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偏瘫失认症的发病机制。

The pathogenesis of anosognosia for hemiplegia.

作者信息

Levine D N, Calvanio R, Rinn W E

机构信息

Neurology Services, Spaulding Rehabilitation Hospital, Boston, MA.

出版信息

Neurology. 1991 Nov;41(11):1770-81. doi: 10.1212/wnl.41.11.1770.

Abstract

We compared patients with unawareness of hemiplegia lasting more than 1 month after right hemisphere stroke with other patients with right hemisphere stroke who became aware of hemiplegia within a few days after onset. Patients with persistent unawareness invariably had severe left hemisensory loss and usually had severe left spatial neglect. They were almost always apathetic; their thought lacked direction, clarity, and flexibility, and they had at least moderate impairment of intellect and memory. Their right hemisphere strokes were large and always affected the central gyri or their thalamic connections and capsular pathways. In addition, there was evidence of at least mild left hemisphere damage, most commonly caused by age-associated atrophy. The pathogenesis of anosognosia for hemiplegia may involve failure to discover paralysis because proprioceptive mechanisms that ordinarily inform an individual about the position and movement of limbs are damaged, and the patient, because of additional cognitive defects, lacks the capacity to make the necessary observations and inferences to diagnose the paralysis. We discuss the implications of this "discovery" theory and contrast it with other explanations of anosognosia.

摘要

我们将右侧半球卒中后偏瘫失认持续超过1个月的患者与其他右侧半球卒中且在发病后几天内就意识到偏瘫的患者进行了比较。持续性失认的患者总是伴有严重的左侧感觉丧失,通常还伴有严重的左侧空间忽视。他们几乎总是表现出冷漠;其思维缺乏方向、清晰度和灵活性,并且至少有中度的智力和记忆力损害。他们的右侧半球卒中范围较大,总是累及中央回或其丘脑连接以及内囊通路。此外,有证据表明至少存在轻度的左侧半球损伤,最常见的原因是与年龄相关的萎缩。偏瘫失认症的发病机制可能涉及因本体感觉机制受损而未能发现瘫痪,而本体感觉机制通常会告知个体肢体的位置和运动情况,并且患者由于其他认知缺陷,缺乏进行必要观察和推理以诊断瘫痪的能力。我们讨论了这种“发现”理论的意义,并将其与失认症的其他解释进行了对比。

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