Changes in excitability and accommodation of human motor axons following brief periods of ischaemia.

Abstract

SUMMARY1. 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 (s< 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. 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. The changes in accommodation and excitability recorded do not, however, provide an explanation for the spontaneous activity occurring after longer periods of ischaemia.

Influence of the skeletal muscle activity on time and frequency domain properties of the body surface ECG during evolving ventricular fibrillation in the pig

“…In our study EMG signals exhibited a very broad spectrum in the measured frequency band (2−250 Hz), which resembles muscular "fibrillation" resulting from asynchronous firing of the individual fibers of a motor unit following denervation [18,19]. Speculatively, the mechanism of SMA observed in our study may involve hyperexcitability in the motor neurons and/or skeletal muscle fibers, resulting from extracellular accumulation of potassium and depolarization of the membrane potential [20,21].…”

The relationship between ischaemic conduction failure and conduction velocity in cat myelinated axons

“…A tourniquet, however, must involve some deformation of the underlying nerve structure (e.g. see Hess, Eames, Darveniza & Gilliatt, 1979) and recent studies indicate that this tourniquet deformation either does (Yarnitsky & Ochoa, 1989), or does not (Bostock, Baker, Grafe & Reid, 1991) influence nerve conduction. Whichever result is correct, since a pure model of nerve ischaemia was desired in the current study tourniquet methods were clearly inappropriate.…”

On the applicability of two different stimulation techniques for intra‐operative peroneal nerve conduction testing

“…Consequently, it is not surprising that dCMAPs were available during proximal conduction block. Additionally, the greatest changes in excitability both during and after ischaemia are known to occur directly beneath the cuff [3]. This increased sensitivity appeared to depend on exclusion of blood supply rather than on mechanical deformation of the nerve.…”

“…These changes in turn yield an axonal depolarization that inactivates sodium channels responsible for action potential generation. As a first consequence conduction velocity is slowed and with further deterioration of the ionic gradients conduction is biocked [3].…”

“…It is well known that ischaemia of a peripheral human nerve leads to a slowing of axonal conduction velocity [3] indicated by a latency shift of the compound muscle action potential. The apparent conduction slowing W Nebelung el al.…”