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Altered thermal sensitivity in injured and demyelinated nerve
  1. Floyd A. Davis,
  2. Samuel Jacobson
  1. Department of Neurology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, U.S.A.

    A possible model of temperature effects in multiple sclerosis1


    Electrophysiological studies were performed on frog and guinea-pig peripheral nerves to determine the effect of temperature on conduction at the site of pressure and demyelinating lesions. An increased susceptibility to thermally-induced conduction blockade has been demonstrated. In pressure-injured frog and guinea-pig nerves, conduction blocks occur at temperatures approximately 6°C lower than in normal nerves. A similar phenomenon occurs in guinea-pig demyelinated nerve (experimental allergic neuritis) and in some cases at temperatures around 15°C lower than in controls. It is suggested that these effects are the result of a critical lowering by temperature of an already markedly depressed conduction safety factor. In support of this, it has been shown that calcium ion depletion, which would be expected to increase the conduction safety factor by lowering the threshold for excitation, counteracts the increased thermal sensitivity of frog pressure-injured nerve. These findings are discussed in relation to well-known temperature effects in multiple sclerosis. They add support to an earlier proposed hypothesis that the changes in signs and symptoms with a change of body temperature in multiple sclerosis may be caused by an effect of temperature on axonal conduction.

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    A possible model of temperature effects in multiple sclerosis1


    • 1 Supported in part by the Morris Multiple Sclerosis Research Fund and by the U.S. Army Medical Research and Development Command (DA Project 3A0256011). Presented in part, at the Seventh International Congress of Electroencephalography and Clinical Neurophysiology, San Diego, California, 13-19 September 1969.