���ルバマゼピン中毒により下眼瞼向き眼振を認めた薬剤性めまい症例

We report the case of a 33-year-old man who presented with disequilibrium and downbeat nystagmus. Balance testing showed failure of visual suppression of caloric nystagmus with insufficient optokinetic nystagmus responses, suggesting central vestibular dysfunction. However, MRI showed no lesions in the brain, including in the cerebellum. The patient had been diagnosed previously as having epilepsy, and the convulsions had remained under control for more than 10 years with a maintenance dose of carbamazepine (900mg/day). Blood tests revealed a serum level of carbamazepine of 10.7mEq/l, which was over the therapeutic range (4.0-10.0mEq/l). Therefore, his carbamazepine dose was reduced, and with a reduction of the dose to 600mg/day, his disequilibrium and downbeat nystagmus gradually disappeared, along with a decrease in return of the serum level of carbamazepine to the therapeutic range. Therefore, we diagnosed the disequilibrium with downbeat nystagmus in this patient as having been caused by carbamazepine intoxication. Although carbamazepine is metabolized by CYP3A4 in the liver, elevated levels of the drug have been reported in cases of renal failure. As he also suffered from polycystic kidneys, we consider that the progressive renal dysfunction in our patient could have precipitated the carbamazepine intoxication.