面肌痉挛发病机制的实验研究

Experimental study on the pathogenesis of hemifacial spasm

目的 通过建立面肌痉挛的动物模型 ,结合电生理检测技术 ,探讨其发病机制。方法2 8只新西兰大白兔随机分为 4组 :面神经脱髓鞘并血管压迫组 (模型组 ) 13只 ;单一面神经血管压迫组 5只 ;单一面神经脱髓鞘组 5只 ;假手术对照组 5只。术后第 3、6周检测并比较各组动物的异常肌反应 (AMR)和F波变化。结果 术后第 3周 ,4组动物均未诱发出AMR ,模型组有 10只动物于术后第6周诱发出典型的AMR ;模型组动物的F/M波幅比率、F波持续时间及其诱发频率均明显高于其他各组动物 (P <0 0 1) ,但各组动物的F波潜伏期差异无显著性意义 (P >0 0 5 )。结论 面神经运动核兴奋性的增高可能是发生面肌痉挛的主要病理生理基础。

Objective To investigate the pathogenesis in hemifacial spasm by establishing animal models of hemifacial spasm and combining with electrophysiological technique. Methods 28 New Zealand white rabbits were randomized into four groups: 13 rabbits underwent both artificial demylination and arterial compression (model group). 5 rabbits underwent only arterial compression, 5 rabbits underwent only artificial demyelination and 5 rabbits underwent sham operation control. Abnormal muscle response (AMR) and F wave changes in all groups were tested and compared at the third or sixth week after operation respectively.Results No AMR was recorded in all four groups at the third week after operation, while a clear AMR was elicited in ten animals in model group rather than in the other groups at the sixth week of postoperation. F/M amplitude ratio, the F wave duration and frequency of F wave appearance in model animals significantly increased as compared with those of the other groups ( P <0 01), however F wave latency in all groups did not significantly differ ( P >0 05). Conclusion The hyperactivity of the facial motonucleus may be the pathophysiological basis of hemifacial spasm.