Gille M, Van den Bergh P, Ghariani S, Guettat L, Delbecq J, Depre A
Service de Neurologie, Clinique Ste-Elisabeth, Bruxelles.
Acta Neurol Belg. 1996 Dec;96(4):307-11.
A 68 year-old man developed progressive hemidystonia and chorea 8 months after a contralateral thalamic stroke. The neurological examination also showed a right pyramidal syndrome without hemiparesis, a right horizontal sectoranopia, and a right hemihypesthesia for all sensory modalities. The MRI revealed infarctions in the left medial temporo-occipital lobes and left posterolateral thalamus, corresponding to the vascular territories of both the thalamo-geniculate and posterolateral choroidal arterial pedicles. The thalamic lesion involved the pulvinar, the lateral geniculate body, and the ventro-postero-lateral, dorso-lateral, posterolateral, and dorso-medial nuclei, but apparently did not extent to the ventrolateral thalamic nucleus, and the subthalamic and midbrain regions. Thalamic and striatopallidal dystonia have not a common pathophysiological mechanism. The involvement of the pulvinar nucleus and of the strategic crossing of proprioceptive, cerebellar, pyramidal, and subthalamic pathways may play a role in the genesis of the posterolateral thalamic dystonia.
一名68岁男性在对侧丘脑中风8个月后出现进行性偏侧肌张力障碍和舞蹈症。神经系统检查还显示右侧锥体束征但无偏瘫、右侧水平扇形视野缺损以及对所有感觉模态的右侧偏身感觉减退。MRI显示左侧颞枕内侧叶和左侧丘脑后外侧梗死,对应丘脑膝状体动脉和脉络膜后外侧动脉蒂的血管区域。丘脑病变累及丘脑枕、外侧膝状体以及腹后外侧核、背外侧核、后外侧核和背内侧核,但显然未累及丘脑腹外侧核以及底丘脑和中脑区域。丘脑性和纹状体苍白球性肌张力障碍没有共同的病理生理机制。丘脑枕核的受累以及本体感觉、小脑、锥体束和底丘脑通路的关键交叉可能在丘脑后外侧肌张力障碍的发生中起作用。