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September 08, 2015; 85 (10) Editorial

Serotonin/dopamine transporter ratio as a predictor of l-dopa–induced dyskinesia

Philippe Huot, William D. Hutchison
First published August 7, 2015, DOI: https://doi.org/10.1212/WNL.0000000000001915
Philippe Huot
From the Department of Pharmacology (P.H.), Faculty of Medicine, University of Montreal, Quebec, Canada; Division of Neurology (P.H.), Centre Hospitalier de l'Université de Montréal, Quebec, Canada; Departments of Surgery and Physiology (W.D.H.), University of Toronto, Ontario, Canada; and Division of Neurosurgery (W.D.H.), Toronto Western Hospital MP11-308 and Toronto Western Research Institute, Ontario, Canada.
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William D. Hutchison
From the Department of Pharmacology (P.H.), Faculty of Medicine, University of Montreal, Quebec, Canada; Division of Neurology (P.H.), Centre Hospitalier de l'Université de Montréal, Quebec, Canada; Departments of Surgery and Physiology (W.D.H.), University of Toronto, Ontario, Canada; and Division of Neurosurgery (W.D.H.), Toronto Western Hospital MP11-308 and Toronto Western Research Institute, Ontario, Canada.
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Citation
Serotonin/dopamine transporter ratio as a predictor of l-dopa–induced dyskinesia
Philippe Huot, William D. Hutchison
Neurology Sep 2015, 85 (10) 840-841; DOI: 10.1212/WNL.0000000000001915

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l-3,4-Dihydroxyphenylalanine (l-dopa)-induced dyskinesia affects virtually every patient with Parkinson disease (PD) after chronic administration.1 The pathophysiology of dyskinesia is complex, and several nondopaminergic systems are involved.2 The serotonin (5-HT) system has received much attention over the past years as a critical player underlying dyskinesia and as a potentially efficacious therapeutic target. 5-HT neurons contain the required enzymes to synthesize dopamine from l-dopa3 but without the regulatory mechanisms required for dopaminergic transmission, resulting in dysregulated, nonphysiologic dopamine release, which underlies the dyskinetic state.4 However, if this aberrant dopamine release by 5-HT fibers is the culprit in dyskinesia, it is also responsible, at least partly, for the antiparkinsonian action of l-dopa.5 As a result, it has proven difficult to achieve an antidyskinetic benefit with agonists of the 5-HT1A receptors, which act by dampening this aberrant dopamine release by 5-HT terminals, without hindering the therapeutic effect of l-dopa in both preclinical and clinical settings.6,7

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  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial.

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  • © 2015 American Academy of Neurology
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