THE THALAMIC ATAXIA SYNDROME

We identified 10 patients with contralateral ataxia and hemisensory lo ss following unilateral thalamic lesions. Seven patients had ischemic infarcts, and three had hemorrhages. Hemiparesis, when present, was on ly a transient finding, whereas ataxia, dysmetria, dysdiadochokinesia, rebound, and hemisensory loss persisted. Two patients had cerebellar outflow tremor. Another developed a severe Dejerine-Roussy pain syndro me. Four patients had lesions of the dominant hemisphere, and two had visual field deficits. None had mutism, aphasia, or astasia. On radiog raphic evaluation, all patients had lesions in the mid to posterior th alamus, a localization consistent with a lesion of the dentatorubrotha lamic and ascending sensory pathways into the thalamus. The thalamic a taxia syndrome has a distinct localizing value that is distinguishable from the ataxic hemiparesis syndrome. Strokes occurring in the ventra l lateral and posterior nuclei of the thalamus produce the clinical pi cture of contralateral ''cerebellar'' dysfunction and sensory loss wit h only transient weakness.