Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks
Identifieur interne : 003141 ( Main/Corpus ); précédent : 003140; suivant : 003142Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks
Auteurs : Bastiaan R. Bloem ; Dennis J. Beckley ; Michael P. Remler ; Raymund A. C. Roos ; J. Gert Van DijkSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1994.
Abstract
Postural reflexes in leg muscles appear to be set at a fixed gain in Parkinson's disease. To further investigate gain adaptation, we instructed 16 patients with idiopathic Parkinson's disease (studied during the ‘off’ phase) and 21 healthy controls to either ‘resist’ or ‘yield’ in response to 20 serial 4 ° toe-up perturbations of a supporting platform on which they were standing. We bilaterally recorded destabilizing medium latency (ML) reflexes from stretched gastrocnemius muscles and corrective long latency (LL) reflexes from shortened tibialis anterior muscles. We also assessed changes in center of foot pressure (CFP) and center of gravity (COG). During the ‘resist’ condition, patients had increased destabilizing ML reflexes, decreased corrective LL reflexes, increased backward displacement of the COG and increased forward (destabilizing) displacement of the CFP. In addition, the backward (corrective) displacement of CFP between 150 and 250 ms was delayed. During the ‘yield’ condition, reflex gains were modified in controls: LL reflexes were markedly attenuated, whereas ML reflexes were markedly increased. Although this reflex pattern resembled the ‘resist’ condition in patients, it was not associated with an increased forward displacement of the CFP, but only with a strongly delayed backward displacement of CFP which started after 150 ms. In patients, ML reflex amplitudes remained unchanged during the ‘yield’ condition, suggesting a fixed reflex gain. LL reflex amplitudes were reduced in patients but significantly less compared to controls, which again suggests a fixed reflex gain. This ‘inflexibility’ of postural reflexes was reflected by the CFP which showed much smaller changes between 0 and 250 ms in patients than controls. These results could not be ascribed to a different ability to yield because posterior displacement of the COG was identical in patients and controls during the ‘yield’ condition. We conclude that (1) patients with Parkinson's disease have abnormal and ‘inflexible’ postural reflexes, associated with delayed corrective movements about the ankle joint and increased body sway; and (2) the increased forward displacement of the CFP in patients likely reflects high stiffness in ankle muscles because reflex changes in controls only affected the CFP more than 150 ms after the perturbation. The increased muscle stiffness and inflexibility of postural reflexes in Parkinson's disease may contribute to balance impairment in daily life.
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DOI: 10.1016/0022-510X(94)00253-K
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks</title><author><name sortKey="Bloem, Bastiaan R" sort="Bloem, Bastiaan R" uniqKey="Bloem B" first="Bastiaan R." last="Bloem">Bastiaan R. Bloem</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Leiden, P.O. Box 9600, 2300 RC Leiden, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Beckley, Dennis J" sort="Beckley, Dennis J" uniqKey="Beckley D" first="Dennis J." last="Beckley">Dennis J. Beckley</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of California, Davis, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Remler, Michael P" sort="Remler, Michael P" uniqKey="Remler M" first="Michael P." last="Remler">Michael P. Remler</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of California, Davis, CA, USA</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, P.O. Box 9600, 2300 RC 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, P.O. 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Box 9600, 2300 RC Leiden, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Beckley, Dennis J" sort="Beckley, Dennis J" uniqKey="Beckley D" first="Dennis J." last="Beckley">Dennis J. Beckley</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of California, Davis, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Remler, Michael P" sort="Remler, Michael P" uniqKey="Remler M" first="Michael P." last="Remler">Michael P. Remler</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of California, Davis, CA, USA</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, P.O. Box 9600, 2300 RC 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, P.O. Box 9600, 2300 RC Leiden, The Netherlands</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1994">1994</date><biblScope unit="volume">129</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="109">109</biblScope><biblScope unit="page" to="119">119</biblScope></imprint><idno type="ISSN">0022-510X</idno></series><idno type="istex">6560A3FE3BDD72B060C79289995F00758AB4B920</idno><idno type="DOI">10.1016/0022-510X(94)00253-K</idno><idno type="PII">0022-510X(94)00253-K</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Postural reflexes in leg muscles appear to be set at a fixed gain in Parkinson's disease. To further investigate gain adaptation, we instructed 16 patients with idiopathic Parkinson's disease (studied during the ‘off’ phase) and 21 healthy controls to either ‘resist’ or ‘yield’ in response to 20 serial 4 ° toe-up perturbations of a supporting platform on which they were standing. We bilaterally recorded destabilizing