Sustained improvement in tardive dyskinesia with diazepam: indirect evidence for corticolimbic involvement.
A rater-bind, ABA's design study of 21 cases indicates that diazepam significantly improves tardive dyskinesia and that some of the improvement persists for an extended period after diazepam is withdrawn. Since benzodiazepine receptors and sites of action seem to be mainly in the neocortex (especially frontal), limbic cortex, and deep limbs nuclei, and these structures provide most of the input into the nigrostriatopallidal system that probably regulates its role in voluntary movement, it may be suggested that impaired corticolimbic control of basal ganglia may be a factor in the pathogenesis of tardive dyskinesia.
D000328:Adult; D000368:Aged; D002540:Cerebral Cortex / Q000032:analysis / Q000503:physiopathology*; D003975:Diazepam / Q000494:pharmacology / Q000627:therapeutic use*; D004409:Dyskinesia, Drug-Induced / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008032:Limbic System / Q000032:analysis / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011956:Receptors, Cell Surface / Q000032:analysis / Q000187:drug effects; D011963:Receptors, GABA-A
D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D003975:Diazepam