Kiernan M C, Mogyoros I, Burke D
Prince of Wales Medical Research Institute and Department of Neurology, Prince of Wales Hospital, Randwick, Sydney, Australia.
Brain. 1999 May;122 ( Pt 5):933-41. doi: 10.1093/brain/122.5.933.
Wrist extension was performed in six healthy subjects to establish, first, whether it would be sufficient to produce conduction block and, secondly, whether the excitability changes associated with this manoeuvre are similar to those produced by focal nerve compression. During maintained wrist extension to 90 degrees, all subjects developed conduction block in cutaneous afferents distal to the wrist, with a marked reduction in amplitude of the maximal potential by >50%. This was associated with changes in axonal excitability at the wrist: a prolongation in latency, a decrease in supernormality and an increase in refractoriness. These changes indicate axonal depolarization. Similar studies were then performed in seven patients with carpal tunnel syndrome. The patients developed conduction block, again with evidence of axonal depolarization prior to block. Mild paraesthesiae were reported by all subjects (normals and patients) during wrist extension, and more intense paraesthesiae were reported following the release of wrist extension. In separate experiments, conduction block was produced by ischaemic compression, but its development could not be altered by hyperpolarizing currents. It is concluded that wrist extension produces a 'depolarization' block in both normal subjects and patients with carpal tunnel syndrome, much as occurs with ischaemic compression, but that this block cannot be altered merely by compensating for the axonal depolarization. It is argued that conduction slowing need not always be attributed to disturbed myelination, and that ischaemic compression may be sufficient to explain some of the intermittent symptoms and electrodiagnostic findings in patients with carpal tunnel syndrome, particularly when it is of mild or moderate severity.
对6名健康受试者进行了腕关节伸展试验，首先是为了确定该动作是否足以产生传导阻滞，其次是为了确定与该动作相关的兴奋性变化是否与局灶性神经受压所产生的变化相似。在将腕关节持续伸展至90度的过程中，所有受试者腕部远端的皮肤传入神经均出现传导阻滞，最大电位幅度显著降低>50%。这与腕部轴突兴奋性的变化有关：潜伏期延长、超常期缩短和不应期延长。这些变化表明轴突去极化。随后对7名腕管综合征患者进行了类似研究。患者出现传导阻滞，同样在阻滞前有轴突去极化的证据。所有受试者（正常人和患者）在腕关节伸展时均报告有轻度感觉异常，在腕关节伸展解除后报告有更强烈的感觉异常。在单独的实验中，缺血性压迫可产生传导阻滞，但其发展不能被超极化电流改变。得出的结论是，腕关节伸展在正常受试者和腕管综合征患者中均产生“去极化”阻滞，这与缺血性压迫时的情况类似，但这种阻滞不能仅通过补偿轴突去极化来改变。有人认为，传导减慢不一定总是归因于髓鞘紊乱，缺血性压迫可能足以解释腕管综合征患者的一些间歇性症状和电诊断结果，尤其是在病情为轻度或中度时。
