现在已有学者认为，帕金森病患者的异常运动很有可能是因为脑组织活动模式的改变。研究发现，正常猴的基底节中有10%的苍白球神经元表现出3~19 Hz微弱的周期性震荡活动，而且苍白球神经元之间的活动是无相关性的。在帕金森病猴模型中，苍白球神经元的震荡活动加强，有41%的苍白球神经元表现出低频的震荡活动，震荡活动的频率主要分布在7 Hz和13 Hz，而且神经元之间的震荡活动呈现出明显的同步化[13]，其他的学者也得出了一些类似的结论。由此可见，帕金森病的运动障碍很有可能是由基底节神经元这些放电模式的改变所引起的。而STN-HFS改变帕金森病运动障碍的机制很有可能就是抑制了这种异常的神经放电模式。近几年国外有学者报道，电刺激丘脑底核神经元同步化活动在20 Hz左右的区域会使GPi 20 Hz左右的神经元同步化活动加剧。而在电刺激丘脑底核同步化活动>70 Hz的区域，信捷职称论文写作发表网，可以抑制内侧苍白球20 Hz左右的神经元同步化活动。STN-HFS和多巴胺能的药物治疗就是使丘脑底核产生一个大于70 Hz的神经元同步化活动来抑制基底节的输出结构GPi的低频同步化活动，从而改善帕金森病的运动症状[14]。
　　综上所述，目前已有的研究主要将STN-HFS的作用机制分为抑制效应与兴奋效应，这个问题不能分开来看，它只是一个问题的两个方面，应该把所有这些试验结果综合起来进行分析。STN-HFS对各种运动障碍症状都有很好的疗效，阐明其作用机制可以更好地了解帕金森病的发病机制，为寻找更好的靶目标及研究新的治疗方法提供理论依据。
　　
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