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

Alberto J. Espay; Francesca Morgante; Aristide Merola; Annamaria Merola; Alfonso Fasano; Luca Marsili; Susan H. Fox; Erwan Bezard; Barbara Picconi; Paolo Calabresi; Anthony E. Lang

doi:10.1002/ana.25364

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

Alberto J. Espay, Francesca Morgante, Aristide Merola, Annamaria Merola, Alfonso Fasano, Luca Marsili, Susan H. Fox, Erwan Bezard, Barbara Picconi, Paolo Calabresi, Anthony E. Lang

Risultato della ricerca: Contributo in rivista › Articolo in rivista

88 Citazioni (Scopus)

Abstract

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.

Lingua originale	English
pagine (da-a)	797-811
Numero di pagine	15
Rivista	Annals of Neurology
Volume	84
DOI	https://doi.org/10.1002/ana.25364
Stato di pubblicazione	Pubblicato - 2018

Keywords

Animals
Antiparkinson Agents
Dose-Response Relationship, Drug
Drug Administration Schedule
Dyskinesia, Drug-Induced
Humans
Levodopa
Parkinson Disease

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10.1002/ana.25364

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title = "Levodopa-induced dyskinesia in Parkinson disease: Current and evolving concepts",

abstract = "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.",

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author = "Espay, {Alberto J.} and Francesca Morgante and Aristide Merola and Annamaria Merola and Alfonso Fasano and Luca Marsili and Fox, {Susan H.} and Erwan Bezard and Barbara Picconi and Paolo Calabresi and Lang, {Anthony E.}",

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doi = "10.1002/ana.25364",

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T1 - Levodopa-induced dyskinesia in Parkinson disease: Current and evolving concepts

AU - Espay, Alberto J.

AU - Morgante, Francesca

AU - Merola, Aristide

AU - Merola, Annamaria

AU - Fasano, Alfonso

AU - Marsili, Luca

AU - Fox, Susan H.

AU - Bezard, Erwan

AU - Picconi, Barbara

AU - Calabresi, Paolo

AU - Lang, Anthony E.

PY - 2018

Y1 - 2018

N2 - 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.

AB - 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.

KW - Animals

KW - Antiparkinson Agents

KW - Dose-Response Relationship, Drug

KW - Drug Administration Schedule

KW - Dyskinesia, Drug-Induced

KW - Humans

KW - Levodopa

KW - Parkinson Disease

KW - Animals

KW - Antiparkinson Agents

KW - Dose-Response Relationship, Drug

KW - Drug Administration Schedule

KW - Dyskinesia, Drug-Induced

KW - Humans

KW - Levodopa

KW - Parkinson Disease

UR - http://hdl.handle.net/10807/170670

U2 - 10.1002/ana.25364

DO - 10.1002/ana.25364

M3 - Article

SN - 0364-5134

VL - 84

SP - 797

EP - 811

JO - Annals of Neurology

JF - Annals of Neurology

ER -

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

Abstract

Keywords

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