ASYMBOLIA FOR PAIN - A SENSORY-LIMBIC DISCONNECTION SYNDROME
ASYMBOLIA FOR PAIN - A SENSORY-LIMBIC DISCONNECTION SYNDROME
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DOI：
10.1002/ana.410240109
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发表时间：
1988-07-01
影响因子：
11.2
通讯作者：
LEIGUARDA, R
中科院分区：
文献类型：
--
作者：
BERTHIER, M;STARKSTEIN, S;LEIGUARDA, R
我们描述了行为和神经解剖学特征的疼痛发生在6例患者后，单侧半球损伤继发于缺血性病变5和外伤性血肿1。在没有初级感觉障碍的情况下，这6名患者表现出缺乏退缩，对施加在整个身体上的疼痛刺激以及威胁性手势缺乏或不充分的情绪反应。五名患者也未能对口头威胁作出反应。患者似乎对缺陷并不关心，似乎无法学习适当的逃避或保护性反应。常见的相关异常是快速缓解性轻偏瘫、皮质型感觉丧失、单侧忽视和身体图式障碍。神经放射学检查显示4例患者左侧大脑半球病变，2例患者右侧大脑半球受累。虽然病变范围不同，但6例患者的岛叶皮质均受损。这些发现表明，岛叶损伤可能通过中断感觉皮层和边缘系统之间的连接在综合征的发展中发挥关键作用。
We describe the behavioral and neuroanatomical features of asymbolia for pain occurring in 6 patients following unilateral hemispheric damage secondary to ischemic lesions in 5 and traumatic hematoma in 1. In the absence of primary sensory deficits, these 6 patients showed a lack of withdrawal and absent or inadequate emotional responses to painful stimuli applied over the entire body, as well as to threatening gestures. Five patients also failed to react to verbal menaces. Patients appeared unconcerned about the defect and seemed unable to learn appropriate escape or protective responses. Common associated abormalities were rapidly resolving hemiparesis, cortical-type sensory loss, unilateral neglect, and body-schema disorders. Neuroradiological examination disclosed left hemispheric lesions in 4 patients and right hemispheric involvement in 2. Although lesion extension differed, the insular cortex was invariably damaged in all 6 patients. These findings suggest that insular damage may play a critical role in the development of the syndrome by interrupting connections between sensory cortices and the limbic system.