Neurocognitive deficits in obsessive–compulsive disorder: A selective review

Obsessive–compulsive disorder (OCD) is a debilitating mental illness characterized by an early onset and chronic course. Evidence from several lines of research suggests significant neuropsychological deficits in patients with OCD; executive dysfunction and nonverbal memory deficits have been reported consistently in OCD. These deficits persist despite controlling potential confounders such as comorbidity, severity of illness, and medications. Neuropsychological impairments are independent of illness severity, thus suggesting that the neuropsychological deficits are trait markers of the disease. In addition, these deficits are seen in first-degree relatives of individuals with OCD. These reports suggest that neuropsychological deficits are potential endophenotype markers in OCD. Neuropsychological studies in pediatric OCD are limited; they show impairments of small effect size across multiple domains but with doubtful clinical significance. Preliminary evidence shows that different symptom dimensions of OCD may have unique neuropsychological deficits suggestive of discrete but overlapping neuroanatomical regions for individual symptom dimensions. Overall, neuropsychological deficits further support the role of frontostriatal circuits in the neurobiology of OCD. In addition, emerging literature also suggests the important role of other areas, in particular parietal cortex. Preliminary evidence suggests the possible role of neuropsychological deficits to be markers of treatment response but needs to be examined in future. Longitudinal studies with examination of patients at different time points and examination of their potential utility as predictors of treatment response are needed in future.