Kuroki A, Møller A R
Department of Surgical Neurology, Yamagata University School of Medicine, Japan.
Acta Neurochir (Wien). 1994;126(2-4):149-57. doi: 10.1007/BF01476426.
It is generally assumed that hemifacial spasm (HFS) is caused by vascular compression of the facial nerve at the root exit zone (REZ), but the mechanism for the development of HFS is not known. Evidence has been previously presented that the signs of HFS are caused by hyperactivity of the facial motonucleus that is caused by the irritation to the facial nerve from the vascular contact. This assumption has been supported by the finding that daily electrical stimulation of the facial nerve in the rat facilitates the development of an abnormal muscle response that is a characteristic sign of HFS in man and is an indication of an abnormal cross-transmission that makes it possible to elicit a contraction of muscles innervated by one branch of the facial nerve by electrically stimulating another branch of the facial nerve. In the present study we show that close contact between a peripheral branch of the facial nerve and an artery also facilitates the development of an abnormal muscle response, but only if the facial nerve has previously been slightly injured (by a chromic suture) at the location of the arterial contact. We also show that blocking neural conduction in the facial nerve proximal to the artificial vascular compression abolishes the abnormal muscle contraction, which supports the assumption that the anatomical location of cross-transmission that is causing the abnormal muscle response is central to the vascular compression, most likely in the facial motonucleus. These findings may explain why the facial nerve is only susceptible to vascular compression near its REZ, where an injury to its myelin is more likely to occur than where the nerve is covered with schwann cell myelin.
一般认为，面肌痉挛（HFS）是由面神经在根部出口区（REZ）受到血管压迫所致，但HFS的发病机制尚不清楚。此前已有证据表明，HFS的症状是由面神经运动核的活动亢进引起的，而这种活动亢进是由血管接触对面神经的刺激所致。这一假设得到了以下发现的支持：每天对大鼠的面神经进行电刺激会促进异常肌肉反应的发展，这种异常肌肉反应是人类HFS的特征性表现，表明存在异常的交叉传导，即通过电刺激面神经的一个分支能够引发由面神经另一分支支配的肌肉收缩。在本研究中，我们发现面神经的外周分支与动脉紧密接触也会促进异常肌肉反应的发展，但前提是面神经在动脉接触部位先前已受到轻微损伤（用铬制缝线）。我们还发现，在人工血管压迫近端阻断面神经的神经传导可消除异常肌肉收缩，这支持了以下假设：导致异常肌肉反应的交叉传导的解剖位置以血管压迫为中心，很可能位于面神经运动核。这些发现可能解释了为什么面神经仅在其REZ附近易受血管压迫，因为在该区域其髓鞘比被施万细胞髓鞘覆盖的部位更容易受损。
