Current psychopathological theories of tardive dyskinesia and their implications for future research.
An understanding of pathophysiology is essential for establishing an etiological relationship between the neuroleptics and tardive dyskinesia, for elucidating specific treatment methods and perhaps for synthesizing new neuroleptics which do not produce this side effect. Our current knowledge has been derived from clues obtained by drug-related factors, therapeutic agents assumed to improve tardive dyskinesia and by neuropathological findings. Among the many theories, dopaminergic hypersensitivity is the most favored and yet unproven. At present the etiology of tardive dyskinesia may be related to the interaction between the exogenous drugs and the endogenous predisposition, the nature of which is so far elusive.
D000109:Acetylcholine / Q000378:metabolism; D000328:Adult; D000368:Aged; D000818:Animals; D014150:Antipsychotic Agents / Q000009:adverse effects*; D001921:Brain / Q000473:pathology; D004298:Dopamine / Q000009:adverse effects / Q000031:analogs & derivatives / Q000378:metabolism; D004409:Dyskinesia, Drug-Induced / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D004967:Estrogens / Q000502:physiology; D005260:Female; D000882:Haplorhini; D006801:Humans; D007980:Levodopa / Q000009:adverse effects; D009638:Norepinephrine / Q000502:physiology; D010302:Parkinson Disease, Secondary / Q000209:etiology; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D014150:Antipsychotic Agents; D004967:Estrogens; D011954:Receptors, Dopamine; D007980:Levodopa; D005680:gamma-Aminobutyric Acid; D014446:Tyrosine 3-Monooxygenase; C001746:3-methoxytyramine; D000109:Acetylcholine; D004298:Dopamine; D009638:Norepinephrine