The effects of a volatile anaesthetic on the excitability of human corticospinal axons

Abstract

The recovery of excitability following a conditioning volley and the strength-duration properties of corticospinal axons were measured in 10 neurologically normal patients in whom corticospinal function was being monitored during scoliosis surgery. Corticospinal volleys were produced using transcranial electrical stimulation of the motor cortex, and recorded from the spinal cord using epidural leads. Administration of a volatile anaesthetic, sevoflurane 2%, increased the threshold current required to produce a submaximal test volley by 35.8% (P = 0.0005), indicating that the anaesthetic depressed the excitability of the site at which the transcranial stimulus activated the corticospinal system. Following a strong transcranial stimulus, axons were relatively refractory for conditioning-test intervals up to ~2.5 ms, and then superexcitable for intervals of > 10 ms. In two patients, the time course and extent of refractoriness and superexcitability did not differ when receiving sevoflurane 2% and after its withdrawal. Strength-duration properties were determined by measuring the stimulus current required to produce a submaximal corticospinal volley of fixed amplitude using test stimuli of different duration, from 50 μs to 1 ms. Strength-duration curves were well described by a hyperbolic function, with which there is a linear relationship between stimulus charge and stimulus duration. In the absence of sevoflurane, the strength-duration time constant (τ(SD)) was 432.2 ± 70.5 μs. When sevoflurane 2% was administered to 6 patients, τ(SD) decreased to 203.7 ± 93.8 μs, a change that was significant (P = 0.04). The decrease in τ(SD) was accompanied by an increase in rheobase. These findings imply that the lowest-threshold component of the corticospinal volley produced by transcranial electrical stimulation probably arises from nodes of Ranvier of corticospinal axons, where it would not be affected by changes in the excitability of cortical neurons. It is suggested that the increase in threshold produced by sevoflurane is due to depression of Na+ currents at the nodes of Ranvier of corticospinal axons.