Mr. A was a 22-year-old student who was seen with paroxysmal depersonalization that had lasted for 6 weeks; he had episodes that lasted from seconds up to 20 minutes. When he was examined, we found left facial dysesthesia, paroxysmal myoclonia, visual impairment, and disturbances of concentration. Oligoclonal banding and multiple periventricular white matter lesions were found with magnetic resonance tomography; possible multiple sclerosis was suggested. Methylprednisolone, given intravenously and tapered orally, however, did not improve his symptoms. Treatment of his paroxysmal depersonalization was begun with carbamazepine, 400 to 600 mg/day; plasma levels of 6–10 mg/liter were achieved. There was a mild improvement in the frequency of his symptoms (from 6–10/day to 2–3/day) and in the severity of his depersonalization attacks.

After 2 months, Mr. A’s treatment with carbamazepine had to be stopped because of a rash. His depersonalization worsened, and he had to be treated with valproic acid. However, to achieve an adequate plasma concentration of the drug (more than 50 mg/liter), a dose of 1800 mg/day was necessary; this resulted in marked sedation accompanied by only a slight improvement of his depersonalization symptoms. Therefore, paroxetine was added, 10 mg/day, and his dose was increased weekly to 40 mg/day, whereas his treatment with valproic acid was discontinued. In the third week of his paroxetine treatment, Mr. A’s depersonalization attacks started to improve. After 4 months of treatment, they occurred only once or twice a week and had markedly decreased intensity. His social withdrawal disappeared as well, and Mr. A started his leisure activities again. However, the facial dysesthesia, myoclonia, and subjective disturbances of concentration persisted. Because of restlessness and sleep disturbances, his paroxetine dose was reduced to 30 mg/day. Two years after the onset of the disease, an acute relapse with neurological symptoms accompanied by typical changes in magnetic resonance tomographic and CSF findings led to the diagnosis of clinically definite, laboratory-supported multiple sclerosis +(3).