| Abstract: | A 66-year-old man with Lambert–Eaton myasthenic syndrome, polyneuropathy, and small cell lung cancer, developed profound muscle weakness with a prolonged period of ventilatory dependency. Electrophysiological studies demonstrated very small compound muscle action potentials in response to supramaximal nerve stimulation, limited tetanic and postexercise facilitation, and prolonged prominent postexercise exhaustion (40–60% of baseline value) persisting up to 20 minutes. It is hypothesized that these changes may reflect both a severe defect in acetylcholine release and decreased availability of releasible acetylcholine from the terminal axon. |
