Elsevier

Comprehensive Psychiatry

Volume 41, Issue 5, September 2000, Pages 373-379
Comprehensive Psychiatry

Phenotypic differences in early- and late-onset obsessive-compulsive disorder

https://doi.org/10.1053/comp.2000.9009Get rights and content

Abstract

Early-onset forms of many medical diseases have been associated with specific genetic anomalies. To assess the potential marker value of onset age in obsessive-compulsive disorder (OCD), we examined and compared the phenotypic characteristics of patients with early and later onset. The study sample included 38 children with DSM-IV OCD and 129 adults 19 years of age or older, 77 of whom reported OCD onset prior to age 18 and 52 of whom reported OCD onset at 18 years of age or older. DSM-IV diagnoses were ascertained for all subjects using an amended version of the Diagnostic Interview for Genetic Studies (DIGS). An initial comparison of children and adults with childhood onset revealed several differences, including an earlier onset of clinically significant symptoms without impairment and earlier onset of DSM-IV OCD, a higher frequency of learning disabilities, and fewer obsessions and compulsions among our child patients. For this reason, subsequent analyses included only adult patients with early and later OCD onset. Nonimpairing symptom onset prior to puberty, a relatively aggressive course, and a greater number of obsessions and compulsions unrelated to the amount of time in illness characterized early-onset OCD. Later-onset OCD was characterized by non-impairing symptom onset during puberty, a static course, and relatively few obsessions and compulsions that were variably related to the amount of time in illness. We conclude that children with OCD and adults with childhood onset differ in their report of clinical characteristics and should be analyzed separately in studies concerning the phenotypic characteristics of OCD. Early- and late-onset forms of OCD appear to be characterized by phenotypic features that have important neurobiologic and perhaps genetic implications.

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Supported by The Rockefeller University and The G. and F. Armour Foundation, and in part by a Lucille P. Markey Clinical Scholarship (C.S.) and an Irma T. Hirschl Career Scientist Award (M.K.). Clinical work at the Rockefeller University Hospital was supported by Grant No. MO1RRO102

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