STUDIES OF THE PATHOPHYSIOLOGY OF HEMIFACIAL SPASM

经典的面肌痉挛（HFS）是在大多数情况下， 由于面部神经入口处的交叉压迫 通过血管到达脑干，但其病理生理学 大部分未知。 关于HFS的原因存在两种假设： 1)它是面神经纤维之间的视神经传递， 导致痉挛和联带运动的压迫部位，以及2） 面部运动神经核参与了这些信号的产生 我们之前已经展示了来自 微血管成形术患者的术中记录 HFS的减压（MVD）操作。 我们发现证据表明 损伤的核心是结构的变化（可能 面神经核），而不是神经本身的损伤， 引起HFS的症状。 我们还发现了证据 少数神经之间的视神经传导 损伤部位的面神经中的纤维可能发生在 罕见的情况下，并在短时间内，当面部 神经被手术操纵，但似乎不太可能， 这种肝纤维化的传播可以产生巨大的肌肉 收缩是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 导致痉挛的生理异常， 异常的肌肉反应 将进行动物实验 目的是在实验动物中复制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，其他疾病的病理生理学 由轻微神经损伤引起的疾病，如各种疼痛 疾病，类似于HFS，我们相信患者 HFS提供了其他神经系统疾病的有价值的模型 是由轻微的神经损伤引起的

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.