Myasthenia gravis (MG) can be exacerbated by a variety of medications, which increase weakness by interrupting neuromuscular junction transmission. Statins, which lower lipids by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, are not commonly known to worsen MG or have activity against the neuromuscular junction. 1 One report suggested that statin therapy produced ocular myasthenia. 2 However, based on the case description, it is not clear that this patient had MG. 3 We present a patient with well-documented MG who experienced worsening of his condition after taking different statins on four separate occasions.Case report. A 55-year-old man with hyperlipidemia and borderline hypertension was evaluated for a 1-year history of intermittent dysarthria. He first noticed dysarthria~1 week after the initiation of atorvastatin. At that time, MRI and blood work revealed no evidence of a stroke or elevation in his creatine kinase (CK) level. He stopped atorvastatin, and within 1 week the dysarthria resolved. During the next 8 months, he tried three other statins (lovastatin, pravastatin, and simvastatin). With each statin, the dysarthria returned in~1 week and resolved after stopping the medication. There was no elevation in his CK after the use of any of the statins. When he sought treatment in our medical center, he had experienced several weeks of dysarthria despite avoiding statin therapy for the previous 4 months. The dysarthria was worse in the evening and after prolonged periods of talking.On examination, he was markedly dysarthric. He had normal tongue movements and was not hypophonic. No cranial nerve abnormalities or proximal muscle weakness was detected. Repetitive nerve stimulation abnormalities were consistent with MG. The facial nerve showed a 50% decrement at baseline and Ͼ50% decrement at 30, 60, 120, and 180 seconds postexercise. The ulnar nerve showed a 6 to 7% decrement, and the spinal accessory nerve showed a 10 to 12% decrement postexercise. His acetylcholine receptor antibody level was Ͼ7.5 nmol/L (normal, Ͻ0.4 nmol/L). EMG did not reveal a myopathy, and CT of the chest did not show a thymoma. He was started on pyridostigmine (60 mg TID) and experienced rapid improvement in his speech.Discussion. To our knowledge, the only report in the literature associating statin use with worsening myasthenic symptoms involved a patient who developed ocular and systemic weakness on four separate occasions: three times with statins and once with a fibrate. 2 However, it is not clear that this patient had MG because no laboratory testing verified the diagnosis. 3 Our patient's history, repetitive nerve stimulation results, acetylcholine receptor antibody levels, and response to pyridostigmine substantiate the diagnosis of MG. It appears likely that statin use exacerbated his symptoms, given that dysarthria occurred on four separate occasions after four different statins, and each time he improved after discontinuation of the medication.Medications that exacerbate MG are thought to interrupt tr...