STUDIES OF THE PATHOPHYSIOLOGY OF HEMIFACIAL SPASM

经典型的面肌痉挛(HFS)在大多数情况下都是 由入口处附近的面神经交叉压迫引起的 通过血管到达脑干，但它的病理生理学 很大程度上是未知的。关于HFS的原因存在两种假设： 1)面神经纤维之间是触觉传递。 导致痉挛和联动的压迫部位，以及2) 面部运动神经核参与了这些信号的产生。 我们早些时候已经展示了来自 微血管手术患者的术中记录 HFS的解压缩(MVD)操作。我们发现有证据表明 结构的改变是损伤的中心(可能 面部神经核)，而不是对神经本身的损伤 会引起HFS的症状。我们还找到了证据 少数神经之间的触觉传递 损伤部位的面神经纤维可能出现在 在极少数情况下和在短时间内面部 神经正在接受手术操作，但似乎不太可能 这种触觉传递可以产生巨大的肌肉 宫缩是HFS的特征。 在拟议的研究中，我们希望延长术中 电生理记录，以确定位置 导致痉挛的生理异常和 肌肉反应异常。将进行动物实验 目的是在实验动物身上复制HFS。 动物实验的基本原理是这样一个模型 将使我们能够直接研究面部运动的参与 原子核。可以假设，其他组织的病理生理学 由轻微损伤的神经引起的疾病，如各种疼痛 疾病，类似于HFS，我们相信患者 HFS为其他神经疾病提供了一个有价值的模型 这是由轻微损伤的神经引起的。

Classical hemifacial spasm (HFS) is in the majority of cases caused by cross-compression of the facial nerve near its entrance to the brainstem by a blood vessel, but its pathophysiology is largely unknown. Two hypotheses exist about the cause of HFS: 1) that it is ephaptic transmission between facial nerve fibers at the site of compression that causes spasm and synkinesis, and 2) that the facial motor nucleus is involved in producing the signs. We have earlier shown electrophysiological results from intraoperative recordings in patients undergoing microvascular decompression (MVD) operations for HFS. We found evidence that it is changes in structures that are central to the injury (probably the facial nucleus) rather than the injury to the nerve itself that give rise to the symptoms of HFS. We have also found evidence that ephaptic transmission between a small number of nerve fibers in the facial nerve at the site of lesion may occur under rare circumstances and for short periods of time when the facial nerve is being surgically manipulated, but it seems unlikely that such ephaptic transmission can generate the massive muscle contractions that are characteristic of HFS. In the proposed study we want to extend the intraoperative electrophysiological recordings in order to identify the location of the physiological abnormality that results in the spasm and abnormal muscle response. Animal experimentation will be done with the purpose of replicating HFS in an experimental animal. The rationale for the animal experimentation is that such a model will allow us to study directly the involvement of the facial motor nucleus. It may be assumed that the pathophysiology of other disorders caused by slightly injured nerves, such as various pain disorders, is similar to that of HFS, and we believe that patients with HFS provide a valuable model of other neurological disorders that are caused by slightly injured nerves.