Obsessive-compulsive disorder (OCD) is a neuropsychiatric disorder characterized by the presence of obsessions (intrusive, repetitive thoughts, images, or impulses) and compulsions (repetitive, overt, and covert behaviors/rituals performed to decrease distress) that can lead to significant impairments across different functional domains, and it constitutes a global burden according to the World Health Organization.1 Although historically perceived as a rare disorder among children and adolescents, more recent prevalence rates range between 0.5% and 4%.2,3 Pediatric OCD causes impairment in multiple functional domains, including day-to-day routines, school performance, and relationships with friends and family, and has a long-term negative impact if not treated.4 The clinical phenomenology and clinical course of pediatric OCD differs from adult OCD and is complicated by overlapping, developmentally typical behaviors.5 Comorbidities are quite prevalent and, therefore, must be taken into account when assessing pediatric OCD and planning for interventions. Our understanding of the neurobiological underpinnings of OCD has undergone significant advances over the past few decades. In one of the early seminal case descriptions (the “Rat Man”), Freud6 described defense mechanisms involved in OCD such as pathological doubts, reaction formation, and isolation of affect. However, recent findings from genetic and neuroimaging studies highlight the complex neurobiological causes for OCD.7 Effective evidence-based treatments for pediatric OCD are available and include psychotherapeutic and pharmacological interventions. These treaments may lead to significant improvements in symptoms and functioning of the affected children and adolescents and their families.8
Important differences do exist between pediatric and adult-onset OCD. According to Geller et al.,9 there are two peaks in pediatric OCD: one in prepuberty and the other in late adolescence or early adulthood. If left untreated, the course of OCD tends to be chronic, with waxing and waning of symptoms over time. Approximately 40% of pediatric OCD persists into adulthood, with a moderate to severe clinical course in approximately one-third of those affected.10,11 Approximately 70% of patients with pediatric OCD present with another mental disorder in adulthood, according to the results of one longitudinal study,12 The co-occurrence of mental disorders is quite common in pediatric OCD, and is estimated at approximately 40%. The most common co-occurring disorders are anxiety disorders, tic disorders, and depressive disorder.12
The etiology of pediatric OCD is multifactorial, with environmental and genetic factors playing a role. Initial theories exploring the etiology of OCD focused on psychoanalytic causes, such as the psychodynamic defense mechanism of reaction formation against latent aggressive impulses, and elevated levels of indirect aggression and anger among patients with OCD;13 however, there is no evidence supporting the role of subconscious conflicts in the etiology of OCD.
Recent technological advances and breakthroughs have shed light on some aspects of the neurobiology of OCD. The most accepted model regarding the neurobiology of OCD is the cortico-striato-thalamo-cortical (CSTC) model.14 Functional and structural neuroimaging studies reported that both adults and children with OCD have an increased activation of the lateral and medial orbitofrontal cortex (OFC),15 and also have increased activity of the head of the caudate nuclei16 and the anterior cingulate cortex (ACC).17 The role of the OFC and ACC in the etiology of OCD has been strengthened by animal studies using optogenetics,18 as the activation of these areas resulted in repetitive behaviors among mice, whereas the deactivation resulted in improved OCD symptoms in a mouse OCD model.
Heritability estimates of OCD are approximately 0.45 to 0.65, which is higher than that of adult-onset OCD.19 Moreover, relatives of children with OCD have greater odds of having neuropsychiatric disorders, such as tic disorders and Tourette syndrome, compared to relatives of adults with OCD. Furthermore, family studies show that OCD (or subthreshold OCD symptoms) are more common among relatives of children with OCD than relatives of adults with OCD.7 These findings suggest that pediatric OCD may be a neurobiologically distinct subtype of OCD. As is the case in many neuropsychiatric disorders, genetic studies indicate that multiple genes with small effects confer the risk of OCD.20 Genetic linkage studies, candidate gene studies, and genome-wide association studies identified multiple genes as being implicated in the etiology of OCD.7 Candidate gene studies were based on the understanding of the neural biology of OCD and focused on genetic variants implicated in serotonergic pathways (5HTTLPR, HTR2A), dopaminergic pathways (DAT1, DRD3), and glutamatergic pathways (SLC1A1). In summary, these studies suggest that OCD has a polygenic etiology stemming from genes that affect glutamatergic, dopaminergic, and serotonergic pathways.
