Abstracts

Patients with temporal lobe epilepsy (TLE) commonly show prominent imaging abnormalities in flurodeoxyglycose positron emission tomography (FDG-PET). The underlying mechanisms responsible for these abnormalities are largely unknown. The kainic acid rat model of TLE demonstrates many of the pathophysiological characteristics of TLE including severe cell loss and synaptic reorganization in the hippocampus resembling hippocampal sclerosis. The present study aimed to determine if the FDG-PET abnormalities seen in TLE patients also developed in this model. Eight male wistar rats were implanted with recording electrodes into the left amygdala one week prior to the induction of status epilepticus (SE n=4, control n=4). SE was induced by hourly injections of kainic acid (5mg/kg i.p.) until continuous seizures were observed by EEG. SE continued for 4 hours before termination by injection of diazepam (4mg/kg). Serial FDG-PET scans were acquired 24 hours, two, four and six weeks post SE. The development of spontaneous recurrent seizures in each animal was confirmed prior to the scans at four and six weeks. FDG-PET demonstrated a distinct decrease in cerebral glucose metabolism 24 hours post SE (31% reduction). This hypometabolism persisted for the following five weeks (2 weeks 32%, 4 weeks 32%, 6 weeks 26%). The degree of hypometabolism did not appear to be affected by the onset of spontaneous recurrent seizures. This persistent hypometabolism was not seen in control animals (p[lt]0.05, repeated measures ANOVA). Kainic acid induced SE results in the development of persistent cerebral hypometabolism. This hypometabolism develops before and remains constant after the onset of spontaneous recurrent seizures. This indicates that the change in glucose utilization seen in this model is related to the process of epileptogenesis rather than being a secondary effect of recurrent seizures. These findings make it possible to conduct an investigation of the pathophysiological processes underlying changes in cerebral glucose metabolism in TLE utilizing this model.