Abstracts

RATIONALE: The mechanisms underlying interictal hypometabolism in and outside the neuropathological lesion in patients with TLE remain unclear. The lithium-pilocarpine model reproduces most aspects of human TLE. We investigated the age-dependent relationship between interictal metabolism and neuronal loss during the chronic period. METHODS: SE was induced by pilocarpine to lithium-pretreated P10, P21 or adults rats. Rats were implanted and monitored for spontaneous seizures (SRS) over 2 to 5 months according to age of SE induction. Then, interictal cerebral glucose utilization was measured with [14C]2-deoxyglucose and neuronal loss was counted on adjacent sections. RESULTS: In P10 rats, 7 months after SE, there were no metabolic changes, no neuronal loss and no epilepsy. In P21 rats, after 74 days, 3 groups of rats were distinguished: rats with SRS (24%), triggered seizures (43%) and no seizures (33%). All adult rats became epileptic after 25 days. In adult and P21 rats, during the chronic phase, interictal hypometabolism occurred in cortical, limbic and thalamic regions while these areas were normometabolic in P21 SRS rats. Neuronal dropout occurred in these regions at P21 but was more robust in adults. CONCLUSIONS: In this model, interictal metabolic changes are age-dependent. There is no obvious correlation between interictal hypometabolism and neuronal loss as reported in human TLE.