Parkinsonism and Cognitive Decline in a 64-Year-Old Woman with Epilepsy

Publisher Summary This chapter examines the case of a patient diagnosed with valproate-induced encephalopathy. A 64-year-old woman with symptomatic epilepsy caused by perinatal brain damage was admitted to the hospital because of progressive deterioration of her general health. Her seizures, which were complex partial and secondary generalized tonic–clonic, had been well controlled over the years with valproate 3000 mg/day and lamotrigine 200 mg/day, a regimen that the patient had tolerated well until 2 weeks before admission. The initial EEG revealed background slowing in the theta range with bilaterally synchronous high-voltage slow wave activity. No epileptiform activity was recorded. Laboratory studies showed elevated levels of blood urea nitrogen (35 mg/dl, normal range 8–20 mg/dl) and ammonia (123 μg/dl, normal range 19–82 μg/dl). The serum concentration of valproate was 134.6 mg/l (normal range 50–100 mg/l), and of lamotrigine was 19.9 mg/l. No other abnormalities were found, including on liver function tests. As the valproate dose was reduced, her physical and cognitive condition improved significantly. Valproate was then completely withdrawn, resulting in complete remission of both the cognitive impairment and the parkinsonian syndrome. In this case, clinical symptoms, hyperammonemia and EEG findings led to the diagnosis of valproate-induced encephalopathy. It should be noted that the serum valproate concentration was only moderately elevated above the therapeutic range.