Magnetic Resonance Imaging in the Study of the Lithium–Pilocarpine Model of Temporal Lobe Epilepsy in Adult Rats
Article first published online: 22 APR 2002
Volume 43, Issue 4, pages 325–335, April 2002
How to Cite
Roch, C., Leroy, C., Nehlig, A. and Namer, Izzie J. (2002), Magnetic Resonance Imaging in the Study of the Lithium–Pilocarpine Model of Temporal Lobe Epilepsy in Adult Rats. Epilepsia, 43: 325–335. doi: 10.1046/j.1528-1157.2002.11301.x
- Issue published online: 22 APR 2002
- Article first published online: 22 APR 2002
- Revision accepted January 2, 2002.
- Temporal lobe epilepsy;
- Hippocampal sclerosis;
- Magnetic resonance imaging
Summary: Purpose: In temporal lobe epilepsy, it remains to be clarified whether hippocampal sclerosis is the cause or the consequence of epilepsy. We studied the temporal evolution of the lesions in the lithium–pilocarpine model of epilepsy in the rat with magnetic resonance imaging (MRI) to determine the progressive morphologic changes occurring before the appearance of chronic epilepsy.
Methods: MRI was performed on an MR scanner operating at 4.7 T. We followed the evolution of lesions using T2- and T1-weighted sequences before and after the injection of gadolinium from 2 h to 9 weeks.
Results: At 2 h after status epilepticus (SE), a blood–brain barrier breakdown could be observed only in the thalamus; it had disappeared by 6 h. At 24 h after SE, edema was present in the amygdala and the piriform and entorhinal cortices together with extensive neuronal loss; it disappeared progressively over a 5-day period. During the chronic phase, a cortical signal reappeared in all animals; this signal corresponded to gliosis, which appeared on glial fibrillary acidic protein (GFAP) immunohistochemically stained sections as hypertrophic astrocytes with thickened processes. In the hippocampus, the correlation between histopathology and T2-weighted signal underscored the progressive constitution of atrophy and sclerosis, starting 2 days after SE.
Conclusions: These data show the reactivity of the cortex that characterizes the initial step leading to the development of epilepsy and the late gliosis that could result from the spontaneous seizures. Moreover, it appears that hippocampal sclerosis progressively worsened and could be both the cause and the consequence of epileptic activity.