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F A Davis

Publications and source records attributed to F A Davis.

88 records · Page 5Linked to original sources

Impairment of repetitive impulse conduction in experimentally demyelinated and pressure-injured nerves.

Repetitive impulse conduction was studied in segmentally demyelinated peripheral nerves in guinea-pigs with experimental allergic neuritis (EAN) and in pressure-injured frog sciatic nerves. Normal guinea-pig sciatic-peroneal nerves maintained at 37°C conducted compound action potentials with only minor amplitude decreases at stimulus frequencies up to 200/sec. In contrast, nerves in EAN guinea-pigs maintained at 37°C demonstrated a rapidly progressive decrease in action potential amplitude when stimulated as slowly as 10-25/sec. The decrease is greater the higher the frequency of stimulation. At 100 stimuli/sec all EAN preparations showed more than a 50% reduction in action potential amplitude. These effects are reversible. In pressure-injured frog sciatic nerves similar effects occurred at stimulus frequencies as low as 50/sec. Normal frog nerves conducted up to 200 impulses/sec with little amplitude decrease. The probable mechanism and clinical significance of these results are discussed.

Action Potentials↗

Altered thermal sensitivity in injured and demyelinated nerve. A possible model of temperature effects in multiple sclerosis.

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.

Action Potentials↗

Effect of intravenous sodium bicarbonate, disodium edetate (Na2EDTA), and hyperventilation on visual and oculomotor signs in multiple sclerosis.

The effects of procedures believed to produce a decrease in serum ionized calcium were tested on visual and oculomotor function in nine multiple sclerosis (MS) patients. Transient improvement in scotomas, nystagmus, and oculomotor paresis occurred with intravenous infusions of NaHCO(3) or Na(2)EDTA. Hyperventilation was also tested for its effect on nystagmus and caused marked decreases in frequency. Control experiments with saline infusions did not produce any effect. The probable mechanism and site of action for these effects is discussed. This study demonstrates that certain signs and symptoms in MS can be altered favourably by changes in the internal chemical environment and offers a new approach to the search for a symptomatic therapy in MS.

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