Dyskinetic Syndrome Research Articles

Neuroleptic-induced acute dyskinesias in squirrel monkeys: correlation with propensity to cause extrapyramidal side effects.

In squirrel monkeys that had undergone repeated treatment with haloperidol at intervals of 7--14 days, subsequent acute administration of haloperidol induced dystonia and dyskinesias. This acute effect of haloperidol was dose-related and occurred at the same doses that impaired Sidman avoidance performance. Chlorpromazine, fluphenazine, metoclopramide, tetrabenazine, and Su-23397, all of which have been associated with extrapyramidal side effects, reliably elicited dyskinesias in these monkeys. Dyskinesias were less mared after thioridazine and absent after clozapine, corresponding to the reported lower incidence of extrapyramidal side effects in the clinic. The non-neuroleptics, baclofen, and diazepam, failed to elicit dyskinesias. In contrast to the dyskinetic syndrome, the incidence of catalepsy or tremor did not accurately predict propensity to elicit extrapyramidal symptomatology. The acute dyskinetic syndrome in squirrel monkeys may therefore serve as an animal model for predicting the ability of antipsychotics to cause extrapyramidal dysfunction, and may yield insight into the mechanisms of these drug-induced motor disorders.

Pharmacological Modification of Experimental Tardive Dyskinesia

Cebus apella monkeys subjected to chronic haloperidol administration develop neurologic disturbances very similar to neuroleptic-induced acute dystonia human beings. After varying lengths of time, certain monkeys develop a prolonged dyskinetic syndrome resembling tardive dyskinesia (TD), as seen clinically. Two monkeys with signs of TD were given single intramuscular injections of various compounds with known effects on the catecholaminergic, cholinergic, serotoninergic and GABA-ergic neurotransmittor systems, and their effect on the TD signs were rated. Dopamine receptor blockers as well as cholinergics had an ameliorating effect on the symptoms. Some compounds known to activate the GABA system, including some benzodiazepines and the GABA-transaminase inhibitor amino-oxyacetic acid, also reduced the symptoms, as did the serotonin precursor L-5HTP. Results with serotonin antagonists were equivocal. It is concluded that dopamine receptor blockade, as well as increased activity within the GABA-ergic or cholinergic systems cause alleviation of TD. The findings are in agreement with earlier reports in man and thus seem to validate this primate model.

High-dose oral dicloxacillin treatment of acute staphylococcal osteomyelitis in children

dyskinetic syndrome in glutaric aciduria, Neuro Pediatr 8:397, 1977. 6. Christensen E, and Brandt NJ: Studies on glutaryl-CoA dehydrogenase in leucocytes, fibroblasts and amniotic fluid ceils. The normal enzyme and the mutant form in patients with glutaric aciduria, Clin Chim Acta 88:267, 1978. 7, Goodman SI, Norenberg MD, Shikes RH, Breslich D J, and Moe PG: Gtutaric aciduria: Biochemical and morphologic considerations, J PEDIArR 90:746, 1977. 8. Brandt N J, Rasmussen K, Brandt S, Kr S, and Schcnheyder F: o-Glyceric acidemia and non-ketotic hyperglycinaemia, Acta Paediatr Scand 65:17, 1976. 9. Thompson JA, and Markey SP: Quantitative metabolic profiling of organic acids by gas-chromatography-mass spectrometry: Comparison of isolation methods, Anal Chim 47:1313, 1975. 10. Besrat A, Polan CE, and Herderson LM: Mammalian metabolism of glutaric acid, J Biol Chem 244:1461, 1969. 11. Stokke O, Goodman SI, and Moe PG: Inhibition of brain glutamate decarboxylase by glutarate, glutaconate, and beta-hydroxyglutarate: Explanation of the symptoms in glutaric aciduria? Clin Chim Acta 66:411, 1976. 12. Robert E: Disinhibition as an organizing principle in the nervous sytem-the role of the GABA system. Application to neurologic and psychiatric disorders, in Robert E, Chaze TN, and Tower DB editors: GABA in nervous system function, New York 1976, Raven Press.

Clinical research techniques in tardive dyskinesia.

The authors have developed standardized assessment and control techniques designed to provide objective measures of tardive dyskinesia in patients progressing through an experimental treatment program. Standardized videotaping is carried out and blind ratings on the Abnormal Involuntary Movement Scale are made by a team of psychiatrists and neurologists. Other assessments include several measurements of vocal function and a quantitative acceleration profile standardized on normal subjects. Such measures allow quantifiable determination of response to drug treatment and may provide clues to the etiology and definition of the dyskinetic syndrome.

Dyskinesias associated with tricyclic antidepressants.

Hyperkinetic 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.

Carbon monoxide poisoning: recovery associated with a transient dyskinetic syndrome.

Carbon monoxide poisoning: recovery associated with a transient dyskinetic syndrome.

DYSKINETIC SYNDROME ASSOCIATED WITH CHLORPROTHIXENE.

DYSKINETIC SYNDROME ASSOCIATED WITH CHLORPROTHIXENE.

Reversible and irreversible dyskinesia after treatment with perphenazine, chlorpromazine, reserpine and electroconvulsive therapy

A dyskinetic syndrome consisting of involuntary grimaces, mastication, and propulsion of the tongue, in some cases in connection with akathisia and tasikinesia, due to electroconvulsive therapy, has been observed in 4 patients.