Levodopa‐induced dyskinesia in Parkinson disease: Current and evolving concepts
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- Alberto J. Espay
- UC Gardner Neuroscience Institute and Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology University of Cincinnati Cincinnati OH
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- Francesca Morgante
- Institute of Molecular and Clinical Sciences St George's University of London London United Kingdom
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- Aristide Merola
- UC Gardner Neuroscience Institute and Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology University of Cincinnati Cincinnati OH
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- Alfonso Fasano
- 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
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- Luca Marsili
- UC Gardner Neuroscience Institute and Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology University of Cincinnati Cincinnati OH
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- Susan H. Fox
- 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
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- Erwan Bezard
- University of Bordeaux, Institute of Neurodegenerative Diseases Bordeaux France
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- Barbara Picconi
- Experimental Neurophysiology Laboratory IRCCS San Raffaele Pisana, University San Raffaele Rome Italy
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- Paolo Calabresi
- Neurological Clinic University of Perugia, Santa Maria della Misericordia Hospital Perugia Italy
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- Anthony E. Lang
- 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
説明
<jats:p>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</jats:p>
収録刊行物
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- Annals of Neurology
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Annals of Neurology 84 (6), 797-811, 2018-11-30
Wiley