Long latency postural reflexes are under supraspinal dopaminergic control
Identifieur interne : 000621 ( Istex/Corpus ); précédent : 000620; suivant : 000622Long latency postural reflexes are under supraspinal dopaminergic control
Auteurs : Bloem ; Dennis J. Beckley ; Jeroen P. P. Van Vugt ; J. Gert Van Dijk ; Michael P. Remler ; J. William Langston ; Raymund A. C. RoosSource :
- Movement Disorders [ 0885-3185 ] ; 1995-09.
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- KwdEn :
Abstract
Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.
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DOI: 10.1002/mds.870100509
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Beckley</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of California, Davis</mods:affiliation></affiliation></author><author><name sortKey="Van Vugt, Jeroen P P" sort="Van Vugt, Jeroen P P" uniqKey="Van Vugt J" first="Jeroen P. P." last="Van Vugt">Jeroen P. P. Van Vugt</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Van Dijk, J Gert" sort="Van Dijk, J Gert" uniqKey="Van Dijk J" first="J. Gert" last="Van Dijk">J. Gert Van Dijk</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Remler, Michael P" sort="Remler, Michael P" uniqKey="Remler M" first="Michael P." last="Remler">Michael P. 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Remler</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of California, Davis</mods:affiliation></affiliation></author><author><name sortKey="Langston, J William" sort="Langston, J William" uniqKey="Langston J" first="J. William" last="Langston">J. William Langston</name><affiliation><mods:affiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Roos, Raymund A C" sort="Roos, Raymund A C" uniqKey="Roos R" first="Raymund A. C." last="Roos">Raymund A. C. Roos</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</mods:affiliation></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="1995-09">1995-09</date><biblScope unit="vol">10</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="580">580</biblScope><biblScope unit="page" to="588">588</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">B501B340D93CAD32DA69B4E24483A43C7C4C801E</idno><idno type="DOI">10.1002/mds.870100509</idno><idno type="ArticleID">MDS870100509</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine</term><term>Long latency reflexes</term><term>Parkinson's disease</term><term>Posture</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Bloem</name><affiliations><json:string>Department of Neurology, University Hospital Leiden, The Netherlands</json:string><json:string>Department of Neurology, School of Medicine, University of California, Davis</json:string><json:string>The Parkinson's Institute, Sunnyvale, California, U.S.A.</json:string></affiliations></json:item><json:item><name>Dennis J. Beckley</name><affiliations><json:string>Department of Neurology, School of Medicine, University of California, Davis</json:string></affiliations></json:item><json:item><name>Jeroen P. P. van Vugt</name><affiliations><json:string>Department of Neurology, University Hospital Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>J. Gert van Dijk</name><affiliations><json:string>Department of Neurology, University Hospital Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Michael P. Remler</name><affiliations><json:string>Department of Neurology, School of Medicine, University of California, Davis</json:string></affiliations></json:item><json:item><name>J. William Langston</name><affiliations><json:string>The Parkinson's Institute, Sunnyvale, California, U.S.A.</json:string></affiliations></json:item><json:item><name>Raymund A. C. Roos</name><affiliations><json:string>Department of Neurology, University Hospital Leiden, The Netherlands</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Posture</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Long latency reflexes</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.</abstract><qualityIndicators><score>7.388</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1513</abstractCharCount><pdfWordCount>5091</pdfWordCount><pdfCharCount>34439</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>199</abstractWordCount></qualityIndicators><title>Long latency postural reflexes are under supraspinal dopaminergic control</title><genre><json:string>Serial article</json:string></genre><host><volume>10</volume><pages><total>9</total><last>588</last><first>580</first></pages><issn><json:string>0885-3185</json:string></issn><issue>5</issue><subject><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>1995</publicationDate><copyrightDate>1995</copyrightDate><doi><json:string>10.1002/mds.870100509</json:string></doi><id>B501B340D93CAD32DA69B4E24483A43C7C4C801E</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/B501B340D93CAD32DA69B4E24483A43C7C4C801E/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/B501B340D93CAD32DA69B4E24483A43C7C4C801E/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/B501B340D93CAD32DA69B4E24483A43C7C4C801E/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Long latency postural reflexes are under supraspinal dopaminergic control</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>1995</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Long latency postural reflexes are under supraspinal dopaminergic control</title><author><persName><surname>Bloem</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, University Hospital, P.O. Box 9600, 2300 RC Leiden, The Netherlands</p></note><affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation><affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation><affiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</affiliation></author><author><persName><forename type="first">Dennis J.