Several environmental factors have been associated with an increased risk of OCD, including perinatal factors21 and psychosocial stressors (including trauma); however, a recent study did not identify a correlation between adverse childhood experiences and OCD.22
In the late 1990s, Swedo et al.23 described a group of people with acute OCD and tic disorders in the context of group A beta-hemolytic streptococcal infections (GABHS), and named this condition pediatric autoimmune neurodevelopmental disorders associated with streptococcus (PANDAS). A meta-analysis of people with OCD reported a greater proportion of anti-basal ganglia antibody among children with OCD compared to controls (odds ratio of 4.97, 95% confidence interval [CI] 2.88–8.55), which was found to be comparable with other autoimmune disorders.24 Furthermore, a recent study using positron emission tomography scans in children with PANDAS reported neuroinflammatory findings in the thalamus and basal ganglia. Nonetheless, there is no clinical indication for neuroimaging in OCD, even when PANDAS is suspected.25 Although some studies point to a subtype of pediatric OCD triggered by GABHS,26 the literature is still not conclusive, and further studies are required to conclude if PANDAS indeed constitutes a true subtype of OCD.27
In a comprehensive overview and attempt to provide an integrative model explaining the etiology of OCD, Pauls et al.7 concluded that people with OCD have a genetic vulnerability to environmental risks that, in turn, trigger changes in the expression of genes in glutamatergic, serotonergic, and dopaminergic systems via epigenetic mechanisms.
Clinical Presentation and Diagnostic Criteria
Pediatric OCD is more prevalent in boys than in girls, with a male to female ratio of 3 to 1, and it usually starts prior to age 12 years.28 The age of onset in pediatric OCD ranges between 7.5 and 12.5 years.9 In children, the course of OCD usually starts with compulsions (mean age, 7.8 years) followed by obsessions (mean age, 9.3 years), whereas obsessions and compulsions start simultaneously in people who are older.29 Furthermore, childhood-onset OCD may be associated with higher symptomatology, especially compulsions, tic-like compulsions, hoarding obsessions, and bodily sensations preceding the compulsions.30 Pediatric OCD is also characterized by a higher level of psychiatric comorbidities, especially tic disorders.5 Other psychiatric comorbidities associated with early-onset OCD include attention-deficit/hyperactivity disorder (ADHD), separation anxiety disorder, agoraphobia, and specific phobias, whereas mood and psychotic disorders are more frequently comorbid with adolescent-onset OCD.31 In the Diagnostic and Statistical Manual for Mental Disorders, fifth edition (DSM-5),32 OCD is in a separate chapter titled “Obsessive-Compulsive and Related Disorders.” Table 1 summarizes DSM-5 criteria for OCD.
Summary of DSM-5 Criteria for Obsessive-Compulsive Disorder
Prognosis and Long-Term Outcomes
In general, the long-term prognosis for pediatric OCD is good, as many children achieve full remission or clinically insignificant symptoms. Factors that are predictive of persistence include younger age of onset, increased duration, inpatient treatment, and the presence of specific subtypes of obsessions including hoarding, sexual, and religious obsessions. Factors that predict poor outcome include comorbid psychiatric disorders and suboptimal response to initial treatment. On the other hand, age and gender, as well as the length of follow-up, are not associated with remission or persistence.33
Assessment of Pediatric OCD
The assessment of pediatric OCD should comprehensively capture the DSM-5 diagnostic criteria, functional impairment, and associated distress, preferably using the clinical assessment in combination with an OCD scale. The Children's Yale-Brown Obsessive-Compulsive Scale (CY-BOCS) rates the clinical severity of obsessions and compulsions and has been validated for use in children.34 Some issues exist when using CY-BOCS and should be considered. For example, avoidance behaviors are not included, which may result in underestimating the severity, and given the heterogeneity of OCD, some atypical symptoms may not be captured. In CY-BOCS, OCD symptoms are assessed across five domains in both obsessions and compulsions that are scored from 0 to 4. The five domains are time spent, associated distress, interference with day-to-day activities, resistance to OCD symptoms, and control over or to the symptoms. A score of 16 is used as a cutoff.
