Striatopallidal and thalamic dystonia. A magnetic resonance imaging anatomoclinical study

S. Lehericy, M. Vidailhet, D. Dormont, L. Pierot, J. Chiras, P. Mazetti, C. Marsault and Y. Agid
INSERM U289, Hopital de la Pitie-Salpetriere, Paris, France.

OBJECTIVE: To determine which brain structures are involved in symptomatic unilateral dystonia caused by localized cerebral infarction. DESIGN: Three-dimensional T1-weighted magnetic resonance imaging sequence and stereotactic analysis were used to analyze the topography of the lesions. Stereotactic localization of thalamic lesions was conducted according to the atlas of Hassler with a Voxtool software (Advantage Windows Workstation, General Electric, Milwaukee, Wis) workstation system. PATIENTS: Eight patients with hemidystonia, segmental dystonia, or focal dystonia were selected from among 51 consecutive patients (between January 1988 and May 1993) with symptomatic unilateral dystonia. RESULTS: Patients had dystonic spasms (n=4) or myoclonic dystonia (n=4). Lesions associated with dystonic spasms were located in the striatopallidal complex, and those with myoclonic dystonia were in the thalamus contralateral to the dystonia. Lesions of the striatopallidal complex involved the putamen posterior to the anterior commissure in all patients and extended variably into the dorsolateral part of the caudate nucleus, the posterior limb of the internal capsule, or the lateral segment of the globus pallidus. These lesions were centered in the "sensorimotor" part of the striatopallidal complex, with a trend toward a somatotopical distribution. Lesions of the thalamus were located in the ventral intermediate and ventral caudal nuclei, while the ventral oral anterior and posterior nuclei (which receive pallidal efferents) were largely spared. CONCLUSIONS: These results suggest that striatopallidal and thalamic dystonia may have different pathophysiologic bases.