Treatment of Pediatric Obsessive-Compulsive Disorder: A Review Elizabeth Mancuso, B.A., 1 Alyssa Faro, B.A., 1 Gagan Joshi, M.D., 1 Daniel A. Geller, MBBS, FRACP 1,2 Abstract Recently, research in pediatric obsessive-compulsive disorder (OCD) has expanded to include large family genetic studies, elaboration of phenotypic dimensions, description of co-morbid disorders and their moderating effects on treatment response and outcome, research on immune-based neuropsychiatric causes, randomized controlled trials of selective serotonin re- uptake inhibitors (SSRIs), randomized controlled trials of cognitive behavioral therapy (CBT), comparative treatment trials; new approaches in behavior therapy, and increased awareness of newer approaches to treatment. The purpose of this article is to review assessment and treatment strategies to include current advances in research. Introduction O bsessive-compulsive disorder (OCD) is now recognized as a relatively common disorder affecting children and adoles- cents and is expected to be among the ten leading causes of global disability by the World Health Organization (WHO) (World Health Organization 2005). In the last decade, our knowledge of pediatric OCD has increased with large family genetic studies, elaboration of phenotypic dimensions, description of co-morbid disorders and their moderating effects on treatment response and outcome, re- search on immune-based neuropsychiatric causes (pediatric neu- ropsychiatric disorders associated with Streptococcus [PANDAS]), publication of randomized controlled trials of selective serotonin reuptake inhibitors (SSRIs), as well as concern and scrutiny regarding safety of these SSRIs in children, the first large-scale randomized controlled trials of cognitive behavioral therapy (CBT) as single and multimodal treatment, new approaches in behavior therapy, and increased awareness of novel approaches to pharma- cotherapy. This review of current treatment strategies aims to in- corporate these new developments. Epidemiology The high prevalence of OCD in children was not generally recognized until the first epidemiological study just over 20 years ago (Flament et al. 1988). Epidemiological studies in the United States and elsewhere report prevalence rates of around 1–2% in the pediatric population. In an early epidemiological study (Flament et al. 1988), most adolescents identified with OCD had been neither diagnosed nor treated, suggesting that the disorder was under rec- ognized and under treated, leading to the notion of pediatric OCD as a ‘‘hidden epidemic.’’ The more recent British Nationwide Survey of Child Mental Health (Heyman et al. 2003) reported similar findings. There appear to be two peaks of incidence for OCD across the life span, one occurring in preadolescent children (Geller et al. 1998b) and a later peak in early adult life (mean age 21 years) (Geller et al. 1998a). Pathophysiology, Neurobiology, and Genetics Several frontal cortico-striatal-thalamic circuits have been implicated in the pathophysiology of OCD, and several neuro- transmitter systems modulate this feedback loop, including the excitatory amine glutamate as well as dopamine and serotonin- containing neurons (Rosenberg and Keshavan 1998). Pediatric imaging studies appear similar to those in adults, detecting struc- tural abnormalities in the cingulate cortex, basal ganglia, and thalami of pediatric OCD patients (Rosenberg and Keshavan 1998; Gilbert et al. 2000). A handful of functional imaging studies con- ducted with children at rest and following treatment have yielded results compatible with those in adults. In a single-photon emission computerized tomography (SPECT) study of 13 adults with early- onset (<10 years) versus later-onset OCD and 22 healthy controls, early-onset cases showed decreased cerebral blood flow in the right thalamus, left anterior cingulate cortex, and bilateral inferior pre- frontal cortex relative to late-onset subjects. In early-onset subjects only, severity of obsessive-compulsive (OC) symptoms correlated positively with left orbitofrontal regional cerebral blood flow (rCBF), suggesting that brain mechanisms in OCD may differ de- pending on the age at which symptoms are first expressed (Busatto et al. 2001). The contribution of genetic factors to the development of OCD has been explored in twin, family genetic, and segregation analyses studies (Pauls et al. 1995; Nestadt et al. 2000; Grados et al. 2001; Reddy et al. 2001; Pato et al. 2002; Hanna et al. 2005). The con- cordance rates for monozygotic twins are significantly higher than 1 Clinical and Research Program in Pediatric Psychopharmacology, Department of Psychiatry, Massachusetts General Hospital, and 2 Harvard Medical School, Boston, Massachusetts. JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY Volume 20, Number 4, 2010 ª Mary Ann Liebert, Inc. Pp. 299–308 DOI: 10.1089/cap.2010.0040 299