Uncini A, Di Muzio A, Awad J, Gambi D
Institute of Clinical Neurology and Behavioral Sciences, University of Chieti, Italy.
Acta Neurol Scand. 1992 Jan;85(1):66-70. doi: 10.1111/j.1600-0404.1992.tb03998.x.
A case of bilateral common peroneal neuropathy following prolonged squatting is reported. Serial peroneal conduction velocities with analysis of compound muscle action potential (CMAP) amplitude, area and duration performed at Days 1, 2, 5, 7, 14, 21, 37, 80 showed conduction block localized at the fibular head which lasted 14 days and paralleled clinical conditions. Axonal loss coexisted as indicated by amplitude reduction of CMAP from peroneal nerve stimulation at the ankle which reached the lowest values at Day 7. Excessive temporal dispersion, as indicated by abnormal increased duration of the CMAP from stimulation above the fibular head, was never detected. Conduction velocity in the segment across the fibular head was reduced as long as conduction block was present, due to preferential block of large diameter, fast conducting, fibers. The rapid resolution of conduction block and the absence of temporal dispersion suggest that compressive conduction block is not necessarily due to demyelination. Mechanical factors or ischemic-metabolic mechanisms might play a role.
报告了一例长时间蹲坐后双侧腓总神经病变的病例。在第1、2、5、7、14、21、37、80天进行了系列腓总神经传导速度测定，并分析复合肌肉动作电位（CMAP）的波幅、面积和时限，结果显示传导阻滞定位于腓骨头处，持续14天，与临床情况相符。踝关节处腓总神经刺激时CMAP波幅降低提示存在轴索损伤，在第7天降至最低值。未检测到腓骨头以上刺激时CMAP时限异常延长所提示的过度时间离散。只要存在传导阻滞，腓骨头节段的传导速度就会降低，这是由于大直径、快速传导纤维的优先阻滞所致。传导阻滞的快速缓解以及无时间离散表明，压迫性传导阻滞不一定是由脱髓鞘引起的。机械因素或缺血-代谢机制可能起作用。
