Magnetic resonance imaging follow-up of progressive hippocampal changes ina mouse model of mesial temporal lobe epilepsy

Citation
V. Bouilleret et al., Magnetic resonance imaging follow-up of progressive hippocampal changes ina mouse model of mesial temporal lobe epilepsy, EPILEPSIA, 41(6), 2000, pp. 642-650
Citations number
54
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EPILEPSIA
ISSN journal
00139580 → ACNP
Volume
41
Issue
6
Year of publication
2000
Pages
642 - 650
Database
ISI
SICI code
0013-9580(200006)41:6<642:MRIFOP>2.0.ZU;2-8
Abstract
Purpose: Hippocampal sclerosis (HS) is the most frequent lesion found in me sial temporal lobe epilepsy (mTLE). MR imaging is considered to be the most sensitive and specific method to detect HS. Despite extensive studies perf ormed on humans and except in a recent study, the morphologic pattern of HS is usually analyzed when the disease has already fully developed, thus not allowing any insight into the mapping of the progressive morphologic chang es inducing the development of mTLE. We have recently characterized a model of mTLE that reproduces the unilateral pattern of I-IS, induced by intrahi ppocampal injection of low doses of kainate (KA) in mice. Methods: In this study, we monitored the temporal evolution of the developm ent of HS in this model of mTLE by using T-2-weighted sequence, T-2-relaxat ion time measurements, and T-1-weighted spin-echo technique after injection of gadolinium, from 1 h to 120 days after KA injection. Results: HS induced by intrahippocampal KA injection occurred in two phases . First, we observed a transient hyperintense T-2-weighted signal in the co rtex above the injected hippocampus, most likely indicative of vasogenic ed ema partly due to the neurotoxic effect of KA. The concomitant increase in the T-2 signal in the injected hippocampus and ipsilateral amygdala likely reflects the phase of cytotoxic edema occurring probably in relation to the excitotoxic consequences of both KA and seizure activity. Second, from 15 days on, a persistent unilateral increased T-2 signal was detected in the h ippocampus, which most probably reflects gliosis. Conclusions: Our findings indicate that longitudinal followup would permit a better understanding of the mechanisms underlying the constitution of HS in humans and eventually development of prevention strategies.