Because more than three-quarters of pediatric OCD cases present with comorbidities, it is extremely important to assess for the presence of psychiatric comorbidities, especially because the presence of comorbidities may affect the treatment response.35 Moreover, the comprehensive assessment of pediatric OCD should include the full medical, developmental, family, and educational history. Furthermore, structured comprehensive diagnostic interviews may be used to assure comprehensiveness of the evaluation, consistency among clinicians, and systematic gathering of required information.36 These interviews include the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children–Present & Lifetime version, and the National Institute of Mental Health Diagnostic Interview Schedule for Children. However, these structured interviews are time intensive and often require extensive training to use properly (Table 2).
General Evaluation Points for Pediatric Obsessive-Compulsive Disorder
Symptoms of Pediatric OCD
Children with OCD present with limited insight. Symptoms among children are usually hidden and poorly articulated. Children may show compulsions without well-defined obsessions. Obsessions may include fear of catastrophic event, contamination, sex, or guilt, and compulsions may include washing, repeating, and checking.5,37 Whereas adults and older adolescents are usually able to link their compulsions with decreasing distress caused by the obsessions, younger children are typically unable to articulate the reason behind their compulsion. Moreover, hoarding has been more frequently reported in pediatric OCD (>50% of girls and >36% of boys) compared to adult OCD.38
It is extremely important to look at the developmental context when assessing a child with OCD. Some of the symptoms of OCD overlap with behaviors that are developmentally normal. For instance, many young children display distress when their routine is disrupted. These behaviors usually start prior to age 2 years, peak around age 3 years, and then decline thereafter. However, this behavior may persist longer in developmentally and cognitively delayed children. Furthermore, clinicians may come across difficulties diagnosing OCD in children with autism spectrum disorder (ASD), given that some of the ASD symptoms, including behavioral rigidity, repetitive movements, and restricted interests, overlap with OCD. One of the main differences, although not always clinically easy to assess, is that OCD is often dysphoric and ego-dystonic, whereas repetitive behaviors and movements in ASD can be self-soothing. Furthermore, the presence of typical OCD symptoms, such as fear of contamination or excessive washing, can help differentiate the two.
Another clinically complicating factor in pediatric OCD is that because some children with OCD present with poor insight about their obsessions, it can be difficult to ascertain whether there are overlapping delusions or psychosis. The presence of other psychotic symptoms may help differentiate the diagnosis. Although personality disorders are not typically diagnosed at a younger age, some children are quite meticulous with minute details, rigidly following the rules, and show significant inflexibility.
Both pharmacological and nonpharmacological treatments have been studied in pediatric OCD. Evidence-based treatment for pediatric OCD relies on cognitive-behavioral therapy (CBT) and medications.39
The effectiveness of CBT for treatment of pediatric OCD has been established in multiple studies.40 A meta-analysis showed reasonable effect size for CBT in treating OCD (effect size = 1.45, 95% CI 0.68–2.22).39 Components of CBT for OCD include cognitive restructuring and exposure/response prevention (ERP). In cognitive restructuring, the patient learns how to connect his or her thoughts with behaviors, and strategies are given to weaken the association and the distress caused by symptoms. CBT for children is usually administered in 50-minute, one-to-one sessions with the child. Furthermore, families are usually requested to be involved in the therapy. In ERP, the child is exposed to a hierarchy of triggers for OCD while being instructed to refrain from engaging in compulsive behaviors to develop tolerance to the stimuli.41 CBT-ERP refers to a type of CBT that is geared toward targeting OCD using ERP techniques.
