Macefield V G
Prince of Wales Medical Research Institute, Randwick, Sydney, NSW, Australia.
Muscle Nerve. 1998 Apr;21(4):461-8. doi: 10.1002/(sici)1097-4598(199804)21:4<461::aid-mus4>3.0.co;2-7.
A quantitative assessment was made of the firing characteristics of repetitive axonal discharges encountered during microneurographic recordings from human peripheral nerves. Spontaneous activity was recorded from 16 single axons using tungsten microelectrodes inserted percutaneously into fascicles of the median or peroneal nerves in normal subjects. These discharges typically consisted of brief bursts of 2-5 spikes occurring at a frequency of 7-10 Hz. Peak instantaneous frequencies usually exceeded 300 Hz. Based on their similarity with spontaneous high-frequency discharges recorded from single axons following nerve damage, ischemia, prolonged electrical stimulation, or hyperventilation, it is concluded that they are generated ectopically at the site of a previous impalement of a nerve fiber. It is suggested that short-term damage to the nerve fiber caused by the microelectrode may allow accumulation of K+ underneath the myelin, triggering an inward flow of K+ and regenerative depolarizations. Alternatively, internodal channels may be exposed following damage to the myelin, resulting in the generation of spontaneous pacemaker potentials and repetitive discharges.
对人体周围神经进行微神经电图记录时遇到的重复性轴突放电的放电特性进行了定量评估。使用钨微电极经皮插入正常受试者正中神经或腓总神经束,从16根单轴突记录自发活动。这些放电通常由2 - 5个尖峰的短暂爆发组成,频率为7 - 10Hz。峰值瞬时频率通常超过300Hz。基于它们与神经损伤、局部缺血、长时间电刺激或过度通气后单轴突记录的自发高频放电的相似性,得出结论:它们是在神经纤维先前被刺入的部位异位产生的。有人提出,微电极对神经纤维造成的短期损伤可能会使K + 在髓鞘下积聚,触发K + 的内流和再生性去极化。或者,髓鞘损伤后节间通道可能暴露,导致自发起搏器电位的产生和重复性放电。