Bostock H, Burke D, Hales J P
Sobell Department of Neurophysiology, National Hospital, London, UK.
Brain. 1994 Apr;117 ( Pt 2):225-34. doi: 10.1093/brain/117.2.225.
The changes in excitability and supernormality of sensory and motor axons of the median (or ulnar) nerve were tracked during and following ischaemia at the wrist for periods of 5-20 min in normal human volunteers. Supernormality was defined as the fractional increase in excitability produced by a maximal conditioning stimulus, 10 ms before the test stimulus. With relatively brief periods of ischaemia (< 10 min), sensory and motor axons behaved similarly, with an increase in excitability (producing a decrease in threshold) and a decrease in supernormality during ischaemia and a long-lasting decrease in excitability (and increase in supernormality) following release of ischaemia. Most subjects reported paraesthesiae during brief periods of ischaemia but not after its release. No one experienced fasciculation. The threshold changes were generally similar during longer periods of ischaemia, but in the post-ischaemic phase the behaviour of sensory and motor axons diverged. After a rapid post-ischaemic increase, the threshold of sensory axons decreased, approaching the pre-ischaemic level, before rising again and then slowly returning to the control level. Sensory axons of different threshold behaved in a qualitatively similar manner, with no evidence of a bimodal distribution of thresholds in the post-ischaemic phase (as occurs with motor axons when the ischaemia is sufficient to produce fasciculation; see Bostock et al. J. Physiol (Lond) 1991; 441: 537-57). The 'notch' on the threshold plot for sensory axons lasted 20-40 min and was accompanied by a relatively small but appropriate change in supernormality. No such 'notch' was seen with motor axons. The changes in latency were generally similar for sensory and motor axons, largely paralleling the supernormality plots, except at the time of the 'notch'. To test the hypothesis that the differences in behaviour of sensory and motor axons resulted from differences in inward rectification activated by hyperpolarization, the changes in threshold produced by long-lasting (300 ms) depolarizing and hyperpolarizing current pulses were compared for sensory and motor axons. In seven of eight subjects, there was evidence of more inward rectification in sensory axons. In the eighth subject, motor axons behaved similarly to sensory axons. It is concluded that a difference in inward rectification contributes to but is insufficient by itself to account for the differences in behaviour of sensory and motor axons and that the greater propensity of sensor y axons to discharge ectopically cannot be attributed to a single factor.
在正常人类志愿者中，追踪了手腕缺血5 - 20分钟期间及之后正中神经（或尺神经）感觉和运动轴突的兴奋性及超常期变化。超常期定义为在测试刺激前10毫秒由最大条件刺激产生的兴奋性分数增加。在相对短暂的缺血期（<10分钟），感觉和运动轴突表现相似，缺血期间兴奋性增加（阈值降低）且超常期降低，缺血解除后兴奋性持续降低（超常期增加）。大多数受试者在短暂缺血期报告有感觉异常，但缺血解除后没有。没有人经历肌束震颤。在较长时间的缺血期，阈值变化通常相似，但在缺血后阶段，感觉和运动轴突的行为出现分歧。缺血后快速增加后，感觉轴突的阈值降低，接近缺血前水平，然后再次升高，随后缓慢恢复到对照水平。不同阈值的感觉轴突表现出定性相似的方式，在缺血后阶段没有阈值双峰分布的证据（运动轴突在缺血足以产生肌束震颤时会出现这种情况；见Bostock等人，《生理学杂志》（伦敦）1991年；441: 537 - 57）。感觉轴突阈值图上的“凹陷”持续20 - 40分钟，并伴有超常期相对较小但适当的变化。运动轴突未见此类“凹陷”。感觉和运动轴突的潜伏期变化通常相似，在很大程度上与超常期图平行，除了在“凹陷”出现时。为了检验感觉和运动轴突行为差异是由超极化激活的内向整流差异导致的这一假设，比较了感觉和运动轴突由持续（300毫秒）去极化和超极化电流脉冲产生的阈值变化。在8名受试者中的7名中，有证据表明感觉轴突的内向整流更强。在第8名受试者中，运动轴突的行为与感觉轴突相似。得出的结论是，内向整流的差异有一定作用，但仅凭其自身不足以解释感觉和运动轴突行为的差异，并且感觉轴突异位放电的更大倾向不能归因于单一因素。
