Non-convulsive status epilepticus secondary to valproic acid-induced hyperammonemic encephalopathy
Authors: Velioğlu, S. K.; Gazioğlu, S.
Source: Acta Neurologica Scandinavica, Volume 116, Number 2, August 2007 , pp. 128-132(5)
Abstract:Velioğlu SK, Gazioğlu S. Non-convulsive status epilepticus secondary to valproic acid-induced hyperammonemic encephalopathy.
Acta Neurol Scand: 116: 128–132.
© 2007 The Authors Journal compilation © 2007 Blackwell Munksgaard. Background –
Valproic acid (VPA) may induce hyperammonemic encephalopathy. On the other hand, seizure-inducing effects of antiepileptic drugs (AEDs) may be a paradoxical reaction or a result of AED-induced encephalopathy (commonly induced by VPA). Methods –
We present the case of a 19-year-old male who developed acute mental status changes consistent with encephalopathy evolving into repetitive seizures with oral automatisms induced by relatively small doses of VPA. Results –
Although serum hepatic enzymes, such as AST and ALT, were normal, serum ammonia concentration was high, i.e. 70 mol/l (normal range 9–33 mol/l). Administration of VPA was discontinued immediately after admission. The patient's condition improved during the second week of hospitalization and ammonium levels returned to normal. Conclusion –
In conclusion, although uncommon, a possible induction of non-convulsive status epilepticus by valproate-induced hyperammonemic encephalopathy should be taken into account and properly managed by discontinuation of the drug.
Document Type: Research Article
Publication date: August 2007