Another important factor is when family members respond to the OCD symptoms by facilitating avoidance and/or allowing and helping in ritualistic behaviors and compulsions. This is sometimes referred to as family accommodation and may hinder the treatment response, as it has been associated with symptom maintenance and poor outcome. Family-based CBT has been demonstrated as an effective intervention for pediatric OCD in a 14-week randomized trial.42
The efficacy of medications and treatment of pediatric OCD has been established, and a meta-analysis of published randomized controlled trials reported an effect size of 0.46 (95% CI 0.37–0.55).43
Selective serotonin reuptake inhibitors. Selective serotonin reuptake inhibitors (SSRIs) are considered the main pharmacological agents for treatment of pediatric OCD because of their established efficacy and tolerability.44 Three SSRIs are approved by the US Food and Drug Administration (FDA) for pediatric OCD—sertraline, fluoxetine, and fluvoxamine. Although not backed by randomized controlled trials, citalopram and escitalopram are commonly used by clinicians in treatment of pediatric OCD.45 There is no evidence for the use of paroxetine and it is usually avoided in children and adolescents due to its side-effect profile. Although the clinical practice is to use higher doses for longer durations in treating pediatric OCD, a recent randomized trial did not support this practice.46
The Pediatric OCD Treatment Study8 is a landmark treatment study for pediatric OCD. This 5-year multisite study compared placebo, an SSRI (sertraline), CBT, and a combination of CBT plus sertraline for the treatment of pediatric OCD. Although all three treatment groups improved, the combined group had a larger effect size compared to CBT alone and sertraline alone (0.97 and 0.67, respectively).8 Furthermore, for children who are treated with medications alone and respond partially, augmentation with CBT results in further improvement.47 In a recent randomized, placebo-controlled trial including 47 children and adolescents (age 7 to 17 years), there was no evidence of greater response in sequentially added sertraline to CBT in pediatric OCD compared with placebo.48
Clomipramine. Varigonda et al.46 conducted a meta-analysis to examine response to SSRIs and clomipramine in pediatric OCD. Although the clinical convention is to use higher doses of SSRIs in pediatric OCD compared to other disorders, this comprehensive meta-analysis did not show a relationship between medication dose and treatment effects. Further, it strengthens the existing evidence supporting clomipramine to have greater efficacy compared to SSRIs.
Other pharmacological agents. Other medications have also been studied in pediatric OCD. Riluzole is a glutamate inhibitor that has been recently studied in both adult and pediatric OCD. Although an initial open-label study showed promising findings, a recent double-blind, placebo-controlled trial did not show symptomatic improvement in pediatric OCD.49 Given its positive effects on facilitating extinction learning, the efficacy of the selective partial N-methyl-D-aspartate receptor agonist, D-cycloserine, has been studied as an adjunct to CBT. A randomized trial was performed on a small number of children with OCD and showed that D-cycloserine improved the efficacy of CBT compared to placebo.50 Other medications that are being studied in adult OCD include ketamine and memantine, but there have been no clinical trials of them for pediatric OCD.
Pediatric OCD is a complex neuropsychiatric disorder that is associated with marked impairments and significant burden. The assessment of pediatric OCD should comprehensively capture the diagnostic criteria, functional impairment, and associated distress, preferably using the clinical assessment in combination with an OCD scale. Childhood-onset OCD is more common in boys than in girls, and usually presents with other neuropsychiatric comorbidities. The first-line treatment for mild to moderate OCD is CBT, and its effectiveness has been demonstrated in different clinical trials. Family-based CBT may also be used as an effective intervention. For moderate to severe cases of pediatric OCD, medications alone or in combination with CBT are recommended. There is evidence for the use of SSRIs, and fluoxetine, fluvoxamine, and sertraline have been approved by the FDA for pediatric OCD. Clomipramine is an effective option but requires close monitoring for side effects. A family approach to the assessment and treatment is necessary in pediatric OCD. Most children with OCD achieve remission or significant improvement in their symptoms.
