Changes in excitability and impulse transmission following prolonged repetitive activity in normal subjects and patients with a focal nerve lesion.

The present study was undertaken to document the excitability changes produced by prolonged high-frequency trains of impulses and to determine whether these changes in excitability would impair neural transmission in cutaneous afferents of patients with focal slowing of conduction across the carpal tunnel. A submaximal test stimulus was used to measure the changes in axonal excitability following trains of supramaximal stimuli delivered at 200 Hz for 30 s, 1 min or 2 min. These trains produced a prolonged depression in excitability in normal axons with gradual recovery to control levels over 20-30 min, presumably due to hyperpolarization associated with activation of the electrogenic Na+/K+ pump. The decrease in excitability was demonstrable at nerve segments remote from the site of tetanic stimulation. Based on these findings, the effects on neural transmission were then assessed in normal subjects and patients using a supramaximal test stimulus following a 1-min tetanic train. In normal subjects there was a small activity-dependent decrease in amplitude of the compound sensory action potential (CSAP) associated with a prolongation in its latency. In patients with focal slowing of conduction across the carpal tunnel there was a more marked post-tetanic prolongation in latency, but the reduction in amplitude of the maximal CSAP was no greater than in the control subjects. It is concluded that activity-dependent conduction block is not a major cause of symptoms in carpal tunnel syndrome. It is suggested that the conduction slowing seen in patients with mild-moderate carpal tunnel syndrome could result from mechanisms other than demyelination.