Contribution of Magnetic Resonance Imaging to the Study of the Lithium-Pilocarpine Model of Temporal Lobe Epilepsy in Adult Rats.
Abstract number :
1.181
Submission category :
Year :
2000
Submission ID :
2887
Source :
www.aesnet.org
Presentation date :
12/2/2000 12:00:00 AM
Published date :
Dec 1, 2000, 06:00 AM
Authors :
Catherine Roch, Claire Leroy, Astrid Nehlig, Christian Marescaux, Izzie J Namer, UPRES-A 7004 CNRS, Strasbourg, France; INSERM U 398, Strasbourg, France; UPRES-A 7004 CNRS, Strabourg, France.
RATIONALE:In temporal lobe epilepsy, we do not know if hippocampal sclerosis is the cause or the consequence of epilepsy. The lithium-pilocarpine model in the rat is a model of epilepsy with the same time course as in patients. After pilocarpine injection, the animals develop a severe status epilepticus (SE) and, after an average 14 days' period of latency, they exhibit spontaneous recurrent seizures with a frequency of 2 to 5 per week. We have studied the temporal evolution of the lesions in this model by the magnetic resonance imaging (MRI) to determine the progressive morphological changes inducing the appearance of chronic epilepsy. METHODS:_SE is induced by lithium administration (3 meq/kg) 20 h before pilocarpine is injected (25 mg/kg). MRI was performed on a MR scanner operating at 4.7T. We followed the evolution of lesions using a T2- and T1-weighted sequences before and after the injection of gadolinium. RESULTS:_24 h after pilocarpine injection, a transient but important increase in T2-weighted signal appeared in the piriform and entorhinal cortex and some thalamic nuclei. This hyper-signal showed an edema without obvious BBB breakdown. Two days after the pilocarpine, a slight increase in T2-weighted signal was seen in dorsal and ventral hippocampus. The signal hyperintensity in the hippocampus, corresponding to an edema, intensified until the end of the study but the hyperintensity of the T2-weighted signal disappeared about 5 days after the pilocarpine in the piriform and entorhinal cortex and subsequently reappeared in almost all animals in the beginning of the chronic phase, i.e an average of 3 weeks after the pilocarpine. This second phase reflects gliosis. CONCLUSIONS: This results show the difference in the reactivity to pilocarpine between the cortex and the hippocampus. Hippocampal sclerosis could be the consequence of recurrent seizures because it progressively gets worse whereas the cortical reaction involves 2 phases: the first caused by a lesion, the second linked to the gliosis resulting from seizures.