Amantadine for levodopa‐induced choreic dyskinesia in compound heterozygotes for GCH1 mutations
Identifieur interne : 003E21 ( Main/Exploration ); précédent : 003E20; suivant : 003E22Amantadine for levodopa‐induced choreic dyskinesia in compound heterozygotes for GCH1 mutations
Auteurs : Yoshiaki Furukawa [Canada] ; James J. Filiano [États-Unis] ; Stephen J. Kish [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2004-10.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Amantadine, Amantadine (therapeutic use), Antiparkinson Agents (adverse effects), Antiparkinson Agents (therapeutic use), Child, Chorea (complications), Chorea (drug therapy), Dopamine Agents (therapeutic use), Dyskinesia, Dyskinesia, Drug-Induced (drug therapy), Dyskinesia, Drug-Induced (etiology), GTP Cyclohydrolase (genetics), GTP cyclohydrolase I deficiency, Heterozygote, Humans, Levodopa, Levodopa (adverse effects), Male, Motor control, Mutation, Nervous system diseases, Parkinson Disease (drug therapy), Parkinson Disease (genetics), Pedigree, Phenotype, Point Mutation (genetics), amantadine, levodopa‐induced dyskinesias.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , genetics : GTP Cyclohydrolase.
- chemical , therapeutic use : Amantadine, Antiparkinson Agents, Dopamine Agents.
- complications : Chorea.
- drug therapy : Chorea, Dyskinesia, Drug-Induced, Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- genetics : Parkinson Disease, Point Mutation.
- Child, Heterozygote, Humans, Male, Pedigree, Phenotype.
Abstract
Amantadine suppressed severe levodopa‐induced choreic dyskinesia, which developed at initiation of levodopa therapy, in two siblings manifesting dystonia with motor delay phenotype of GTP cyclohydrolase I deficiency caused by compound heterozygous GCH1 mutations. Our finding suggests a beneficial effect of amantadine on this type of dyskinesia frequently observed in relatively severe dopamine‐deficient metabolic disorders. © 2004 Movement Disorder Society
Url:
DOI: 10.1002/mds.20194
Affiliations:
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Le document en format XML
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Filiano</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics/Neurology, Dartmouth–Hitchcock Medical Center, Lebanon, New Hampshire</wicri:regionArea><placeName><region type="state">New Hampshire</region></placeName></affiliation></author><author><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J." last="Kish">Stephen J. Kish</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Human Neurochemical Pathology Laboratory, Centre for Addiction and Mental Health—Clarke Division, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-10">2004-10</date><biblScope unit="vol">19</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1256">1256</biblScope><biblScope unit="page" to="1258">1258</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">19E87E9E42A5799A024DE5A9F3F2BA61D713A376</idno><idno type="DOI">10.1002/mds.20194</idno><idno type="ArticleID">MDS20194</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amantadine</term><term>Amantadine (therapeutic use)</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Child</term><term>Chorea (complications)</term><term>Chorea (drug therapy)</term><term>Dopamine Agents (therapeutic use)</term><term>Dyskinesia</term><term>Dyskinesia, Drug-Induced (drug therapy)</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>GTP Cyclohydrolase (genetics)</term><term>GTP cyclohydrolase I deficiency</term><term>Heterozygote</term><term>Humans</term><term>Levodopa</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Motor control</term><term>Mutation</term><term>Nervous system diseases</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (genetics)</term><term>Pedigree</term><term>Phenotype</term><term>Point Mutation (genetics)</term><term>amantadine</term><term>levodopa‐induced dyskinesias</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>GTP Cyclohydrolase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Amantadine</term><term>Antiparkinson Agents</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Chorea</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Chorea</term><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term><term>Point Mutation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Child</term><term>Heterozygote</term><term>Humans</term><term>Male</term><term>Pedigree</term><term>Phenotype</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Amantadine</term><term>Contrôle moteur</term><term>Dyskinésie</term><term>Lévodopa</term><term>Mutation</term><term>Système nerveux pathologie</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Amantadine suppressed severe levodopa‐induced choreic dyskinesia, which developed at initiation of levodopa therapy, in two siblings manifesting dystonia with motor delay phenotype of GTP cyclohydrolase I deficiency caused by compound heterozygous GCH1 mutations. Our finding suggests a beneficial effect of amantadine on this type of dyskinesia frequently observed in relatively severe dopamine‐deficient metabolic disorders. © 2004 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>New Hampshire</li></region></list><tree><country name="Canada"><noRegion><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name></noRegion><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J." last="Kish">Stephen J. Kish</name></country><country name="États-Unis"><region name="New Hampshire"><name sortKey="Filiano, James J" sort="Filiano, James J" uniqKey="Filiano J" first="James J." last="Filiano">James J. Filiano</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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