- Kessler RC, Aguilar-Gaxiola S, Alonso J, et al. The global burden of mental disorders: an update from the WHO World Mental Health (WMH) surveys. Epidemiol Psichiatr Soc. 2009;18(1):23–33. doi:10.1017/S1121189X00001421 [CrossRef]
- Heyman I, Fombonne E, Simmons H, et al. Prevalence of obsessive-compulsive disorder in the British nationwide survey of child mental health. Br J Psychiatry. 2001;179:324–329. doi:10.1192/bjp.179.4.324 [CrossRef]
- Ford T, Goodman R, Meltzer H. The British Child and Adolescent Mental Health Survey 1999: the prevalence of DSM-IV disorders. J Am Acad Adoslec Psychiatry. 2003;42(10):1203–1211. doi:. doi:10.1097/00004583-200310000-00011 [CrossRef]
- Cooper M. Obsessive-compulsive disorder: effects on family members. Am J Orthopsychiatry. 1996;66(2):296–304. doi:10.1037/h0080180 [CrossRef]
- Geller DA, Biederman J, Faraone S, et al. Developmental aspects of obsessive compulsive disorder: findings in children, adolescents, and adults. J Nerv Ment Dis. 2001;189(7):471–477. doi:10.1097/00005053-200107000-00009 [CrossRef]
- Freud S. (1909). Notes upon a case of obsessional neurosis. In: Strachey J, ed. (translated). The Standard Edition of the Complete Psychological Works of Sigmund Freud. Volume 10. London, UK. Hogarth Press; 1974.
- Pauls DL, Abramovitch A, Rauch SL, Geller DA. Obsessive-compulsive disorder: an integrative genetic and neurobiological perspective. Nat Rev Neurosci. 2014;15(6):410–424. doi:. doi:10.1038/nrn3746 [CrossRef]
- Pediatric OCD Treatment Study (POTS) Team. Cognitive-behavior therapy, sertraline, and their combination for children and adolescents with obsessive-compulsive disorder: the Pediatric OCD Treatment Study (POTS) randomized controlled trial. JAMA. 2004;292(16):1969–1976. doi:. doi:10.1001/jama.292.16.1969 [CrossRef]
- Geller D, Biederman J, Jones J, et al. Is juvenile obsessive-compulsive disorder a developmental subtype of the disorder? A review of the pediatric literature. J Am Acad Adolesc Psychiatry. 1998;37(4):420–427. doi:. doi:10.1097/00004583-199804000-00020 [CrossRef]
- Stewart SE, Geller DA, Jenike M, et al. Long-term outcome of pediatric obsessive-compulsive disorder: a meta-analysis and qualitative review of the literature. Acta Psychiatrica Scand. 2004;110(1):4–13. doi:. doi:10.1111/j.1600-0447.2004.00302.x [CrossRef]
- Bloch MH, Peterson BS, Scahill L, et al. Adulthood outcome of tic and obsessive-compulsive symptom severity in children with Tourette syndrome. Arch Pediatr Adolesc Med. 2006;160(1):65–69. doi:. doi:10.1001/archpedi.160.1.65 [CrossRef]
- Micali N, Heyman I, Perez M, et al. Long-term outcomes of obsessive-compulsive disorder: follow-up of 142 children and adolescents. Br J Psychiatry. 2010;197(2):128–134. doi:. doi:10.1192/bjp.bp.109.075317 [CrossRef]
- Moritz S, Kempke S, Luyten P, Randjbar S, Jelinek L. Was Freud partly right on obsessive-compulsive disorder (OCD)? Investigation of latent aggression in OCD. Psychiatry Res. 2011;187(1–2):180–184. doi:. doi:10.1016/j.psychres.2010.09.007 [CrossRef]
- Saxena S, Rauch SL. Functional neuroimaging and the neuroanatomy of obsessive-compulsive disorder. Psychiatr Clin North Am. 2000;23(3):563–586. doi:. doi:10.1016/S0193-953X(05)70181-7 [CrossRef]
- Fitzgerald KD, Welsh RC, Stern ER, et al. Developmental alterations of frontal-striatal-thalamic connectivity in obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry. 2011;50(9):938–948.e3. doi:10.1016/j.jaac.2011.06.011 [CrossRef]
- Abramovitch A, Mittelman A, Henin A, Geller D. Neuroimaging and neuropsychological findings in pediatric obsessive-compulsive disorder: a review and developmental considerations. Neuropsychiatry. 2012;2(4):313–329. doi:. doi:10.2217/npy.12.40 [CrossRef]
