpersonal histories. [2]

Initial successes in treatment of OCD with selective serotonin reuptake inhibitors (SSRIs) have led to a neuropsychiatric explanation of a serotonin-mediated “grooming behavior” that has been disrupted. In addition, clear family genetic studies demonstrate that, in some cases, OCD and Tourette syndrome may represent expressions of the same gene. Tic disorders occur more frequently in individuals who have OCD, and first-degree relatives of patients with OCD have higher rates of tic disorders, a full Tourette syndrome (TS), and OCD. While there exists some overlap in the genetic basis of OCD and TS, the conditions represent two unique genetic structures. [6]

OCD may result from excessive glutamatergic activity in the prefrontal and orbitofrontal cortex. [7, 8, 9]

Neuroimaging studies suggest abnormalities in neurologic circuits that link cortical areas to the basal ganglia. These circuits appear to change in response to successful treatment with either SSRI medication or cognitive behavior therapies (CBTs). Increased emotional processing-related activation has been demonstrated in limbic, frontal, and temporal regions. [10] Also, neurotransmitter and neuroendocrine abnormalities have been documented in childhood-onset OCD. Anti-basal ganglia antibodies had been shown to be five times more likely to be detected in the serum of individuals with primary OCD in comparison with healthy controls, and patients with various psychiatric, neurological, and autoimmune disorders. [11]

In addition, investigators have found OCD symptoms that arise from, or are strongly exacerbated in, the context of group A beta-hemolytic streptococcal (GABHS) infection. Such conditions are referred to as pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). Sudden exacerbation of OCD symptoms in the presence of upper respiratory tract illness marks these cases. The mechanism is believed to be caused by antineuronal antibodies formed against group beta-hemolytic streptococcal cell wall antigens, which cross-react with caudate neural tissue and initiate OCD symptoms.

Reactions against other infections, including viral agents, are also being considered. Current research is evaluating this particular factor in the development of OCD. These cases are believed to make up a fairly small percentage (ie, < 5%) of all persons with OCD, but this may be an important mechanism in children who may have had some tendencies or subclinical OCD symptoms prior to infection.

In the United States, obsessive-compulsive disorder (OCD) is substantially more common in children and adolescents than was once believed. It has a 6-month prevalence of approximately 1 in 200 children and adolescents, while the prevalence of OCD occurring at any time during childhood is assumed to be 2–3 per 100 children. [12]

Among adults with OCD, interview data indicate that one third to one half developed the disorder during childhood. Unfortunately, this disorder often goes unrecognized in children and adolescents. Onset in childhood or adolescence can lead to a lifetime of OCD. However, 40% of individuals with early onset may experience remission by early adulthood. [13]

In clinical samples, OCD was found to be more common in white children than in African American children. However, epidemiologic data suggest no differences in prevalence as a function of ethnic group or geographic region.

Boys are more likely to have a prepubertal onset and a family member with OCD or Tourette syndrome. Girls are more likely to have onset of OCD during adolescence.

OCD has been studied most comprehensively at the National Institute of Mental Health with referred patients, who likely represent more severe cases. In those studies, the modal age of onset was 7 years; the mean age was 10.2 years. These figures imply the possible existence of an early-onset group and a second group with onset in adolescence. [14]

No specific predictors of treatment outcome have been identified for pediatric obsessive-compulsive disorder (OCD). Children who can identify their obsessions as senseless and their rituals as useless and distressing are more motivated and better candidates for cognitive-behavioral therapy (CBT). A calm, supportive family environment in which parents and/or caregivers actively can support the child’s coping strategies also should improve outcome. [15]  Pediatric OCD appears to have a better prognosis than adult-onset OCD. [16]  

Comorbidity of OCD with other disorders, specifically oppositional disorders and/or attention deficit/hyperactivity disorder (ADHD), makes compliance with OCD treatment more difficult.

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James Robert Brasic, MD, MPH Assistant Professor, Russell H Morgan Department of Radiology and Radiological Science, Division of Nuclear Medicine, Johns Hopkins University School of Medicine; Active Staff, Department of Radiology and Radiological Science, Division of Nuclear Medicine, Johns Hopkins Hospital; Courtesy Staff, Department of Radiology, Johns Hopkins Bayview Medical Center

James Robert Brasic, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, International Parkinson and Movement Disorder Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Johns Hopkins University School of Medicine<br/>Received research grant from: National Institutes of Health<br/>Received income in an amount equal to or greater than $250 from: Brand Institute, Inc.<br/>Received royalty from Medscape for other; Received royalty from Neuroscience-Net, LLC for other; Received grant/research funds from National Institutes of Health for other.

Farzaneh Farhadi, MD 

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Caroly Pataki, MD Health Sciences Clinical Professor of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, David Geffen School of Medicine

Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

This research is supported by the Essel Foundation, the Brain and Behavior Research Foundation (NARSAD), the Tourette Syndrome Association Inc, and the National Institutes of Health.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author W Douglas Tynan, PhD, to the development and writing of the source article.

Pediatric Obsessive-Compulsive Disorder

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