INTERICTAL SPIKING INCREASES 2-DEOXY(C-14)GLUCOSE UPTAKE AND C-FOS-LIKE REACTIVITY

Although interictal spikes are thought to share pathophysiological mec hanisms with partial-onset seizure discharges, positron emission tomog raphic studies of the interictal state have paradoxically shown focal hypometabolism whereas seizures produce hypermetabolism To address thi s question, we performed functional mapping studies in an interictal s piking model in the rat. Recording screw electrodes were inserted thro ugh the skull bone so as to depress underlying cortex. Interictal spik ing was subsequently induced by systemic administration of bicuculline methiodide. 2-deoxy[C-14]glucose studies revealed increased glucose u tilization in superficial and middle cortical layers at spiking screw sites. Nonspiking screw sites in the same animals and in controls did not show increased uptake. Convulsive seizures caused additional 2-deo xy[C-14]glucose uptake at screw sites and in widespread forebrain area s. c-fos immunoreactivity occurred in superficial cortex at interictal spiking, but not nonspiking, sites. Convulsive seizures induced wides pread forebrain c-fos immunoreactivity. These data suggest interictal epileptiform activity occurs in cells adjacent to cortical injury; the se activate deeper layers via local connections. Interictal and ictal epileptiform states share common mechanisms, as both induce glucose hy permetabolism and immediate-early gene product activation. Possible re asons for failure to detect hypermetabolism in interictal human subjec ts are discussed.