- Brennan BP, Tkachenko O, Schwab ZJ, et al. An examination of rostral anterior cingulate cortex function and neurochemistry in obsessive-compulsive disorder. Neuropsychopharmacology. 2015;40(8):1866–1876. doi:. doi:10.1038/npp.2015.36 [CrossRef]
- Burguière E, Monteiro P, Feng G, Graybiel AM. Optogenetic stimulation of lateral orbitofronto-striatal pathway suppresses compulsive behaviors. Science. 2013;340(6137):1243–1246. doi:. doi:10.1126/science.1232380 [CrossRef]
- van Grootheest DS, Cath DC, Beekman AT, Boomsma DI. Twin studies on obsessive-compulsive disorder: a review. Twin Res Hum Genet. 2005;8(5):450–458. doi:. doi:10.1375/twin.8.5.450 [CrossRef]
- Mattheisen M, Samuels JF, Wang Y, et al. Genome-wide association study in obsessive-compulsive disorder: results from the OCGAS. Mol Psychiatry. 2014;20(3):337–344. doi:. doi:10.1038/mp.2014.43 [CrossRef]
- Geller DA, Wieland N, Carey K, et al. Perinatal factors affecting expression of obsessive compulsive disorder in children and adolescents. J Child Adolesc Psychopharmacol. 2008;18(4):373–379. doi:10.1089/cap.2007.0112 [CrossRef].
- Visser HA, van Minnen A, van Megen H, et al. The relationship between adverse childhood experiences and symptom severity, chronicity, and comorbidity in patients with obsessive-compulsive disorder. J Clin Psychiatry. 2014;75(10):1034–1039. doi:. doi:10.4088/JCP.13m08825 [CrossRef]
- Swedo SE, Leonard HL, Garvey M, et al. Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: clinical description of the first 50 cases. Am J Psychiatry. 1998;155(2):264–271. doi:10.1176/ajp.155.2.264 [CrossRef].
- Pearlman DM, Vora HS, Marquis BG, Najjar S, Dudley LA. Anti-basal ganglia antibodies in primary obsessive-compulsive disorder: systematic review and meta-analysis. Br J Psychiatry. 2014;205(1):8–16. doi:. doi:10.1192/bjp.bp.113.137018 [CrossRef]
- Kumar A, Williams MT, Chugani HT. Evaluation of basal ganglia and thalamic inflammation in children with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection and tourette syndrome: a positron emission tomographic (PET) study using 11C-[R]-PK11195. J Child Neurol. 2015;30(6):749–756. doi:. doi:10.1177/0883073814543303 [CrossRef]
- Leslie DL, Kozma L, Martin A, et al. Neuropsychiatric disorders associated with streptococcal infection: a case-control study among privately insured children. J Am Acad Child Adolesc Psychiatry. 2008;47(10):1166–1172. doi:. doi:10.1097/CHI.0b013e3181825a3d [CrossRef]
- de Oliveira SKF, Pelajo CF. Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS): a controversial diagnosis. Curr Infect Dis Rep. 2010;12(2):103–109. doi:. doi:10.1007/s11908-010-0082-7 [CrossRef]
- Garcia AM, Freeman JB, Himle MB, et al. Phenomenology of early childhood onset obsessive compulsive disorder. J Psychopathol Behav Assess. 2009;31(2):104–111. doi:. doi:10.1007/s10862-008-9094-0 [CrossRef]
- Rosario-Campos MC, Leckman JF, Mercadante MT, et al. Adults with early-onset obsessive-compulsive disorder. Am J Psychiatry. 2001;158(11):1899–1903. doi:10.1176/appi.ajp.158.11.1899 [CrossRef]
- do Rosario Campos MC, Leckman JF, Curi M, et al. A family study of early-onset obsessive-compulsive disorder. Am J Med Genet. 2005;136B(1):92–97. doi:. doi:10.1002/ajmg.b.30149 [CrossRef]
- Geller DA, Biederman J, Faraone SV, et al. Disentangling chronological age from age of onset in children and adolescents with obsessive-compulsive disorder. Int J Neuropsychopharmacol. 2001;4(2):169–178. doi:. doi:10.1017/S1461145701002395 [CrossRef]
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Publishing; 2013.