medium latency (ML) reflexes from stretched gastrocnemius muscles and corrective long latency (LL) reflexes from shortened tibialis anterior muscles. We also assessed changes in center of foot pressure (CFP) and center of gravity (COG). During the ‘resist’ condition, patients had increased destabilizing ML reflexes, decreased corrective LL reflexes, increased backward displacement of the COG and increased forward (destabilizing) displacement of the CFP. In addition, the backward (corrective) displacement of CFP between 150 and 250 ms was delayed. During the ‘yield’ condition, reflex gains were modified in controls: LL reflexes were markedly attenuated, whereas ML reflexes were markedly increased. Although this reflex pattern resembled the ‘resist’ condition in patients, it was not associated with an increased forward displacement of the CFP, but only with a strongly delayed backward displacement of CFP which started after 150 ms. In patients, ML reflex amplitudes remained unchanged during the ‘yield’ condition, suggesting a fixed reflex gain. LL reflex amplitudes were reduced in patients but significantly less compared to controls, which again suggests a fixed reflex gain. This ‘inflexibility’ of postural reflexes was reflected by the CFP which showed much smaller changes between 0 and 250 ms in patients than controls. These results could not be ascribed to a different ability to yield because posterior displacement of the COG was identical in patients and controls during the ‘yield’ condition. We conclude that (1) patients with Parkinson's disease have abnormal and ‘inflexible’ postural reflexes, associated with delayed corrective movements about the ankle joint and increased body sway; and (2) the increased forward displacement of the CFP in patients likely reflects high stiffness in ankle muscles because reflex changes in controls only affected the CFP more than 150 ms after the perturbation. The increased muscle stiffness and inflexibility of postural reflexes in Parkinson's disease may contribute to balance impairment in daily life.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Bastiaan R. Bloem</name><affiliations><json:string>Department of Neurology, University Hospital Leiden, P.O. Box 9600, 2300 RC Leiden, The Netherlands</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, CA, USA</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, CA, USA</json:string></affiliations></json:item><json:item><name>Raymund A.C. Roos</name><affiliations><json:string>Department of Neurology, University Hospital Leiden, P.O. Box 9600, 2300 RC 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, P.O. Box 9600, 2300 RC Leiden, The Netherlands</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Clinical section</value></json:item><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>Postural set</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Reflex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Gain</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Balance</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Instability</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Postural reflexes in leg muscles appear to be set at a fixed gain in Parkinson's disease. To further investigate gain adaptation, we instructed 16 patients with idiopathic Parkinson's disease (studied during the ‘off’ phase) and 21 healthy controls to either ‘resist’ or ‘yield’ in response to 20 serial 4 ° toe-up perturbations of a supporting platform on which they were standing. We bilaterally recorded destabilizing medium latency (ML) reflexes from stretched gastrocnemius muscles and corrective long latency (LL) reflexes from shortened tibialis anterior muscles. We also assessed changes in center of foot pressure (CFP) and center of gravity (COG). During the ‘resist’ condition, patients had increased destabilizing ML reflexes, decreased corrective LL reflexes, increased backward displacement of the COG and increased forward (destabilizing) displacement of the CFP. In addition, the backward (corrective) displacement of CFP between 150 and 250 ms was delayed. During the ‘yield’ condition, reflex gains were modified in controls: LL reflexes were markedly attenuated, whereas ML reflexes were markedly increased. Although this reflex pattern resembled the ‘resist’ condition in patients, it was not associated with an increased forward displacement of the CFP, but only with a strongly delayed backward displacement of CFP which started after 150 ms. In patients, ML reflex amplitudes remained unchanged during the ‘yield’ condition, suggesting a fixed reflex gain. LL reflex amplitudes were reduced in patients but significantly less compared to controls, which again suggests a fixed reflex gain. This ‘inflexibility’ of postural reflexes was reflected by the CFP which showed much smaller changes between 0 and 250 ms in patients than controls. These results could not be ascribed to a different ability to yield because posterior displacement of the COG was identical in patients and controls during the ‘yield’ condition. We conclude that (1) patients with Parkinson's disease have abnormal and ‘inflexible’ postural reflexes, associated with delayed corrective movements about the ankle joint and increased body sway; and (2) the increased forward displacement of the CFP in patients likely reflects high stiffness in ankle muscles because reflex changes in controls only affected the CFP more than 150 ms after the perturbation. The increased muscle stiffness and inflexibility of postural reflexes in Parkinson's disease may contribute to balance impairment in daily life.