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Experimental tardive dyskinesia.

P J Bédard, R Boucher, L Larochelle

    Progress in Neuro-Psychopharmacology & Biological Psychiatry
    |January 1, 1982
    PubMed
    Summary
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    Researchers induced tardive dyskinesia-like symptoms in monkeys using haloperidol and midbrain lesions. These models offer insights into movement disorders and potential therapeutic targets.

    Area of Science:

    • Neuroscience
    • Pharmacology
    • Primate Models

    Background:

    • Tardive dyskinesia is a movement disorder often associated with antipsychotic use.
    • Reproducing tardive dyskinesia in animal models is crucial for understanding its mechanisms and developing treatments.

    Purpose of the Study:

    • To investigate two distinct methods for inducing dyskinesia resembling tardive dyskinesia in macaca mulatta.
    • To explore the neurological underpinnings of drug-induced and lesion-induced movement disorders.

    Main Methods:

    • Administered haloperidol (0.25 mg/kg daily for six months) to six monkeys, observing behavioral changes and inducing tremors.
    • Created electrolytic lesions in the midbrain of twelve monkeys, assessing subsequent motor function and dyskinesia.
    • Administered harmaline to assess potential damage to the rubro-olivo-cerebello rubral loop.

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  • Performed histological analysis of brain tissue to identify lesions and abnormalities.

    • Main Results:

    • Haloperidol administration induced restlessness, akinesia, and tremor. One monkey developed persistent buccolingual dyskinesia.
    • Midbrain lesions resulted in tremor in one monkey and buccolingual dyskinesia in five monkeys, lasting over a year.
    • The induced dyskinesia was exacerbated by dopaminergic agents and inhibited by haloperidol.
    • Histological analysis revealed lesions in the nucleus parafascicularis thalami region but spared the substantia nigra.

    Conclusions:

    • Both chronic haloperidol administration and midbrain lesions can elicit dyskinetic movements in non-human primates.
    • The findings suggest the involvement of specific brain pathways, potentially excluding the substantia nigra, in the pathophysiology of tardive dyskinesia.
    • These primate models provide valuable tools for studying dopamine-related movement disorders.