Related Experiment Videos
Tardive dyskinesia: pathophysiology and animal models
1Mental Illness Research, Education and Clinical Center, Veterans Affairs Medical Center, Portland, OR 97201, USA. daniel.casey@med.va.gov
The Journal of Clinical Psychiatry
|March 30, 2000
Summary
Tardive dyskinesia research explores antipsychotic mechanisms. Atypical antipsychotics appear to reduce tardive dyskinesia risk, though underlying causes remain under investigation.
Area of Science:
- Neuroscience
- Pharmacology
- Psychiatry
Background:
- Tardive dyskinesia (TD) is a motor disorder linked to antipsychotic medications.
- Understanding TD mechanisms is crucial for developing safer treatments.
- Antipsychotic drug action research is extensive, with various animal models employed.
Purpose of the Study:
- To review current understanding of tardive dyskinesia pathophysiology.
- To explore the mechanisms behind typical and atypical antipsychotic-induced TD.
- To discuss the roles of dopamine, GABA, and structural factors in TD.
Main Methods:
- Review of animal models (homologous, analogous, correlational) for TD.
- Analysis of leading hypotheses on TD pathophysiology.
- Consideration of contributing factors like psychosis and aging.
Main Results:
- Typical neuroleptics are associated with TD, while atypical agents show a lower risk.
- Hypotheses including dopamine receptor hypersensitivity, GABA insufficiency, and structural abnormalities are debated.
- The precise contributions of psychosis and aging to TD remain challenging to quantify.
Conclusions:
- Atypical antipsychotics significantly decrease the risk of developing tardive dyskinesia.
- The mechanisms by which atypical agents mitigate TD risk require further investigation.
- Further research is needed to fully elucidate the complex pathophysiology of tardive dyskinesia.