Levodopa-induced dyskinesias
Identifieur interne : 001615 ( PascalFrancis/Checkpoint ); précédent : 001614; suivant : 001616Levodopa-induced dyskinesias
Auteurs : Giovanni Fabbrini [Italie] ; Jonathan M. Brotchie [Canada] ; Francisco Grandas [Espagne] ; Masahiro Nomoto [Japon] ; Christopher G. Goetz [États-Unis]Source :
- Movement disorders [ 0885-3185 ] ; 2007.
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- Pascal (Inist)
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Abstract
Levodopa-induced dyskinesias (LID) are common and difficult to treat. This review focuses on three issues related to LID: clinical features, classification and rating, pathophysiology and pathogenesis, and management. The three primary clinical syndromes are OFF-period dystonia, peak-dose dyskinesia, and diphasic dyskinesia. Several other forms also occur, making the evaluation and choice of treatment complicated. A core component of the pathophysiology of LID is overactivity of the direct striatal output pathway. This pathway provides a direct GABAergic connection by which the striatum inhibits the output regions of the basal ganglia, i.e., the internal globus pallidus and the substantia nigra pars reticulata. Altering dopaminergic dosing and timing can abate dyskinesias, but usually impact the control of parkinsonism. Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α2 adrenergic, serotonergic (5HT1A, 5HT2A), opioid, histamine H3, adenosine A2A receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence-based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. New rating measures to assess severity and disability related to dyskinesia are in the process of development and clinimetric testing.
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Brotchie</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Toronto Western Research Institute, Toronto Western Hospital</s1><s2>Toronto</s2><s3>CAN</s3><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto</wicri:noRegion></affiliation></author><author><name sortKey="Grandas, Francisco" sort="Grandas, Francisco" uniqKey="Grandas F" first="Francisco" last="Grandas">Francisco Grandas</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Department of Neurology, Hospital General Universitario "Gregorio Marañón"</s1><s2>Madrid</s2><s3>ESP</s3><sZ>3 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Nomoto, Masahiro" sort="Nomoto, Masahiro" uniqKey="Nomoto M" first="Masahiro" last="Nomoto">Masahiro Nomoto</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Therapeutic Medicine, Faculty of Medicine, Ehime University Hospital</s1><s2>Ehime</s2><s3>JPN</s3><sZ>4 aut.</sZ></inist:fA14><country>Japon</country><wicri:noRegion>Ehime</wicri:noRegion></affiliation></author><author><name sortKey="Goetz, Christopher G" sort="Goetz, Christopher G" uniqKey="Goetz C" first="Christopher G." last="Goetz">Christopher G. Goetz</name><affiliation wicri:level="2"><inist:fA14 i1="05"><s1>Department of Neurological Sciences, Rush University Medical Center</s1><s2>Chicago, Illinois</s2><s3>USA</s3><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Illinois</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dyskinesia</term><term>Levodopa</term><term>Nervous system diseases</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Système nerveux pathologie</term><term>Dyskinésie</term><term>Lévodopa</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Levodopa-induced dyskinesias (LID) are common and difficult to treat. This review focuses on three issues related to LID: clinical features, classification and rating, pathophysiology and pathogenesis, and management. The three primary clinical syndromes are OFF-period dystonia, peak-dose dyskinesia, and diphasic dyskinesia. Several other forms also occur, making the evaluation and choice of treatment complicated. A core component of the pathophysiology of LID is overactivity of the direct striatal output pathway. This pathway provides a direct GABAergic connection by which the striatum inhibits the output regions of the basal ganglia, i.e., the internal globus pallidus and the substantia nigra pars reticulata. Altering dopaminergic dosing and timing can abate dyskinesias, but usually impact the control of parkinsonism. Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α<sub>2</sub> adrenergic, serotonergic (5HT<sub>1A,</sub> 5HT<sub>2A</sub>), opioid, histamine H<sub>3,</sub> adenosine A<sub>2A</sub> receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence-based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. 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Altering dopaminergic dosing and timing can abate dyskinesias, but usually impact the control of parkinsonism. Putative therapies to reduce the problem of dyskinesias could focus on the glutamatergic, GABAergic, α<sub>2</sub> adrenergic, serotonergic (5HT<sub>1A,</sub> 5HT<sub>2A</sub>), opioid, histamine H<sub>3,</sub> adenosine A<sub>2A</sub> receptors, the monoamine transport or cannabinoid CB1 receptors systems. The only currently available drug with an evidence-based recommendation on efficacy for dyskinesia is amantadine. Therapy goals include the prevention of dyskinesia and treatment of dyskinesias that are troublesome clinically. 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Brotchie</name></noRegion></country><country name="Espagne"><region name="Communauté de Madrid"><name sortKey="Grandas, Francisco" sort="Grandas, Francisco" uniqKey="Grandas F" first="Francisco" last="Grandas">Francisco Grandas</name></region></country><country name="Japon"><noRegion><name sortKey="Nomoto, Masahiro" sort="Nomoto, Masahiro" uniqKey="Nomoto M" first="Masahiro" last="Nomoto">Masahiro Nomoto</name></noRegion></country><country name="États-Unis"><region name="Illinois"><name sortKey="Goetz, Christopher G" sort="Goetz, Christopher G" uniqKey="Goetz C" first="Christopher G." last="Goetz">Christopher G. Goetz</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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