OBJECTIVE: To examine the relative impact of depression on executive function deficits in obsessive-compulsive disorder (OCD). BACKGROUND: Existing data suggest that OCD is associated with basal ganglia and orbital frontal dysfunction, and neurobehavioral abnormalities that are putatively associated with these regions have been demonstrated in OCD. Nonetheless, few studies have accounted for the effects of depression, which is a common concurrent symptom among those with OCD. METHOD: A broad battery of neuropsychological tests, including measures of executive function and sensory-motor function, was administered to 20 adults with OCD and 31 control subjects. To assess depressive severity, participants were administered the depression scale from the Minnesota Multiphasic Personality Inventory. RESULTS: Data were analyzed using a regression model in two steps. In step one, patient group was entered, and patients with OCD demonstrated a pattern of executive function and sensory-motor deficits, similar to those shown in previous research. In step two, self-reported depressive symptom severity was entered as a predictor. As a consequence, depression accounted for some executive function deficits, whereas presence of OCD only predicted performance on measures of sensory-motor function. CONCLUSIONS: These data suggest that abnormalities involving executive function in OCD are related to co-morbid depressive severity. However, sensory-motor deficits seem to be more consistent with basal ganglia/orbital frontal dysfunction in OCD.
OBJECTIVE: To examine the relative impact of depression on executive function deficits in obsessive-compulsive disorder (OCD). BACKGROUND: Existing data suggest that OCD is associated with basal ganglia and orbital frontal dysfunction, and neurobehavioral abnormalities that are putatively associated with these regions have been demonstrated in OCD. Nonetheless, few studies have accounted for the effects of depression, which is a common concurrent symptom among those with OCD. METHOD: A broad battery of neuropsychological tests, including measures of executive function and sensory-motor function, was administered to 20 adults with OCD and 31 control subjects. To assess depressive severity, participants were administered the depression scale from the Minnesota Multiphasic Personality Inventory. RESULTS: Data were analyzed using a regression model in two steps. In step one, patient group was entered, and patients with OCD demonstrated a pattern of executive function and sensory-motor deficits, similar to those shown in previous research. In step two, self-reported depressive symptom severity was entered as a predictor. As a consequence, depression accounted for some executive function deficits, whereas presence of OCD only predicted performance on measures of sensory-motor function. CONCLUSIONS: These data suggest that abnormalities involving executive function in OCD are related to co-morbid depressive severity. However, sensory-motor deficits seem to be more consistent with basal ganglia/orbital frontal dysfunction in OCD.