Levodopa-induced dyskinesia in Parkinson disease: Current and Evolving Concepts.

Alberto J. Espay, Francesca Morgante, Aristide Merola, Alfonso Fasano, Luca Marsili, Susan H. Fox, Erwan Bezard, Barbara Picconi, Paolo Calabresi, Anthony E. Lang
Ann Neurol.. 2018-11-30; 84(6): 797-811
DOI: 10.1002/ana.25364

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1. Ann Neurol. 2018 Dec;84(6):797-811. doi: 10.1002/ana.25364. Epub 2018 Nov 30.

Levodopa-induced dyskinesia in Parkinson disease: Current and evolving concepts.

Espay AJ(1), Morgante F(2), Merola A(1), Fasano A(3)(4), Marsili L(1), Fox
SH(3)(4), Bezard E(5)(6), Picconi B(7), Calabresi P(8), Lang AE(3)(4).

Author information:
(1)UC Gardner Neuroscience Institute and Gardner Family Center for Parkinson’s
Disease and Movement Disorders, Department of Neurology, University of
Cincinnati, Cincinnati, OH.
(2)Institute of Molecular and Clinical Sciences, St George’s University of
London, London, United Kingdom.
(3)Edmond J. Safra Program in Parkinson’s Disease, Morton and Gloria Shulman
Movement Disorders Clinic, Toronto Western Hospital, University Health Network,
Division of Neurology, University of Toronto, Toronto, Ontario, Canada.
(4)Krembil Brain Institute, Toronto, Ontario, Canada.
(5)University of Bordeaux, Institute of Neurodegenerative Diseases, Bordeaux,
(6)National Center for Scientific Research, Institute of Neurodegenerative
Diseases, Bordeaux, France.
(7)Experimental Neurophysiology Laboratory, IRCCS University San Raffaele Pisana,
University San Raffaele, Rome, Italy.
(8)Neurological Clinic, University of Perugia, Santa Maria della Misericordia
Hospital, Perugia, Italy.

Levodopa-induced dyskinesia is a common complication in Parkinson disease.
Pathogenic mechanisms include phasic stimulation of dopamine receptors,
nonphysiological levodopa-to-dopamine conversion in serotonergic neurons,
hyperactivity of corticostriatal glutamatergic transmission, and overstimulation
of nicotinic acetylcholine receptors on dopamine-releasing axons. Delay in
initiating levodopa is no longer recommended, as dyskinesia development is a
function of disease duration rather than cumulative levodopa exposure. We review
current and in-development treatments for peak-dose dyskinesia but suggest that
improvements in levodopa delivery alone may reduce its future prevalence. Ann
Neurol 2018;84:797-811.

© 2018 American Neurological Association.

DOI: 10.1002/ana.25364
PMID: 30357892

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