A 22-year-old woman had been suffering from blepharoptosis and fatigabilities of both shoulders for a year. She had been administered phenytoin since age 4 to prevent febrile convulsion. On admission, she had bilateral blepharoptosis with left one being more severely affected. Her pupils and eye movement were normal. Other cranial nerve functions were normal. Her both deltoid muscles were mildly weak. A repetitive stimulation study revealed a 35% decline of the evoked responses recorded from either the orbicularis oculi or the abductor pollicis brevi muscle. Antibody activity for acetylcholine receptor was higher than normal range. Her blepharoptosis transiently disappeared after an intravenous administration of 5mg of edrophonium. She was diagnosed as having myasthenia gravis. Her myasthenic signs had continued one month after phenytoin withdrawal, then an extended thymectomy was done. The thymus was histologically hypertrophic. Although a direct blocking at a neuromuscular junction by phenytoin has been reported in animal experiments, our case is not likely to be affected by this effect. Since a large population of young epileptic patients needs a long-term phenytoin therapy, detailed investigation is necessary to elucidate how frequently they manifest myasthenia gravis.