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Obsessive-compulsive disorder associated with brain lesions

Clinical phenomenology, cognitive function, and anatomic correlates

From the Neurology Service (Drs. Berthier and Heras), Virgen de la Victoria University Hospital, Malaga; and the Department of Neurology (Drs. Kulisevsky and Gironell), Sant Pau Hospital, University of Barcelona, Barcelona, Spain.
Presented in part at the 46th annual meeting of the American Academy of Neurology, Washington, DC, May 1994.
Received October 12, 1995. Accepted in final form January 19, 1996.
Address correspondence and reprint requests to Dr. Marcelo L. Berthier, Servicio de Neurologia, Hospital Universitario Virgen de la Victoria, Campus Universitario Teatinos-Apartado 3091 (29010), Malaga, Espana.

We studied the behavioral, cognitive, and neuroimaging characteristics of obsessive-compulsive disorder (OCD) in 13 patients with focal brain lesions (acquired OCD) and compared their clinical features and the severity of obsessive and compulsive (OC) symptoms with patients with idiopathic OCD. Both OCD groups were further compared with matched normal controls on a series of neuropsychological tests. Patients with acquired OCD had a negative familial history and later age at onset of OCD symptoms than patients with idiopathic OCD. The two OCD groups showed relatively similar clinical phenomenology, severity of OC symptoms, and profile of neuropsychological deficits. Compared with normal control subjects, both OCD groups showed cognitive deficits affecting attention, intellectual function, memory, word retrieval, and motor and executive functions. Eight of the 13 patients with acquired OCD had abnormal neurologic examinations, whereas only 3 of the 13 patients with idiopathic OCD had abnormal neurologic examinations. Neuroimaging in the acquired OCD group disclosed a variety of lesions involving exclusively the cerebral cortex (frontal, temporal, or cingulate regions), the basal ganglia, or both. These results suggest that acquired and idiopathic OCDs may share a common pathophysiologic mechanism, and that structural damage to specific frontal-limbic-subcortical circuits plays an important role in the pathogenesis of acquired OCD.

NEUROLOGY 1996;47: 353-361

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