Brain, Vol 120, Issue 2 317-325, Copyright © 1997 by Oxford University Press
I Mogyoros, MC Kiernan, D Burke and H Bostock
This study was undertaken to compare the excitability changes of sensory
and motor axons during hyperventilation and ischaemia, and to determine why
ectopic impulse activity develops more readily during hyperventilation, and
in sensory fibres. During hyperventilation for 20 min, all six subjects
reported paraesthesiae in the hand and face, and four out of the six
developed muscle twitching and cramps, associated with significant
decreases of 20-30% in the threshold current required to produce sensory
and motor potentials of constant size. During ischaemia four out of the six
subjects reported paraesthesiae, but none reported muscle twitching. There
were significant decreases of 15-20% in threshold for sensory and motor
fibres. Ischaemia produced a marked decrease in supernormality, an increase
in refractoriness and an increase in latency of the test compound sensory
or motor potential, changes that were not seen with hyperventilation. The
decrease in threshold during these manoeuvres was associated with a
significant increase in strength--duration time constant (tau SD),
indicating a relatively greater decrease in rheobase current. Using the
technique of latent addition, we found that the changes in tau SD were
consistent with a recently proposed model in which non-inactivating,
voltage- dependent 'threshold channels' (presumably persistent Na+
channels) are active at resting potential. The failure of hyperventilation
to alter conduction velocity, refractoriness or supernormality appreciably
indicates that, unlike ischaemic depolarization, hyperventilation does not
increase inactivation of conventional Na+ channels or activation of K+
channels, and this implies that the hyperventilation-induced increase in
excitability is not the result of conventional depolarization, as seems to
occur during ischaemia. These results suggest that hyperventilation has a
rather selective action on the threshold channels, and they help to explain
its greater effectiveness compared with ischaemia in provoking ectopic
discharges. The greater expression of threshold channels in sensory than in
motor fibres can explain why hyperventilation induces paraesthesiae before
fasciculation and why only paraesthesiae occur during ischaemia.
ARTICLES
Excitability changes in human sensory and motor axons during hyperventilation and ischaemia
Prince of Wales Medical Research Institute, Sydney, Australia.
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