Abstract

Previous studies in experimentally demyelinated mammalian nerves have demonstrated that a reversible conduction block occurs with small increases of temperature within the animal's normal body temperature range. This phenomenon is believed to be the mechanism for clinical temperature effects in multiple sclerosis. This study examines some quantitative thermal relationships in demyelinated nerves of guinea pigs with experimental allergic neuritis. The observed results in normal and experimental animals are in good agreement with previous theoretical calculations based on the effects of temperature on the voltage and time-dependent behavior of the ionic permeabilities of the nodes of Ranvier. Guinea pigs with increasing motor dysfunction generally exhibited corresponding increases in the overall latency of the conducted action potential, as well as decreases in amplitude. In addition, the lower the initial velocity increment per degree of temperature elevation, the lower was the temperature at which conduction block began to occur. Except for a few cases in which the recorded action potential was bimodal, with response at both normal and prolonged latency, the results tended to indicate a remarkedly uniform involvement of the sciatic nerve within the region of temperature control.