</forename><surname>Beckley</surname></persName><affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation></author><author><persName><forename type="first">Jeroen P. P.</forename><surname>van Vugt</surname></persName><affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation></author><author><persName><forename type="first">J. Gert</forename><surname>van Dijk</surname></persName><affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation></author><author><persName><forename type="first">Michael P.</forename><surname>Remler</surname></persName><affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation></author><author><persName><forename type="first">J. William</forename><surname>Langston</surname></persName><affiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</affiliation></author><author><persName><forename type="first">Raymund A. C.</forename><surname>Roos</surname></persName><affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation></author></analytic><monogr><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="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-09"></date><biblScope unit="vol">10</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="580">580</biblScope><biblScope unit="page" to="588">588</biblScope></imprint></monogr><idno type="istex">B501B340D93CAD32DA69B4E24483A43C7C4C801E</idno><idno type="DOI">10.1002/mds.870100509</idno><idno type="ArticleID">MDS870100509</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>Posture</term></item><item><term>Long latency reflexes</term></item><item><term>Dopamine</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-02-15">Registration</change><change when="1995-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/B501B340D93CAD32DA69B4E24483A43C7C4C801E/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Box 9600, 2300 RC Leiden, The Netherlands</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870100509.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="43"></count></countGroup><titleGroup><title type="main" xml:lang="en">Long latency postural reflexes are under supraspinal dopaminergic control</title><title type="short" xml:lang="en">LL REFLEXES IN HYPODOPAMINERGIC SYNDROMES</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2 #af3" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Bastiaan R.</givenNames><familyName>Bloem</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Dennis J.</givenNames><familyName>Beckley</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jeroen P. P.</givenNames><familyName>van Vugt</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>J. Gert</givenNames><familyName>van Dijk</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Michael P.</givenNames><familyName>Remler</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>J. William</givenNames><familyName>Langston</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Raymund A. C.</givenNames><familyName>Roos</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="NL" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital Leiden, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, School of Medicine, University of California, Davis</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">Posture</keyword><keyword xml:id="kwd3">Long latency reflexes</keyword><keyword xml:id="kwd4">Dopamine</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Long latency postural reflexes are under supraspinal dopaminergic control</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>LL REFLEXES IN HYPODOPAMINERGIC SYNDROMES</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Long latency postural reflexes are under supraspinal dopaminergic control</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Bloem</namePart><affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation><affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation><affiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</affiliation><description>Correspondence: Department of Neurology, University Hospital, P.O. Box 9600, 2300 RC Leiden, The Netherlands</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dennis J.</namePart><namePart type="family">Beckley</namePart><affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeroen P. P.</namePart><namePart type="family">van Vugt</namePart><affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. Gert</namePart><namePart type="family">van Dijk</namePart><affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael P.</namePart><namePart type="family">Remler</namePart><affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. William</namePart><namePart type="family">Langston</namePart><affiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Raymund A. C.</namePart><namePart type="family">Roos</namePart><affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1995-09</dateIssued><dateValid encoding="w3cdtf">1995-02-15</dateValid><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">2</extent><extent unit="references">43</extent></physicalDescription><abstract lang="en">Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>Posture</topic><topic>Long latency reflexes</topic><topic>Dopamine</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>580</start><end>588</end><total>9</total></extent></part></relatedItem><identifier type="istex">B501B340D93CAD32DA69B4E24483A43C7C4C801E</identifier><identifier type="DOI">10.1002/mds.870100509</identifier><identifier type="ArticleID">MDS870100509</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1995 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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