Gamma-vinyl-GABA treatment of tardive dyskinesia and other movement disorders

1985 ◽  
Vol 20 (8) ◽  
pp. 888-893 ◽  
Author(s):  
Stephen M. Stahl ◽  
Joe E. Thornton ◽  
Mary L. Simpson ◽  
Philip A. Berger ◽  
Michael J. Napoliello
Author(s):  
Susan H. Fox

Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement (i.e., chorea or dystonia) is important because treatment options can differ according to the type of dyskinesia present.


1992 ◽  
Vol 22 (1) ◽  
pp. 69-77 ◽  
Author(s):  
K. W. Brown ◽  
T. White ◽  
D. Palmer

SYNOPSISNeuropsychological tests of frontal lobe functions were undertaken in 46 chronic schizophrenic patients who were also rated for movement disorders. Tardive dyskinesia was found to have significant associations with most of these psychological tests. The possible mechanisms are discussed within the context of known neostriatal psychological functions.


1976 ◽  
Vol 128 (5) ◽  
pp. 490-493 ◽  
Author(s):  
William E. Fann ◽  
John L. Sullivan ◽  
Bruce W. Richman

SummaryHyperkinetic movement disorders may occur as side effects of antipsychotic drugs; and a hyperdopaminergic state induced by the neuroleptic compounds is thought to be a cause of extrapyramidal disorders such as tardive dyskinesia. We have observed two cases of the dyskinetic syndrome in patients receiving tricyclic antidepressants (TCA). Because the TCA are known to have little effect on striatal dopamine but do share with the neuroleptics potent anticholinergic activity, these cases appear to support the hypothesis that the drug-induced hyperkinetic disorders are related to a diminution of CNS acetylcholine activity as well as to an increase in dopamine activity.


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