[Physiopathology and curative treatment of tardive dyskinesia].
Tardive dyskinesia is a common complication of neuroleptic treatment. Current physiopathological theories emphasize the role of dopaminergic, cholinergic and GABAergic systems. The experimental bases of these hypotheses have been presented in detail. A critical review of the main clinical trials allows us to evaluate the effectiveness of our treatment and the validity of our theoretical models.
D000612:4-Aminobutyrate Transaminase; D000109:Acetylcholine / Q000031:analogs & derivatives; D014150:Antipsychotic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D018492:Dopamine Antagonists; D004409:Dyskinesia, Drug-Induced / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D008094:Lithium / Q000627:therapeutic use; D011950:Receptors, Cholinergic / Q000502:physiology; D011954:Receptors, Dopamine / Q000502:physiology; D011963:Receptors, GABA-A / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000031:analogs & derivatives
D014150:Antipsychotic Agents; D018492:Dopamine Antagonists; D011950:Receptors, Cholinergic; D011954:Receptors, Dopamine; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D008094:Lithium; D000612:4-Aminobutyrate Transaminase; D000109:Acetylcholine
Physiopathologie et traitement curatif des dyskinésies tardives.