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Bostock, Hugh; Baker, M.; Grafe, Peter and Reid, G. (1991): Changes in excitability and accommodation of human motor axons following brief periods of ischaemia. In: The Journal of Physiology, Vol. 441: pp. 513-535 [PDF, 2MB]

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1. The mechanism of post-ischaemic ectopic impulse generation in nerve is not known, and previous measurements of excitability changes in human motor axons have appeared to conflict. We have used automatic threshold tracking and different stimulus-response combinations to follow the effects on excitability of brief (5-10 min) periods of ischaemia, too short to induce motor fasciculations. Excitability changes have been compared at different sites in axons innervating hand, arm and foot muscles. 2. Threshold was determined as the percutaneous stimulus current required to excite a single motor unit, or to evoke a constant multiunit response, after rectifying and integrating the electromyogram (EMG). Three different waveforms of stimulus current were compared: short (less than or equal to 2 ms) pulses, long (100-200 ms) pulses to measure rheobase, and 100 ms current ramps. We also measured accommodation by recording the effects of subthreshold depolarizing currents on excitability. 3. Ischaemic and post-ischaemic excitability changes were greatest in the proximal parts of the longest motor axons, and greater if the sphygmomanometer cuff was inflated over, rather than proximal to, the stimulating site. 4. Using integrated EMG responses from abductor digiti minimi, the ulnar nerve stimulated above the elbow became rapidly much less excitable after ischaemia when tested with short pulses, but more excitable when tested with current ramps. The rheobase rose briefly, but then fell, often below resting level, always staying below the pulse and ramp thresholds. 5. The latency of the response to a rheobasic stimulus altered in parallel with the threshold to short current pulses, and increased dramatically after ischaemia. This latency increase was associated with a prolonged phase of 'negative accommodation', i.e. the continued increase in excitability to a maintained subthreshold depolarizing current. 6. Changes in excitability and accommodation similar to those occurring after ischaemia were recorded following high frequency trains of stimuli. They were attributed primarily to hyperpolarization by the electrogenic sodium pump, since comparable changes could be induced by passing a steady hyperpolarizing current through the stimulating electrode. 7. Threshold and latency recordings from single motor units during and after ischaemia resembled in most respects the multiunit responses, but single unit rheobase did not show a post-ischaemic fall below the resting level. Repetitive firing contributed to the low multiunit thresholds recorded with long current pulses during the post-ischaemic period. 8. We conclude that human motor nerves become simultaneously both more and less excitable than normal after 10 min of ischaemia, depending on the choice of stimulus and response.

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