Evoked metabolic responses in the limbic-striate system produced by stimulation of anterior thalamic nucleus in man.
Six human subjects (5 male, 1 female, age 23.7 + 5.7 years) with incapacitating partial seizure disorders intractable to medical therapy have been treated by ongoing pulsed electrical stimulation of anterior nucleus of the thalamus. Four of the six patients have demonstrated statistically significant clinical control of the seizure disorder. One patient (D.L.) has been seizure-free for the last two years. In two of these six patients, it was possible to study not only electrophysiological activity of the brain, but also regional cerebral glucose metabolism by the (18F) 2-fluoro-2-deoxy-D-glucose method, blood cortisol levels, and blood levels of valproic acid, diphenylhydantoin, and carbamazepine. Significant changes were seen during periods of stimulation compared with control periods without stimulation. These results imply that stimulation of the principal thalamic relay nucleus of the limbic system causes clinical, behavioral, cerebral metabolic, electroencephalographic, endocrinologic, and pharmacokinetic responses.
D000328:Adult; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism; D002220:Carbamazepine / Q000097:blood; D004599:Electric Stimulation Therapy; D004833:Epilepsy, Temporal Lobe / Q000628:therapy*; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008032:Limbic System / Q000502:physiology*; D008297:Male; D010672:Phenytoin / Q000097:blood; D011877:Radionuclide Imaging; D013787:Thalamic Nuclei / Q000502:physiology*; D014635:Valproic Acid / Q000097:blood
D002220:Carbamazepine; D014635:Valproic Acid; D010672:Phenytoin; D005947:Glucose; D006854:Hydrocortisone