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Valproate-induced hyperammonemic encephalopathy (VHE) is an unusual complication characterized by a decreasing level of consciousness, focal neurological deficits, cognitive slowing, vomiting, drowsiness, and lethargy. VHE may occur in people with normal liver function, despite normal doses and serum levels of valproic acid (VPA). We describe a case of valproic acid-induced hyperammonemic encephalopathy in a bipolar disorder patient with therapeutic VPA levels. We report a case of a 50 year-old woman with bipolar disorder who presented to the inpatient psychiatry clinic with a manic episode. Sodium valproate was started at a dosage of 500 mg two times a day together with the extended release form of quetiapine 400 mg once a day. After a week she was confused about the day of the week, but was oriented to month, year, person, and place. Her vital signs were stable. The patient reported that she did not feel better and said that she felt slowed down and depressed. The next day she gradually became lethargic, proceeding to stuporous, and she had vomiting and drowsiness. Her blood level of valproic acid was at 97.2 μg/ml. Liver function tests were normal. The blood urea level was 33 mg/dL. Her blood ammonia level was 304 μmol/L, more than ten times the upper limit of the normal range. All psychotropic medications were stopped. After three days her vital signs were stable, and she had no obvious neurological deficits. She recovered fully. Clinical manifestations and hyperammonemia tend to normalize after VPA withdrawal. VHE is a serious condition that can lead to coma and even death. It can, however, be reversed if a precocious diagnosis is made and VPA treatment is discontinued (1). VHE is clinically characterized by an acute or subacute decreasing level of consciousness that goes from drowsiness to lethargy and coma, ataxia, vomiting, and focal neurological deficits (1). Laboratory tests usually show normal liver functions with hyperammonemia. Blood VPA levels are within therapeutic range in most VHE cases (2). The primary treatment for VHE is stopping VPA. Complete recovery generally occurs over a period of one to a few days (3). Etiopathogenesis is not completely understood, although hyperammonemia has been postulated as the main cause of the clinical syndrome (4). Psychiatrists and the other staff may need to be informed about the potential for hyperammonemia when starting valproic acid, and patients whose tolerance for valproic acid is unknown may need to be monitored for liver functions and blood levels of urea and ammonia.