A 66-year-old man with Lambert-Eaton myasthenic syndrome, polyneuropat
hy, and small cell lung cancer, developed profound muscle weakness wit
h a prolonged period of ventilatory dependency. Electrophysiological s
tudies demonstrated very small compound muscle action potentials in re
sponse to supramaximal nerve stimulation, limited tetanic and postexer
cise facilitation, and prolonged prominent postexercise exhaustion (40
-60% of baseline value) persisting up to 20 minutes. It is hypothesize
d that these changes may reflect both a severe defect in acetylcholine
release and decreased availability of releasible acetylcholine from t
he terminal axon.