Pathophysiological basis of drug-induced dyskinesias in Parkinson's disease.
Drug-induced dyskinesias (DID) represent a troublesome, dose-limiting, and common complication of long-term pharmacotherapy in Parkinson's disease (PD) patients. The pathophysiological basis and clinical nature of DID is of major interest for clinicians and neuroscientists. In this review article, we evaluate the theories of pathophysiology and molecular basis of DID, validity of various animal models used in DID related research, and electrophysiological characteristics of various basal ganglia nuclei during DID. We also discuss the relevance of various treatment strategies to the pathophysiological mechanisms.
Deogaonkar
Milind
M
Department of Neuroscience, NB 20, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. deoganm@ccf.org
Subramanian
Thyagarajan
T
D000818:Animals; D000978:Antiparkinson Agents / Q000009:adverse effects* / Q000493:pharmacokinetics; D004195:Disease Models, Animal; D004409:Dyskinesia, Drug-Induced / Q000209:etiology* / Q000235:genetics / Q000628:therapy; D006801:Humans; D008954:Models, Biological; D009479:Neuropeptides / Q000378:metabolism; D010300:Parkinson Disease / Q000188:drug therapy; D017981:Receptors, Neurotransmitter / Q000145:classification / Q000378:metabolism
D000978:Antiparkinson Agents; D009479:Neuropeptides; D017981:Receptors, Neurotransmitter