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Predictive Value of Cortical Injury for the Development of Temporal Lobe Epilepsy in 21‐day‐old Rats: An MRI Approach Using the Lithium‐pilocarpine Model
Author(s) -
Roch Catherine,
Leroy Claire,
Nehlig Astrid,
Namer Izzie J.
Publication year - 2002
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1046/j.1528-1157.2002.17802.x
Subject(s) - epilepsy , status epilepticus , temporal lobe , piriform cortex , hippocampal sclerosis , pilocarpine , entorhinal cortex , hippocampus , population , psychology , medicine , neuroscience , anesthesia , environmental health
Summary: Purpose: Patients with temporal lobe epilepsy (TLE) usually had an initial precipitating injury in early childhood. However, epilepsy does not develop in all children who have undergone an early insult. As in patients, the consequences of the lithium‐pilocarpine‐induced status epilepticus (SE) are age dependent, and only a subset of 21‐day‐old rats will develop epilepsy. Thus with magnetic resonance imaging (MRI), we explored the differences in the evolution of lesions in these two populations of rats. Methods: SE was induced in 21‐day‐old rats by the injection of lithium and pilocarpine. T 2 ‐weighted images and T 2 relaxation‐time measurements were used for detection of lesions from 6 h to 4 months after SE. Results: Three populations of rats could be distinguished. The first one had neither MRI anomalies nor modification of the T 2 relaxation time, and these rats did not develop epilepsy. In the second one, a hypersignal appeared at the level of the piriform and entorhinal cortices 24 h after SE (increase of 49% of the T 2 relaxation time in the piriform cortex) that began to disappear 48–72 h after SE; epilepsy developed in all these animals. The third population of rats showed a more moderate increase of the T 2 relaxation time in cortices (14% in the piriform cortex) that could not be seen on T 2 ‐weighted images. Epilepsy developed in all these rats. Only in a subpopulation of the 21‐day‐old rats with epilepsy did hippocampal sclerosis develop. Conclusions: These results suggest that the injury of the piriform and entorhinal cortices during SE play a critical role for the installation of the epileptic networks and the development of epilepsy.