Aberrant cortical functionality and somatosensory deficits after stroke.

Aberrant cortical functionality and somatosensory deficits after stroke.
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中风后皮质功能异常和体感缺陷。

DOI:
10.1097/wnp.0b013e318176c0d4
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发表时间:
2008
期刊:
Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society
影响因子:
--
通讯作者:
Papanicolaou,AndrewC
Papanicolaou,AndrewC
中科院分区:
--
文献类型:
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作者:
Castillo,EduardoM;Boake,Corwin;Breier,JoshuaI;Men,Disheng;Garza,HectorM;Passaro,Anthony;Papanicolaou,AndrewC

文献摘要

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中风后初级躯体感觉皮层(SI)的损伤和/或连接中断会导致触觉障碍。我们使用脑磁图来测试躯体感觉皮质的特定功能模式是否与急性后不同程度的躯体感觉障碍有关。对19例急性单侧卒中后不同程度躯体感觉障碍的患者(6例不存在,6例中度,7例重度)和8例年龄匹配的对照组进行了高分辨率MRI和全头脑磁图的体感诱发电场和自发慢振荡活动的记录。比较四组受试者患侧和非患侧触觉刺激后SI的激活幅度和中央后区的增量偶极子密度(DDD)。所有病例均伴有严重的急性后躯体感觉障碍,患手对刺激缺乏SI反应,中央后DDD向患侧明显不对称。中度感觉丧失患者的中枢性DDD不对称(4例偏向患侧,2例偏向健侧),但SI激活无异常波幅。没有躯体感觉缺陷的中风患者的SI波幅或中枢后DDD的记录与对照组没有差异。在卒中患者中,SI反应幅度与中枢后DDD呈负相关。刺激患手后SI皮层缺乏激活和中枢后区自发慢振荡活动是卒中后急性期躯体感觉障碍的神经生理学相关因素。
Damage and/or disconnection of the primary somatosensory cortex (SI) after stroke leads to deficits in touch perception. We used magnetoencephalography to test whether specific patterns of functionality of the somatosensory cortex are associated with different degrees of postacute somatosensory deficit. Nineteen postacute unilateral stroke patients suffering different degrees of somatosensory deficit (six inexistent, six moderate, and seven severe) and eight aged-matched controls underwent high-resolution MRI and whole-head magnetoencephalography recordings of somatosensory-evoked fields and of spontaneous slow oscillatory activity. Amplitude of SI activation after tactile stimulation in the affected and nonaffected hemispheres and delta dipole density (DDD) in the postcentral areas were estimated and compared across the four groups. Severe postacute somatosensory deficit was accompanied, in all cases, with absence of SI responses to stimulation in the affected hand and a significant asymmetry in postcentral DDD toward the affected hemisphere. Patients with moderate sensory loss showed asymmetry in their postcentral DDD (four cases toward the affected hemisphere and two toward the unaffected) but no atypical amplitudes in SI activation. Recordings in stroke patients without somatosensory deficit did not differ from those obtained in controls for SI amplitude or postcentral DDD. In stroke patients, amplitude of SI responses and postcentral DDD show a negative correlation. Lack of activation of SI cortex after stimulation of the affected hand and spontaneous slow oscillatory activity in postcentral areas are neurophysiological correlates of somatosensory deficit in the postacute phase of stroke.