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Fieberkrampf und Magnetresonanztomographie

Febrile seizures and magnetic resonance imaging

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Zusammenfassung

Selten folgt eine therapierefraktäre Epilepsie unmittelbar auf einen Fieberkrampf. Trotzdem berichten Populationsstudien über einen Zusammenhang zwischen kompliziertem Fieberkrampf in der Kindheit (KFK; fokal, prolongier, als Status oder Serie) und einer Temporallappenepilepsie mit mesialer Temporallappensklerose (MTS), typischerweise mit einem Beginn in der Jugend. Es wird kontrovers diskutiert, warum einem frühen, andernfalls oft harmlosen Ereignis, das der unkomplizierte Fieberkrampf darstellt, mit einer Latenz die Ausbildung eines spezifischen, oftmals therapierefraktären Epilepsiesyndroms folgt. Drei verschiedene Erklärungshypothesen wurden formuliert: 1. „Innocent-Bystander-Hypothese“: ein normaler Hippokampus wird durch den KFK geschädigt, und diese Schädigung entwickelt sich zur MTS; 2. „Two-hit-Hypothese“: subtile, präexistierende, strukturelle hippokampale Veränderungen oder genetische Prädisposition führen zu einer Empfindlichkeit, KFK zu entwickeln und statusbedingte Schäden zu erleiden, die sich zur MTS entwickelt; 3. „Been there, done that-Hypothese“: eine präexistierende MTS zeigt sich nach KFK mit akutem Ödem. Bildgebungsuntersuchungen weisen bei Patienten mit KFK auf eine postiktale Schädigung hippokampaler Strukturen hin. Subtile hippokampale Veränderungen im Sinne von Malformationen scheinen dabei die Anfälligkeit für die Entstehung einer MTS nach KFK zu erhöhen. Biomarker für die Epileptogenese ist möglicherweise ein erhöhtes hippokampales T2-Signal unmittelbar nach fieberassoziierten Anfällen. Patienten mit postiktalen hippokampalen Veränderungen sind möglicherweise eine Zielgruppe für präventive Therapieansätze.

Abstract

It is rare that a febrile seizure results immediately in a pharmacoresistant focal epilepsy. Population-based studies, however, report an association between complicated febrile seizures (i.e., those with focal features, a prolonged course, or an occurrence as status epilepticus) in childhood and temporal lobe epilepsy with mesial temporal sclerosis in early adolescence. There is controversy whether a seemingly harmless event like a febrile seizure can lead to treatment refractory epilepsy after a silent period often of many years. Three main hypotheses are formulated: 1. “Innocent bystander” hypothesis: a normal hippocampus is damaged by the complicated febrile seizure and the damage develops to become mesial temporal sclerosis; 2. “Two hit” hypothesis: subtle pre-existing structural changes in the hippocampus and temporal lobe predispose for hippocampal damage by febrile status epilepticus which develops to mesial temporal sclerosis; 3. “Been there, done that” hypothese: mesial temporal sclerosis exist prior to febrile seizures and develops further afterwards. Neuroimaging studies demonstrate postictal hippocampal damage after complicated febrile seizures. Subtle hippocampal malformations, in the sense of malformations, seem to increase the susceptibility to damage following febrile seizures. A prominent MRI feature after febrile seizures might be hippocampal edema. Patients with hippocampal edema after febrile seizures might be a target group for the pharmacological prevention of the further development towards mesial temporal sclerosis.

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  1. MRT, Krankenhaus Mara, Epilepsiezentrum Bethel, 33617, Bielefeld, Deutschland

    F.G. Woermann

  2. Institute of Neurology, University College London, London, UK

    M.J. Koepp

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  1. F.G. Woermann
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  2. M.J. Koepp
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Correspondence to F.G. Woermann.

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Woermann, F., Koepp, M. Fieberkrampf und Magnetresonanztomographie. Z. Epileptol. 22, 220–224 (2009). https://doi.org/10.1007/s10309-009-0077-2

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  • DOI: https://doi.org/10.1007/s10309-009-0077-2

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