- Practice parameter for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry. 2012;51(1):98–113. doi:. doi:10.1016/j.jaac.2011.09.019 [CrossRef]
- Scahill L, Riddle MA, McSwiggin-Hardin M, et al. Children's Yale-Brown Obsessive Compulsive Scale: reliability and validity. J Am Acad Child Adolesc Psychiatry. 1997;36(6):844–852. doi:. doi:10.1097/00004583-199706000-00023 [CrossRef]
- Storch EA, Merlo LJ, Larson MJ, et al. Impact of comorbidity on cognitive-behavioral therapy response in pediatric obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry. 2008;47(5):583–592. doi:. doi:10.1097/CHI.0b013e31816774b1 [CrossRef]
- Lewin AB, Piacentini J. Evidence-based assessment of child obsessive compulsive disorder: recommendations for clinical practice and treatment research. Child Youth Care Forum. 2010;39(2):73–89. doi:. doi:10.1007/s10566-009-9092-8 [CrossRef]
- Rettew DC, Swedo SE, Leonard HL, Lenane MC, Rapoport JL. Obsessions and compulsions across time in 79 children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry. 1992;31(6):1050–1056. doi:. doi:10.1097/00004583-199211000-00009 [CrossRef]
- Mataix-Cols D, Nakatani E, Micali N, Heyman I. Structure of obsessive-compulsive symptoms in pediatric OCD. J Am Acad Child Adolesc Psychiatry. 2008;47(7):773–778. doi:. doi:10.1097/CHI.0b013e31816b73c0 [CrossRef]
- Watson HJ, Rees CS. Meta-analysis of randomized, controlled treatment trials for pediatric obsessive-compulsive disorder. J Child Psychol Psychiatr. 2008;49(5):489–498. doi:. doi:10.1111/j.1469-7610.2007.01875.x [CrossRef]
- Wu Y, Lang Z, Zhang H. Efficacy of cognitive-behavioral therapy in pediatric obsessive-compulsive disorder: a meta-analysis. Med Sci Monit. 2016;22:1646–1653. doi:. doi:10.12659/MSM.895481 [CrossRef]
- McKay D, Sookman D, Neziroglu F, et al. Efficacy of cognitive-behavioral therapy for obsessive-compulsive disorder. Psychiatry Res. 2015;227(1):104–113. doi:. doi:10.1016/j.psychres.2015.02.004 [CrossRef]
- Freeman J, Sapyta J, Garcia A, et al. Family-based treatment of early childhood obsessive-compulsive disorder: the Pediatric Obsessive-Compulsive Disorder Treatment Study for Young Children (POTS Jr)—a randomized clinical trial. JAMA Psychiatry. 2014;71(6):689–698. doi:. doi:10.1001/jamapsychiatry.2014.170 [CrossRef]
- Geller DA, Biederman J, Stewart SE, et al. Which SSRI? A meta-analysis of pharmacotherapy trials in pediatric obsessive-compulsive disorder. Am J Psychiatry. 2003;160(11):1919–1928. doi:. doi:10.1176/appi.ajp.160.11.1919 [CrossRef]
- Grados MA, Torrico H, Frederick J, Riley T. Pediatric obsessive-compulsive disorder: a psychopharmacology update. Child Adolesc Psychopharmacol News. 2016;21(1):1–6. doi:10.1521/capn.2016.21.1.1 [CrossRef]
- Zohar J. Escitalopram in the treatment of obsessive-compulsive disorder. Expert Rev Neurother. 2008;8(3):339–349. doi:. doi:10.1586/1473718.104.22.1689 [CrossRef]
- Varigonda AL, Jakubovski E, Bloch MH. Systematic review and meta-analysis: early treatment responses of selective serotonin reuptake inhibitors and clomipramine in pediatric obsessive-compulsive disorder. J Am Acad Adolesc Psychiatry. 2016;5(10):851–859.e852. doi:. doi:10.1016/j.jaac.2016.07.768 [CrossRef]
