Predicting the development of levodopa-induced dyskinesias: a presynaptic mechanism?
After chronic levodopa use, many patients with Parkinson disease (PD) develop involuntary movements. Whether disabling or minor, levodopa-induced dyskinesia (LID) constitutes an undesirable outcome calling for better treatment strategies. Options for managing LID include delaying its onset by combining a dopaminergic agonist with levodopa from the start(1) or symptomatic control using amantadine. However, fundamental questions about LID remain: by what mechanisms does it develop, and why don't all patients go on to experience LID after sustained levodopa exposure?
From the Department of Neurology (P.A.L.), Henry Ford Hospital, Bloomfield; the Department of Neurology (P.A.L.), Wayne State University School of Medicine, Detroit, MI; and Center for Neurodegenerative and Neuroimmunologic Diseases (M.M.M.), Department of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ.
Peter A
PA
Lewitt
M Maral
MM
Mouradian
D000547:Amantadine / Q000627:therapeutic use; D000977:Antiparasitic Agents / Q000009:adverse effects*; D004409:Dyskinesia, Drug-Induced / Q000175:diagnosis / Q000000981:diagnostic imaging / Q000473:pathology*; D019788:Fluorodeoxyglucose F18; D006801:Humans; D007980:Levodopa / Q000009:adverse effects*; D010300:Parkinson Disease / Q000188:drug therapy; D049268:Positron-Emission Tomography; D017729:Presynaptic Terminals / Q000000981:diagnostic imaging / Q000473:pathology*
D000977:Antiparasitic Agents; D019788:Fluorodeoxyglucose F18; D007980:Levodopa; D000547:Amantadine