The pathophysiology of dystonia.
Dystonia occurs frequently following administration of neuroleptic or antiemetic drugs. This acute manifestation is not likely to be a simple consequence of reduced dopaminergic activity, because it was never reported to occur following the use of drugs which deplete dopamine stores, like reserpine and tetrabenazine. Based on the fact that dopamine-beta-hydroxylase levels are frequently elevated in patients with the dominant form of torsion dystonia it is suggested that dystonia results from impairment of a normal dopaminergic-noradrenergic balance, in which noradrenergic tone preponderates. A relative norepinephrine hyperactivity may be caused by dopaminergic blockade (as occurs in drug-induced dystonia) or from enhanced release of norepinephrine (in idiopathic torsion dystonia).
D001921:Brain / Q000503:physiopathology*; D004298:Dopamine / Q000378:metabolism; D004299:Dopamine beta-Hydroxylase / Q000097:blood; D004421:Dystonia / Q000139:chemically induced / Q000188:drug therapy / Q000503:physiopathology*; D009638:Norepinephrine / Q000378:metabolism; D010643:Phenoxybenzamine / Q000627:therapeutic use; D011954:Receptors, Dopamine / Q000187:drug effects
D011954:Receptors, Dopamine; D010643:Phenoxybenzamine; D004299:Dopamine beta-Hydroxylase; D004298:Dopamine; D009638:Norepinephrine