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.