Molecular neuropathology of human mesial temporal lobe epilepsy

Citation
I. Blumcke et al., Molecular neuropathology of human mesial temporal lobe epilepsy, EPILEPSY R, 36(2-3), 1999, pp. 205-223
Citations number
135
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
EPILEPSY RESEARCH
ISSN journal
09201211 → ACNP
Volume
36
Issue
2-3
Year of publication
1999
Pages
205 - 223
Database
ISI
SICI code
0920-1211(199909)36:2-3<205:MNOHMT>2.0.ZU;2-7
Abstract
With the recent progress in surgical treatment modalities, human brain tiss ue from patients with intractable focal epilepsies will increasingly become available for studies on the molecular pathology, electrophysiological cha nges and pathogenesis of human focal epilepsies. An inherent problem for st udies on human temporal lobe epilepsy (TLE) is the lack of suitable control s. Strategies to alleviate this obstacle include the use of human post mort em samples, hippocampus from experimental animals and, in particular, the c omparative analysis of surgical specimens from patients with Ammon's horn s clerosis (AHS) and with focal temporal lesions but anatomically preserved h ippocampal structures. In this review we focus on selected aspects of the m olecular neuropathology of TLE: (1) the potential impact of persisting calr etinin-immunoreactive neurons with Cajal-Retzius cell morphology, (2) astro cytic tenascin-C induction and redistribution as potential regulator of abe rrant axonal sprouting and (3) alterations of Ca2+-mediated hippocampal sig nalling pathways. The diverse and complex changes described so far in human TLE specimens require a systematic interdisciplinary approach to distingui sh primary, epileptogenic alterations and secondary, compensatory mechanism s in the pathogenesis of human temporal lobe epilepsies. (C) 1999 Elsevier Science B.V. All rights reserved.