Brain Neurorehabil.  2013 Sep;6(2):86-89. 10.12786/bn.2013.6.2.86.

Valproate-induced Hyperammonemic Encephalopathy: A Case Report

• Yoo JY
• Yang HS

• KMID: 1797952
• DOI: http://doi.org/10.12786/bn.2013.6.2.86

Abstract

Valproate is widely used because of broad spectrum of action, but it can produce an encephalopathy resulting from hyperammonemia even at the therapeutic range of valproate and is called as valproate-induced encephalopathy (VHE). Delay in recognition of VHE can result in the development of potentially life-threatening complications. Fortunately, it is reversible with discontinuing valproate. A 65-year-old man became progressively lethargic with impaired gait and poor cognitive function while taking valproate as alternative to zonisamide. Routine investigations of admission profiles were performed but revealed no abnormalities. Next, we checked serum ammonia level to identify other possible causes and detected hyperammonemia despite the therapeutic range of valproate in the absence of any abnormalities in liver enzymes. On cessation of valproate, he has achieved dramatic clinical improvement including the reversal of hyperammonemia. We confirmed the diagnosis of VHE. This emphasizes the importance of rapid diagnosis and proper management of VHE in order to prevent the neurological damage and minimize complications.

Keyword

encephalopathy; hyperammonemia; valproate

MeSH Terms

Aged
Ammonia
Gait
Humans
Hyperammonemia
Isoxazoles
Liver
Valproic Acid
Ammonia
Isoxazoles
Valproic Acid

Figure

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  Fig. 1 Magnetic resonance imaging (MRI) of brain showed multifocal encephalomalacias in right frontotemporal lobe and a few old lacunes in both basal ganglia, but there were no newly appeared lesions, compared to previous imaging.

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