S. Lehericy et al., STRIATOPALLIDAL AND THALAMIC DYSTONIA - A MAGNETIC-RESONANCE-IMAGING ANATOMOCLINICAL STUDY, Archives of neurology, 53(3), 1996, pp. 241-250
Objective: To determine which brain structures are involved in symptom
atic unilateral dystonia caused by localized cerebral infarction. Desi
gn: Three-dimensional T-1-weighted magnetic resonance imaging sequence
and stereotactic analysis were used to analyze the topography of the
lesions. Stereotactic localization of thalamic lesions was conducted a
ccording to the atlas of Hassler with a Voxtool software (Advantage Wi
ndows Workstation, General Electric, Milwaukee, Wis) workstation syste
m. Patients: Eight patients with hemidystonia, segmental dystonia, or
focal dystonia were selected from among 51 consecutive patients (betwe
en January 1988 and May 1993) with symptomatic unilateral dystonia. Re
sults: Patients had dystonic spasms (n=4) or myoclonic dystonia (n=4).
Lesions associated with dystonic spasms were located in the striatopa
llidal 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 pati
ents and extended variably into the dorsolateral part of the caudate n
ucleus, the posterior limb of the internal capsule, or the lateral seg
ment of the globus pallidus. These lesions were centered in the ''sens
orimotor'' part of the striatopallidal complex, with a trend toward a
somatotopical distribution. Lesions of the thalamus were located in th
e ventral intermediate and ventral caudal nuclei, while the ventral or
al anterior and posterior nuclei (which receive pallidal efferents) we
re largely spared. Conclusion: These results suggest that striatopalli
dal and thalamic dystonia may have different pathophysiologic bases.