The role of sensorimotor cortex (anterior and posterior sigmoid gyri)
as the origin of enflurane-induced generalized seizures was examined a
nd compared to that of lidocaine-induced seizures in cats. The inhaled
enflurane concentration was adjusted at 3.5% in oxygen, the maximum p
otency to induce generalized seizures. Repetitive electrical stimulati
on with supramaximum intensity at a forepaw (2 Hz, 0.5 ms, 10 V) induc
ed generalized seizures, which ended with a sudden appearance of isoel
ectricity in the electroencephalogram (EEG), the so-called ''postictal
depression.'' Repetitive auditory stimuli also induced similar grand
mal-type EEGs.Unilateral ablation of the sensorimotor cortex completel
y blocked the induction of generalized seizures by contralateral somat
osensory stimuli. However, it had little effect on the induction of se
izures by ipsilateral somatosensory stimuli or bilateral auditory stim
uli. In contrast, bilateral ablation of the sensorimotor cortex did no
t have a significant effect on the lidocaine-induced seizures. These f
indings indicate that the involvement of the sensorimotor cortex is es
sential for the development of enflurane-induced but not lidocaine-ind
uced seizures.