Catherine Roch1, Claire Leroy, Astrid Nehlig, Izzie J Namer. 1. Institut de Physique Biologique (UMR 7004 ULP/CNRS/IFR37), Faculté de Médecine, 4 rue Kirschleger, 67085 Strasbourg Cedex, France. roch@ipb.u-strasbg.fr
Abstract
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 T(2)- and T(1)-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 T(2)-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.
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 T(2)- and T(1)-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 T(2)-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.
Authors: J P Munasinghe; M Banerjee; M T Acosta; M Banks; A Heffer; A C Silva; A Koretsky; W H Theodore Journal: Acta Neurol Scand Date: 2009-11-25 Impact factor: 3.209
Authors: Maria Thom; Sofia Eriksson; Lillian Martinian; Luis O Caboclo; Andrew W McEvoy; John S Duncan; Sanjay M Sisodiya Journal: J Neuropathol Exp Neurol Date: 2009-08 Impact factor: 3.685