Sodium Valproate-Induced Encephalopathy: A Case Report

Valproic acid is widely used in neurological and psychiatric practice and is generally well tolerated; however, valproate-induced encephalopathy (VIE) is a rare but clinically significant adverse reaction that may occur even at therapeutic serum concentrations and in the absence of hyperammonaemia or hepatic dysfunction. We report the case of a 63-year-old woman on long-term valproic acid therapy who presented with progressive gait instability, fluctuating consciousness, and marked sinus bradycardia. Neuroimaging, cerebrospinal fluid analysis, and metabolic investigations were unremarkable, with normal serum ammonia and valproate levels within the therapeutic range. Electroencephalography demonstrated generalised cerebral dysfunction without epileptiform activity. Discontinuation of valproic acid led to rapid and complete resolution of both the encephalopathy and the bradycardia, supporting a direct causal relationship. VIE may occur via hyperammonaemic or normoammonaemic mechanisms; this case exemplifies the latter, demonstrating that normal ammonia levels must not be used to exclude the diagnosis. The concurrent sinus bradycardia is an atypical feature rarely described outside the context of overdose, and its co-resolution with the encephalopathy following drug withdrawal further supports a valproate-mediated aetiology. This case highlights that serious neuro-cardiac adverse effects traditionally associated with valproate toxicity may arise during routine therapeutic use, and that prompt recognition and withdrawal of valproate can be curative.