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NEUROLOGY 1980;30:126
© 1980 American Academy of Neurology

Antiabsence drugs and inhibitory pathways

Gerhard H. Fromm, M. D., Jay D. Glass, Ph.D., Amrik S. Chattha, M. D., A. Julio Martinez, M. D. and Michael Silverman, B.S.

Departments of Neurology (Drs. Fromm and Chattha and Mr. Silverman), Pharmacology (Dr. Glass), and Pathology (Dr. Martinez), University of Pittsburgh School of Medicine, Pittsburgh, PA.

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 drugs 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.

Address correspondence and reprint requests to Dr. Fromm, Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15261.

Accepted for publication July 11, 1979.

Presented in part at the thirtieth annual meeting of the American Academy of Neurology, Los Angeles, April 1978.

Supported in part by Grant No. S-10 from the Health Research Services Foundation of Pittsburgh.






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