- Franklin ME, Sapyta J, Freeman JB, et al. Cognitive behavior therapy augmentation of pharmacotherapy in pediatric obsessive-compulsive disorder: the Pediatric OCD Treatment Study II (POTS II) randomized controlled trial. JAMA. 2011;306(11):1224–1232. doi:. doi:10.1001/jama.2011.1344 [CrossRef]
- Storch EA, Bussing R, Small BJ, et al. Randomized, placebo-controlled trial of cognitive-behavioral therapy alone or combined with sertraline in the treatment of pediatric obsessive-compulsive disorder. Behav Res Ther. 2013;51(12):823–829. doi:. doi:10.1016/j.brat.2013.09.007 [CrossRef]
- Grant PJ, Joseph LA, Farmer CA, et al. A 12-week, placebo-controlled trial of add-on riluzole in the treatment of childhood-onset obsessive-compulsive disorder. Neuropsychopharmacology. 2014;39(6):1453–1459. doi:. doi:10.1038/npp.2013.343 [CrossRef]
- Farrell LJ, Waters AM, Boschen MJ, et al. Difficult-to-treat pediatric obsessive-compulsive disorder: feasibility and preliminary results of a randomized pilot trial of D-cycloserine-augmented behavior therapy. Depress Anxiety. 2013;30(8):723–731. doi:. doi:10.1002/da.22132 [CrossRef]
Summary of DSM-5 Criteria for Obsessive-Compulsive Disordera
Compulsionsa are defined by (1) or (2)
Presence of obsessions, compulsions, or both
Obsessions are defined by (1) or (2)
Recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance, as intrusive and unwarranted, and that in most people cause marked anxiety or distress
The person attempts to ignore or suppress such thoughts, urges, or images, or to neutralize them with some other thought or action
Repetitive behaviors in which the person feels driven to perform in response to an obsession or according to the rules that must be applied rigidly
The behaviors are aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation; however, these behaviors are not connected in a realistic way with what they are designed to neutralize or prevent, or are clearly excessive
The obsessions or compulsions are time-consuming or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning
The obsessive-compulsive symptoms are not attributable to the physiological effects of a substance
The disturbance is not better explained by the symptoms of another mental disorder
General Evaluation Points for Pediatric Obsessive-Compulsive Disorder
Conduct a detailed clinical interview, including some time with the child/adolescent alone
Obtain detailed information about the obsession/compulsion presentation, and screen for other forms of obsessions and compulsions
Ask for triggers including streptococcal infections
Be aware of developmental variations of symptomatology when assessing children younger than age 6 years
Documentation of the level of symptoms and associated impairment is essential for diagnosis and monitoring of treatment response using CY-BOCS
Specifically inquire about avoidance behaviors as they are not included in CY-BOCS, which may result in underestimating the severity
Assess for the presence of psychiatric comorbidities especially because the presence of comorbidities may impact the treatment response, including tic disorders, anxiety disorders, and ADHD
Obtain a full medical, developmental, family, and educational history
Considerusing formal assessment tools for pediatric obsessive-compulsive disorder when available such as
Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present & Lifetime version
National Institute of Mental Health Diagnostic Interview Schedule for Children