The transient decrease in muscle strength during short, intensive courses of corticotropin therapy in myasthenic patients was accompanied by more pronounced progressive decrease in amplitude of evoked muscle action potentials, and therapeutically useful increase in muscle strength after the course was accompanied by lesser decrease in amplitude of successive muscle action potentials and increase in response to intra-arterial injections of acetylcholine chloride or neostigmine methylsulfate. The maximum conduction velocity of motor and sensory nerves and electromyographic findings were unchanged. The evoked muscle action potentials and the response to acetylcholine were unchanged before and after intraarterial injections of corticotropin or hydrocortisone. These findings indicate that the changes in muscle strength accompanying corticotropin therapy in myasthenic patients are due to changes in neuromuscular transmission, and not to direct action of corticotropin or glucocorticoids on neuromuscular junctions.