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Neuropathologische Befunde bei Fieberkrämpfen

Neuropathological findings in patients with prolonged febrile seizures

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Zusammenfassung

Fieberkrämpfe treten bei Epilepsiepatienten im Vergleich zur Gesamtbevölkerung häufiger auf. Zudem findet sich eine enge Assoziation zwischen frühkindlichen Fieberkrämpfen vor dem 4. Lebensjahr und der Entwicklung einer chronischen, pharmakoresistenten Schläfenlappenepilepsie („temporal lobe epilepsy“, TLE). Tierexperimentelle Modelle bestätigen diese Beobachtung. Wird bei jungen Ratten durch eine Hyperthermie ein Fieberkrampf ausgelöst, entwickeln 35% der Tiere eine limbische Epilepsie. Diese Ergebnisse legen nahe, dass frühkindliche, prolongierte Fieberkrämpfe eine Ursache für die Entstehung der TLE darstellen, v. a., da regionen- und zellspezifische Veränderungen im Hippocampus der behandelten Tiere nachzuweisen sind. In diesem Artikel sollen diejenigen molekularbiologischen und neuropathologischen Befunde diskutiert werden, welche die Entstehung einer chronischen pharmakoresistenten Temporallappenepilepsie infolge frühkindlicher Fieberkrämpfe erklären helfen.

Abstract

Patients suffering from drug-resistant temporal lobe epilepsy (TLE) frequently reported about prolonged febrile seizures during their early childhood. Neuropathological evaluation of neurosurgical specimens obtained from TLE patients with prolonged febrile seizures before the age of 4 years compared with specimens from TLE patients without febrile seizures has revealed a few interesting differences: Segmental neuronal cell loss is usually more severe, the architecture of the granule cell layer is usually more disturbed, and postsurgical seizure control is usually more successful. On the other hand, hippocampal cell loss was not observed in a rat model of febrile seizures. In this model, young rats were submitted to hyperthermia and experienced prolonged febrile convulsions. One-third of the animals developed chronic limbic epilepsy. This animal model, by unraveling the effects of prolonged febrile seizures on neuronal function, thereby identified several molecular pathomechanisms and the potential contribution of such seizures to epilepsy.

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Blümcke, I. Neuropathologische Befunde bei Fieberkrämpfen. Z. Epileptol. 22, 216–219 (2009). https://doi.org/10.1007/s10309-009-0060-y

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