Abstracts

Rationale: Lithium-pilocarpine status epilepticus (SE) in rats heralds spontaneous recurrent seizures after a latent period. It therefore reproduces the temporal course of mesial temporal lobe epilepsy in humans. Focal ictal hypermetabolism and postictal hypometabolism are common findings in epileptic patients evaluated by positron emission tomography (PET). The aim of our study is to determine the very early modifications of regional utilization of glucose after SE using 2-[18F]-fluoro-2-deoxy-D-glucose small animal PET (microPET). Methods: Young adult rats were subjected to lithium-pilocarpine induced SE (n=8). Controls were injected lithium and saline (n=7). Brain microPET (4 and 48 h after SE) and MRI (24 h after SE) were performed under isoflurane anesthesia. Regional glucose uptake was determined in 18 regions of interest formerly assigned on MRI. Results were normalized to brain global glucose uptake. Results: All rats treated with lithium and pilocarpine became epileptic. Twenty four hours after SE, these animals exhibited dramatic T2 hypersignal in hippocampus, parahippocampal cortices, amygdala and thalamic nuclei. Four hours after SE, lithium-pilocarpine treated rats exhibited a significant increase in glucose uptake in CA3 ( 17%) and parahippocampal structures: amygdala complex ( 10%), piriform cortex ( 23%) and entorhinal cortex ( 14%). This hypermetabolism did not last since by 48 h brain global hypometabolism was recorded, more strikingly in para-hippocampal cortices (-23%). Conclusions: Our study reproduced early MRI and microPET findings after lithium-pilocarpine induced SE. We also showed a transient increase in CA3 and para-hippocampal structures at the early acute phase of the SE. These regions are known to exhibit the marked neuronal loss in this model and to be key structures involved in epileptogenesis.