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

C Roch, C Leroy, A Nehlig, IJ Namer - Epilepsia, 2002 - Wiley Online Library
C Roch, C Leroy, A Nehlig, IJ Namer
Epilepsia, 2002Wiley Online Library
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 …
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. T2‐weighted images and T2 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 T2 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 T2 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 T2 relaxation time in cortices (14% in the piriform cortex) that could not be seen on T2‐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.
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