Letters to the Editor Letters to the Editor will be published, if suitable, as space permits. They should not exceed 1,000 words (typed double-spaced) in length, and may be subject to editing or abridgement. Ataxic Hemiparesis — Ventrolateral Nucleus of t

To the Editor: Thalamic vascular lesions usually produce objective sensory distur-bances and sometimes may be associated with aphasia, amnesia, and neglect. Rarely ataxia and choreoathetotic movements can be seen.121 describe a patient with ataxic hemiparesis in whom computed tomog-raphy (CT scan) showed an isolated hypodense area in the thalamus compatible with lacunar infarct. A 60-year-old man, a known hypertensive, suddenly experienced clumsiness of his left arm and leg associated with weakness and heavi-ness. He was conscious and well-oriented without any memory or other higher function abnormalities; there was minimal left-sided weakness. Tendon reflexes were hyperactive on that side with upgoing plantar. He had difficulty in accomplishing finger-nose and heel-shin tests on the left side with dysdiadochokinesia and intention tremor. Touch and pain sensations were mildly impaired. CT scan showed a small hypodense lesion in the thalamus on the right side (Figure 1). His pyramidal weakness and sensory disturbances improved within 5 days, his ataxia in 10 days. Garcin3 and Garcin and Lapresele4 described two cases with unilater-al cerebellar ataxia in whom infarction of the contralateral thalamus was demonstrated at autopsy. One patient had associated numbness and paresis of the lower limb.4 Cases of thalamic lesion presenting as pain-ful ataxic hemiparesis5 and hypesthetic ataxic hemiparesis6 have been documented. Ataxia is due to the involvement of the dentatorubro tha-lamic fibers in the ventrolateral nucleus of the thalamus. Hemiparesis is due to extension of the lesion to the adjacent internal capsule