Responses of human sensory and motor axons to the release of ischaemia and to hyperpolarizing currents

Abstract

This study compared directly the post‐ischaemic behaviour of sensory and motor axons in the human median nerve, focusing on the excitability changes produced by ischaemia and its release and by continuous polarizing DC. The decrease in threshold during ischaemia for 13 min was greater, the post‐ischaemic increase in threshold was more rapid, and the return to the pre‐ischaemic excitability took longer in sensory axons. However, a transient depolarizing threshold shift developed in sensory axons a few minutes after release of ischaemia. This pattern could not be reproduced by polarizing currents designed to mimic the probable pump‐induced changes in membrane potential, even though the applied currents produced greater changes in threshold. Hyperpolarizing currents of equivalent intensity produced a greater increase in threshold for motor axons than sensory axons and, in studies of threshold electrotonus using graded hyperpolarizing DC, accommodation was greater in sensory than motor axons. The post‐ischaemic changes in threshold were not uniform for axons of different threshold, whether sensory or motor, the threshold increase was usually less prominent for low‐threshold axons. A transient post‐ischaemic depolarization could be produced in motor axons with ischaemia of 20 min duration. Greater ischaemic and post‐ischaemic changes in threshold for sensory axons could reflect greater dependence on the electrogenic Na+‐K+ pump to maintain resting membrane potential and/or greater extracellular K+ accumulation in ischaemic sensory axons. Inward K+ currents due to extracellular K+ accumulation would then be more likely to trigger a depolarizing shift in membrane potential, the degree of K+ accumulation and pump activity being dependent on the duration of ischaemia. In sensory axons the greater tendency to accommodate to hyperpolarizing stimuli presumably contributes to shaping their post‐ischaemic behaviour but is probably insufficient to explain why their behaviour differs from that of motor axons.

Ulnar nerve conduction abnormalities in carpal tunnel syndrome

“…This may be explained by the general belief that, due to biophysical differences, sensory fibers are more susceptible to mechanical stress than motor fibers. 27 On the other hand, as suggested earlier, standard electrophysiological tests may not be sensitive enough to detect minimal conduction abnormalities when applied to a limited sample of patients. 22 This may also explain why, although there was a statistically significant difference in motor and sensory branches of the ulnar nerve passing through the Guyon canal in CTS patients compared with controls, only a small proportion of our patients had conduction abnormalities that exceeded our laboratory limits.…”

Anomalies of ulnar nerve conduction in different carpal tunnel syndrome stages

“…This was not so, and possible reasons could be: (1) minimal impairment of ulnar nerve motor fibers may not be detectable by standard electrophysiology 13 ; and (2) biophysical differences in the properties of sensory and motor axons could account for a lower susceptibility of motor axons to compression with respect to sensory axons. 18 …”

Evaluation of Na+/K+ pump function following repetitive activity in mouse peripheral nerve

“…Activity-dependent hyperpolarization may, however, impair conduction in demyelinated axons (Bostock and Grafe, 1985;Kiernan et al, 1996a). Demyelinated motor axons are especially prone to activitydependent conduction block (Cappelen-Smith et al, 2000, 2003Kaji et al, 2000) as they express less inward rectification than sensory axons Kiernan et al, 2004;Lin et al, 2002). Reducing Na + /K + pump activity improves conduction in demyelinated axons in experimental (Kaji and Sumner, 1989a,b) and clinical trials (Kaji et al, 1990).…”