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Fortschr Neurol Psychiatr 2010; 78(10): 590-598
DOI: 10.1055/s-0029-1245632
Übersicht

© Georg Thieme Verlag KG Stuttgart · New York

Antiepileptika-induzierte Enzephalopathie

Antiepileptic Drug-Induced EncephalopathyN. Hansen1 , M. Finzel2 , F. Block3
  • 1Neurologische Klinik und Poliklinik, Julius-Maximilians-Universität Würzburg
  • 2Kleinwachau, Sächsisches Epilepsiezentrum Radeberg gemeinnützige GmbH, Radeberg
  • 3Neurologische Klinik, Helios-Kliniken Schwerin
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Publikationsverlauf

Publikationsdatum:
06. Oktober 2010 (online)

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Zusammenfassung

Eine durch Antiepileptika induzierte Enzephalopathie (AIE) kann sich klinisch durch eine Verwirrtheit, eine Bewusstseinseinschränkung, neurologische Defizite oder eine Zunnahme der Anfallsfrequenz auszeichnen. Im Elektroencephalogramm können sich eine Allgemeinveränderung oder epileptische Entladungen finden. Laborchemisch charakteristisch sind die nicht toxischen Serumspiegel des Antiepileptikums. Unter der Behandlung von Valproinsäure, Phenytoin und Carbamazepin wurde bereits mehrfach eine AIE beschrieben. Seltener wurde eine AIE nach der Einnahme von Vigabatrin, Lamotrigin und Topiramat beobachtet. Als potenzielle pathogene Mechanismen werden die Hyperammonämie, intrinsische Wirkungen auf zerebrale Rezeptoren, medikamentöse Wechselwirkungen, hepatische Enzyminteraktionen, metabolische Ursachen oder paradoxe epileptogene Effekte der Antikonvulsiva diskutiert. Die Therapie besteht in der medikamentösen Umstellung der Antiepileptika sowie dem Absetzen des verantwortlichen Präparats.

Abstract

The clinical features of an antiepileptic drug-induced encephalopathy (ADE) are confusion, reduction of vigilance, neurological deficits or an increase of the seizure frequency. In the electroencephalogram a general slowing or epileptic discharges are found. Characteristic are non-toxic blood levels of the antiepileptic drugs. So far an ADE was reported under phenytoin, carbamazepine or valproatic acid (valproate) therapy. More seldom, an ADE has been described after the intake of vigabatrine, lamotrigine und topiramate. Potential pathogenic mechanisms of AED are hyperammonemia, intrinsic effects on cerebral receptors, drug interactions, hepatic enzyme interactions, metabolic reasons or paradoxical proconvulsive effects of antiepileptic drugs. The medicamentous therapy consists of an immediate discontinuation of the antiepileptic drug.

Schlüsselwörter

Valproinsäure - Antiepileptika-induzierte Enzephalopathie - Hyperammonämie - Zentrales Nervensystem - epileptische Entladungen

Keywords

valproatic acid (valproate) - antiepileptic drug-induced encephalopathy - hyperammonemia - central nervous system - epileptic discharges

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Dr. med. Niels Hansen

Neurologische Klinik und Poliklinik

Julius- Maximilians-Universität

Josef-Schneider-Straße 11

97080 Würzburg

eMail: Hansen_N@klinik.uni-wuerzburg.de

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