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
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