Abstracts

Evidence is accumulating that absence seizures have a cortical origin. Based on neurophysiological studies, immunocytochemistry, morphometric in vitro and pharmacological studies in vivo it has been demonstrated that various disturbances in the somatosensory cortex in WAG/Rij, but also in GAERS, might underly the origin of the spike-wave discharges (SWD), the electroencephalographic hallmark of absence seizures. Here we investigated whether local (at the somatosensory cortex) application of phenytoine, a drug that promotes SWD after systemic administration, is effective in reducing the number of SWD. Adult male WAG/Rij rats were equipped cortical EEG electrodes and bilateral canulla[apos]s for cortical administraion of the drug. Canulla[apos]s were located at the peri-oral part of the somatosensory cortex. Rats were either systemically injected with a dose of 40 mg/kg phenytoin or saline, or with 360 pmol/500 nl per side and Ringer as control. EEG[apos]s were recorded one hour before and after two hours after administration, number and mean duration of SWD were quantified. Systemic injection of phenytoin doubled the number (p[lt].05) the number of SWD, the effect ocured immediately and persisted for 2 hours. In contrast, local injection of phenytoin reduced (p[lt].01) the number of SWD, also for at least 2 hours. In fact all SWDs were nearly abolished. The results demonstrate that phenytoin has opposite effects on absence seizures: the are aggravated after systemic administration, but reduced after administration to the somatosensory cortex. The results are also in favour of the cortical focus theory of absence epilepsy which suggests that absence epilepsy is secondary generalized.