Valproic acid. a b s t r a c t. Valproate-induced hyperammonemic encephalopathy is an unusual but serious adverse effect that is usually characterized by the ...
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Case Reports / Journal of Clinical Neuroscience 21 (2014) 690–691
Valproate induced hyperammonemic encephalopathy successfully treated with levocarnitine Andrea Rigamonti a,⇑, Giuseppe Lauria b, Gianluca Grimod c, Graziella Bianchi a, Andrea Salmaggi a a b c
Department of Neurology, Alessandro Manzoni Hospital, Via Dell’Eremo 9/11, 23900 Lecco, Italy Neuromuscular Diseases Unit, Carlo Besta Neurological Institute, IRCCS Foundation, Milan, Italy Department of Neurosurgery, Alessandro Manzoni Hospital, Lecco, Italy
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Article history: Received 13 December 2012 Accepted 21 April 2013
Keywords: Encephalopathy Hyperammonemia Levocarnitine Valproic acid
a b s t r a c t Valproate-induced hyperammonemic encephalopathy is an unusual but serious adverse effect that is usually characterized by the acute onset of impaired consciousness, focal neurological symptoms and increased seizure frequency. It has been reported to occur at therapeutic valproate levels. We report a patient who developed valproate-induced hyperammonemic encephalopathy after a short treatment with valproate and was successfully treated with levocarnitine. We discuss this patient and review the literature regarding the use of levocarnitine in similar patients. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction Valproate-induced hyperammonemic encephalopathy (VHE) is an unusual but serious adverse event that has been reported at a therapeutic valproate (VPA) [1] dosage. We describe a patient in whom VHE was successfully treated with levocarnitine and review the literature on this topic [2–5].
2. Case report A 31-year-old right-handed man was admitted to the emergency department of our hospital soon after a generalized tonicclonic seizure. Brain CT scan disclosed a right temporal-insular lesion 4 cm in diameter confirmed by brain MRI and suggestive of a glioma. VPA was immediately started at 500 mg daily and increased to 1500 mg daily in the following 7 days. Two days after admission, the patient underwent neurosurgery with complete resection of the tumor. His post-operative course was uneventful until his sixth day after admission, when he became lethargic with a Glasgow Coma Scale score of 9. Complete blood cell count, erythrocyte sedimentation rate, electrolytes, liver and renal function values were normal, whereas his ammonia plasma level was 204 lmol/L (normal,
