Segmental inhibition was elicited in the spinal trigeminal nucleus of cats by delivering a conditioning stimulus to the maxillary nerve 100 msec before the test stimulus. Carbamazepine, baclofen, and phenytoin markedly facilitated this segmental inhibition, as well as depressing the response to an unconditioned maxillary nerve stimulus. Phenobarbital, on the other hand, usually depressed the segmental inhibition. These results suggest that drugs that relieve trigeminal neuralgia both facilitate inhibitory mechanisms and depress excitatory mechanisms in the spinal trigeminal nucleus. The facilitation of inhibitory mechanisms appears to be at least as important as the depression of excitatory mechanisms and suggests that a failure of inhibitory mechanisms may play a significant role in the pathogenesis of trigeminal neuralgia.

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A double-blind crossover study with imipramine was conducted in 10 patients with absence and myoclonic-astatic seizures who had not responded to conventional medications. Imipramine produced a significant initial decrease in seizure frequency in 5 of the 10 patients, and in 2 patients the beneficial effect was maintained for more than 1 year. An open trial of imipramine in another 16 patients showed an initial reduction in seizure frequency in 10 patients (63 percent), and this decrease persisted for more than 1 year in 4 patients (25 percent). The effect of imipramine on the EEG did not always correlate with the clinical response. Serum content of imipramine in the patients who showed a long-term response was 40 to 120 ng per milliliter, on a total daily dose of 0.7 to 3.5 mg per kilogram. These results suggest that imipramine is a valuable addition to the treatment of seizures.

Conditioning stimuli to the coronal gyrus or periventricular gray matter inhibit the activity of spinal trigeminal neurons. Valproate decreased the corticofugal inhibition of the spinal trigeminal nucleus, as did ethosuximide, trimethadione, and imipramine. Valproate and ethosuximide also decreased the periventricular inhibition of the spinal trigeminal nucleus, indicating that antiabsence drug depress subcortical inhibitory pathways as well as pathways of cortical origin. These results support the hypothesis that ability to depress inhibitory pathways is an important characteristic of antiabsence drugs. The effect of valproate and ethosuximide on periventricular inhibition also suggests that these anticonvulsants may act by preventing the spread of seizure activity through subcortical pathways.