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

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.