Abstract

We sought to evaluate the effect of hyperthermia (HT) on central conduction pathways by alterations in pattern visual evoked potentials (PVEPs) in normal and demyelinated optic nerves. We studied PVEP peak latency and amplitudes in 10 normal subjects and six patients with demyelinating optic neuropathy before and during HT. In normal subjects, a mean rise in temperature of 2.5 degrees C resulted in a decrease in the second positive peak (P2) latency of 6.1 ms (p < 0.0001) and a slight decline in P2 amplitude of 1.16 muV (p < 0.009). These results were compared to those obtained from six patients with multiple sclerosis. These patients had a history of monocular optic neuritis; two patients had had bilateral optic neuritis, and one patient had not had involvement of the optic nerve. Average temperature elevations during PVEPs were 1.60 degrees C. PVEPs among these patients showed decrease in mean P2 latencies, except in patients with multiple sclerosis, who showed an increase in latency with 60 min check size in the left eyes. There was a consistent decline in P2 amplitudes. Loss of amplitude was greater among the six optic nerves of those patients having transient, mild losses in visual acuity during HT. Reductions in P2 amplitude were best explained by partial or complete conduction block. These changes in conduction time and amplitude during HT provide a neurophysiologic correlation to the well-known sensitivity of demyelinated optic nerves to elevated temperatures. They are also relevant to the monitoring of central pathways in the operative or intensive care setting. The demonstrated reversible loss of amplitudes also gives promise to therapeutic manipulation of impaired pathways by impeding the loss of current from denuded nerve fibers.

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