Seizure activity per se does not induce tissue damage markers in human neocortical focal epilepsy

Summary

Objective The contribute of recurring seizures to the progression of epileptogenesis is debated. Seizure-induced brain damage is not conclusively demonstrated both in humans and in animal models of epilepsy. We evaluated the expression of brain injury biomarkers on post-surgical brain tissue obtained from 20 patients with frequent seizures and a long history of drug-resistant focal epilepsy.

Methods The expression patterns of specific glial, neuronal and inflammatory molecules was evaluated by immunohistochemistry in the core of type II focal cortical dysplasias (FCD-II), at the FCD boundary (perilesion) and in the adjacent normal-appearing area included in the epileptogenic region. We also analysed surgical specimens from cryptogenic patients not presenting structural alterations at imaging.

Results Astroglial and microglial activation, reduced neuronal density, peri-vascular CD3-positive T lymphocytes clustering and fibrinogen extravasation were demonstrated in the core of FCD-II lesions. No pathological immunoreactivity was observed outside the FCD-II and in cryptogenetic specimens, where the occurrence of interictal and ictal epileptiform activity was confirmed by either stereo-EEG or intraoperative electrocorticography.

Interpretation Recurrent seizures do not induce the expression of brain damage markers in non-lesional epileptogenic cortex studied on post-surgical tissue from cryptogenic and FCD patients. This evidence argues against the hypothesis that epileptiform activity per se contributes to focal brain injury, at least in the neocortical epilepsies here considered. This article is protected by copyright. All rights reserved.

http://ift.tt/2vMwF18