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Altered cortical excitability in obsessive–compulsive disorder

From the Adult OCD Research Unit, Laboratory of Clinical Science, National Institute of Mental Health, and the National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.

Address correspondence and reprint requests to Dr. Benjamin D. Greenberg, Adult OCD Research Unit, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1264, Bethesda, MD 20892-1264, or to Dr. Eric M. Wassermann, 10 Center Drive, MSC 1428, Bethesda, MD 20892-1428.

OBJECTIVE: To assess cortical inhibitory and excitatory mechanisms in obsessive–compulsive disorder (OCD).

BACKGROUND: Transcranial magnetic stimulation (TMS) studies have found decreased neuronal inhibition and a reduced cortical silent period in the primary motor area in Tourette’s syndrome, focal dystonia, and other disorders believed to involve dysfunction of subcortical structures, including the basal ganglia. Dysfunction of the basal ganglia and linked regions also has been implicated in OCD, which has significant clinical and familial overlap with tic disorders.

METHODS: We applied the TMS techniques previously used in Tourette’s syndrome to a group of 16 OCD patients (seven unmedicated) and 11 age-matched healthy volunteers extensively screened for psychopathology. Measures of motor cortex excitability included resting and active motor threshold, cortical silent period duration, and intracortical inhibition and facilitation using a paired-pulse TMS technique with a subthreshold conditioning stimulus.

RESULTS: Similar to recent findings in Tourette’s syndrome and focal dystonia, this study reports significantly decreased intracortical inhibition (ICI) relative to the volunteers at interstimulus intervals from 2 to 5 msec. We also found decreased active and resting motor evoked potential threshold in the OCD patients, another indication of increased cortical excitability. Neither abnormality appeared medication related. The decreases in ICI and motor threshold were greatest in OCD patients with comorbid tics, but remained significant in patients without tics.

CONCLUSIONS: The data suggest abnormal cortical excitability in obsessive–compulsive disorder. These findings are congruent with the hypothesis that Tourette’s syndrome and obsessive–compulsive disorder (OCD) are analogous disorders with overlapping dysfunction in corticobasal circuits. Patients with tic-related OCD may have more abnormal motor cortex excitability than OCD patients without tics.

Key words: Obsessive–compulsive disorder—Transcranial magnetic stimulation—Intracortical inhibition—Basal ganglia

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