Transcallosal inhibition in cortical and subcortical cerebral vascular lesions
Transcallosal inhibition in cortical and subcortical cerebral vascular lesions
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DOI：
10.1016/s0022-510x(96)00222-5
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发表时间：
1996-12-01
影响因子：
4.4
通讯作者：
Ferbert, A
中科院分区：
文献类型：
--
作者：
Boroojerdi, B;Diefenbach, K;Ferbert, A
对10例单纯皮层下脑血管病和22例皮层-皮层下脑血管病患者经颅磁刺激后运动皮层的兴奋性进行了研究。在第一次调查中，我们应用磁双刺激在两个运动皮层不同的刺激间隔。第一个（条件反射）刺激施加到受影响的半球和第二个刺激（测试刺激）的未受影响的一侧。第一背侧骨间（FDI）肌肉，对侧的测试刺激，单独应用测试刺激后，并在5毫秒，7毫秒，15毫秒，30毫秒和60毫秒的刺激间隔记录的反应。在第二次调查中，患者被要求激活他们的非麻痹的第一背侧骨间肌肉和磁刺激施加在受影响的半球。对EMG反应进行校正和平均。半卵圆中心以下皮质下大脑病变的患者（即，对经胼胝体纤维没有影响）在刺激对侧后显示出对一个运动皮层的明显抑制，与正常受试者相当。皮质-皮质下脑损伤患者的运动皮质抑制仅部分减少，但该组的结果并不一致。由于抑制保留在皮质下病变，这破坏了皮质脊髓束的患者，我们得出结论，这种抑制是不通过同侧的投影介导，但通过经胼胝体的路线。
The excitability of the motor cortex after transcranial magnetic stimulation was investigated in 10 patients with purely subcortical, and in 22 patients with cortical-subcortical cerebrovascular lesions. In the first investigation we applied magnetic double stimuli over both motor cortices with different inter-stimulus intervals. The first (conditioning) stimulus was applied to the affected hemisphere and the second stimulus (test stimulus) to the unaffected side. The responses of the first dorsal interosseal (FDI) muscle, contralateral to the lest stimulus, were recorded after applying the test stimulus alone and at inter-stimulus intervals of 5 ms, 7 ms, 15 ms, 30 ms and 60 ms. In a second investigation the patients were asked to activate their non-paretic first dorsal interosseus muscle and the magnetic stimulus was applied over the affected hemisphere. The EMG responses were rectified and averaged. Patients with subcortical cerebral lesions below the centrum semiovale (i.e., having no effect on the transcallosal fibres) displayed a pronounced inhibition of one motor cortex after the stimulation of the contralateral side, comparable with normal subjects. Patients with cortical-subcortical cerebral lesions displayed only partly less inhibition of their motor cortex but the results in this group were not uniform. Since inhibition was preserved in patients with subcortical lesions, which had destroyed the corticospinal tract, we conclude that this inhibition is not mediated through an ipsilateral projection but via a transcallosal route.