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丘脑豆状核缺血导致的感觉运动性卒中

Sensorimotor stroke due to thalamocapsular ischemia.

作者信息

Mohr J P, Kase C S, Meckler R J, Fisher C M

出版信息

Arch Neurol. 1977 Dec;34(12):739-41. doi: 10.1001/archneur.1977.00500240027004.

Abstract

A 61-year-old hypertensive diabetic man awoke with a numb, heavy right arm and leg; symptoms progressed within 30 hours to a dense right hemisensory syndrome involving head, face, trunk, arm, and leg, accompanied by a right hemiparesis, involving tongue, face, arm, and leg with extensor plantar response, leaving him barely able to move the arm and leg against gravity. No impairment in alertness, memory, language, praxic, or visual functions was evident at any time. Improvement in motor function began in 24 hours and progressed to walking status by discharge on day 23. Eight days passed before the sensory deficit showed improvement, and it was still prominent at discharge. Autopsy three months later showed a 4 X 2 X 4-mm lacune in the ventral posterior nucleus of the left thalamus, with a zone of pallor on stained microscopic sections extending into the immediately adjacent posterior limb of the internal capsule. This case appears to be unique in that a sensorimotor stroke has been produced by a confirmed thalamocapsular infarct.

摘要

一名61岁的高血压糖尿病男性醒来时感到右侧手臂和腿部麻木、沉重;症状在30小时内进展为累及头部、面部、躯干、手臂和腿部的严重右侧半身感觉综合征,伴有右侧偏瘫,累及舌头、面部、手臂和腿部,伴有跖伸反应,导致他几乎无法克服重力移动手臂和腿部。在任何时候,警觉性、记忆力、语言、运动能力或视觉功能均未出现损害。运动功能在24小时内开始改善,并在第23天出院时进展到可步行状态。感觉缺陷在8天后才开始改善,出院时仍然很明显。3个月后的尸检显示左丘脑腹后核有一个4×2×4毫米的腔隙,染色显微镜切片上的苍白区延伸至紧邻的内囊后肢。该病例似乎很独特,因为已证实的丘脑-内囊梗死导致了感觉运动性中风。

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