Predictive Value of Cortical Injury on the Development of Temporal Lobe Epilepsy in Immature Rats: An MRI Approach Using the Lithium-Pilocarpine Model.
Abstract number :
3.046
Submission category :
Year :
2001
Submission ID :
2297
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
C. Roch, PhD student, UPRES-A 7004 ULP/CNRS, Strasbourg, France; C. Leroy, PhD student, INSERM U398, Strasbourg, France; A. Nehlig, PhD, INSERM U398, Strasbourg, France; I.J. Namer, MD, UPRES-A 7004 ULP/CNRS, Strasbourg, France
RATIONALE: In humans, it has been reported that patients with temporal lobe epilepsy (TLE) presented in their early childhood an initial precipitating injury (complicated febrile seizures, encephalitis, head trauma, etc.). However, not all children who have undergone injury have become epileptic. In parallel, the lithium-pilocarpine model of TLE leads after an initial status epilepticus (SE) to chronic epilepsy, with a intermediate silent phase characterized by neuronal lesions causing circuits to be reorganized. In 21-day old rats, only 67% became epileptic. A non invasive technique such as magnetic resonance imaging (MRI) enabled us to follow the evolution of the lesions after the SE in these rats and may explain the differences which make that one becomes epileptic or not.
METHODS: The SE was induced by administrating lithium (3 meq/kg) 18 h before pilocarpine was injected (30 mg/kg). MRI was performed on a MR scanner operating at 4.7 T. A 40 mm field of view, 256 x 256 pixel matrix and 1 mm slice thickness were used as imaging parameters. We followed the evolution of lesions, using a T2-weighted sequence, from 6 h to 3 months after pilocarpine injection.
RESULTS: Two populations of rats could be distinguished 24 h after the SE. In the first, a hypersignal appeared at the level of the piriform and entorhinal cortices, that disappeared 48 h after the SE while a hippocampal T2-weighted signal progressively developed; these animals did all become epileptic (6/11). The rest of the population, without MRI anomaly, could be subdivided into two groups when the chronic phase was reached: the first did not become epileptic (2/11), whereas the second did (3/11). A preliminary quantitative study, with T2 relaxation time measurements seems to show increased T2 times in the piriform and entorhinal cortices 24 h after the SE in the rats that became epileptic, but which did not present any qualitative anomaly on the T2-weighted images.
CONCLUSIONS: These first results suggest that the piriform and entorhinal cortices characterize the initial step leading to the development of epilepsy. However, the fact that some rats did become epileptic even though no cortical edema could be observed on qualitative images shows the limit of the sensitivity of T2-weighted images. A more sensitive technique such as diffusion, should allow to confirm these results.
Support: UPRES-A 7004 ULP/CNRS and INSERM U398