Non-convulsive status epilepticus secondary to valproic acid-induced hyperammonemic encephalopathy
ACTA NEUROLOGICA SCANDINAVICA, cilt.116, sa.2, ss.128-132, 2007 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 116 Sayı: 2
- Basım Tarihi: 2007
- Doi Numarası: 10.1111/j.1600-0404.2006.00793.x
- Dergi Adı: ACTA NEUROLOGICA SCANDINAVICA
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.128-132
- Anahtar Kelimeler: EEG, encephalopathy, hypermmonemia, non-convulsive status epilepticus, valproic acid, adverse effects, antiepileptic drugs, seizures, DRUGS, RATS
- Karadeniz Teknik Üniversitesi Adresli: Evet
Özet
ackground –Valproic acid (VPA) may induce hyperammonemic
encephalopathy. On the other hand, seizure-inducing effects of
antiepileptic drugs (AEDs) may be aparadoxical 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.70lmol/l (normal range 9–33lmol/l). Administration of
VPA was discontinued immediatelyafter 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-inducedhyperammonemic encephalopathy
should be taken into account and properly managed by
discontinuation of the drug