CHANGES IN EXCITABILITY AND IMPULSE TRANSMISSION FOLLOWING PROLONGED REPETITIVE ACTIVITY IN NORMAL SUBJECTS AND PATIENTS WITH A FOCAL NERVELESION

Citation
Mc. Kiernan et al., CHANGES IN EXCITABILITY AND IMPULSE TRANSMISSION FOLLOWING PROLONGED REPETITIVE ACTIVITY IN NORMAL SUBJECTS AND PATIENTS WITH A FOCAL NERVELESION, Brain, 119, 1996, pp. 2029-2037
Citations number
29
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
BrainACNP
ISSN journal
00068950
Volume
119
Year of publication
1996
Part
6
Pages
2029 - 2037
Database
ISI
SICI code
0006-8950(1996)119:<2029:CIEAIT>2.0.ZU;2-L
Abstract
The present study was undertaken to document the excitability changes produced by prolonged high-frequency trains of impulses and to determi ne whether these changes in excitability would impair neural transmiss ion in cutaneous afferents of patients with focal slowing of conductio n across the carpal tunnel. A submaximal test stimulus was used to mea sure the changes in axonal excitability following trains of supramaxim al 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 g radual recovery to control levels over 20-30 min, presumably due to hy perpolarization associated with activation of the electrogenic Na+/Kpump. 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 subjec ts and patients using a supramaximal test stimulus following a 1-min t etanic 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 control subjects. It is con cluded that activity-dependent conduction block is not a major cause o f symptoms in carpal tunnel syndrome. It is suggested that the conduct ion slowing seen in patients with mild-moderate carpal tunnel syndrome could result from mechanisms other than demyelination.