</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>2494</abstractCharCount><pdfWordCount>6464</pdfWordCount><pdfCharCount>44026</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>369</abstractWordCount></qualityIndicators><title>Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks</title><pii><json:string>0022-510X(94)00253-K</json:string></pii><genre><json:string>research-article</json:string></genre><host><volume>129</volume><pii><json:string>S0022-510X(00)X0021-4</json:string></pii><pages><last>119</last><first>109</first></pages><issn><json:string>0022-510X</json:string></issn><issue>2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Journal of the Neurological Sciences</title><publicationDate>1995</publicationDate></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROIMAGING</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>1994</publicationDate><copyrightDate>1995</copyrightDate><doi><json:string>10.1016/0022-510X(94)00253-K</json:string></doi><id>6560A3FE3BDD72B060C79289995F00758AB4B920</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6560A3FE3BDD72B060C79289995F00758AB4B920/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6560A3FE3BDD72B060C79289995F00758AB4B920/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6560A3FE3BDD72B060C79289995F00758AB4B920/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6560A3FE3BDD72B060C79289995F00758AB4B920/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1995</date></publicationStmt><notesStmt><note type="content">Section title: Research article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks</title><author><persName><forename type="first">Bastiaan R.</forename><surname>Bloem</surname></persName><note type="correspondence"><p>Corresponding author. Tel.: (071) 263920; Fax: (071) 248253.</p></note><affiliation>Department of Neurology, University Hospital Leiden, P.O. Box 9600, 2300 RC Leiden, The Netherlands</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, CA, USA</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, CA, USA</affiliation></author><author><persName><forename type="first">Raymund A.C.</forename><surname>Roos</surname></persName><affiliation>Department of Neurology, University Hospital Leiden, P.O. Box 9600, 2300 RC 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, P.O. Box 9600, 2300 RC Leiden, The Netherlands</affiliation></author></analytic><monogr><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="pISSN">0022-510X</idno><idno type="PII">S0022-510X(00)X0021-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1994"></date><biblScope unit="volume">129</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="109">109</biblScope><biblScope unit="page" to="119">119</biblScope></imprint></monogr><idno type="istex">6560A3FE3BDD72B060C79289995F00758AB4B920</idno><idno type="DOI">10.1016/0022-510X(94)00253-K</idno><idno type="PII">0022-510X(94)00253-K</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Postural reflexes in leg muscles appear to be set at a fixed gain in Parkinson's disease. To further investigate gain adaptation, we instructed 16 patients with idiopathic Parkinson's disease (studied during the ‘off’ phase) and 21 healthy controls to either ‘resist’ or ‘yield’ in response to 20 serial 4 ° toe-up perturbations of a supporting platform on which they were standing. We bilaterally recorded destabilizing medium latency (ML) reflexes from stretched gastrocnemius muscles and corrective long latency (LL) reflexes from shortened tibialis anterior muscles. We also assessed changes in center of foot pressure (CFP) and center of gravity (COG). During the ‘resist’ condition, patients had increased destabilizing ML reflexes, decreased corrective LL reflexes, increased backward displacement of the COG and increased forward (destabilizing) displacement of the CFP. In addition, the backward (corrective) displacement of CFP between 150 and 250 ms was delayed. During the ‘yield’ condition, reflex gains were modified in controls: LL reflexes were markedly attenuated, whereas ML reflexes were markedly increased. Although this reflex pattern resembled the ‘resist’ condition in patients, it was not associated with an increased forward displacement of the CFP, but only with a strongly delayed backward displacement of CFP which started after 150 ms. In patients, ML reflex amplitudes remained unchanged during the ‘yield’ condition, suggesting a fixed reflex gain. LL reflex amplitudes were reduced in patients but significantly less compared to controls, which again suggests a fixed reflex gain. This ‘inflexibility’ of postural reflexes was reflected by the CFP which showed much smaller changes between 0 and 250 ms in patients than controls. These results could not be ascribed to a different ability to yield because posterior displacement of the COG was identical in patients and controls during the ‘yield’ condition. We conclude that (1) patients with Parkinson's disease have abnormal and ‘inflexible’ postural reflexes, associated with delayed corrective movements about the ankle joint and increased body sway; and (2) the increased forward displacement of the CFP in patients likely reflects high stiffness in ankle muscles because reflex changes in controls only affected the CFP more than 150 ms after the perturbation. The increased muscle stiffness and inflexibility of postural reflexes in Parkinson's disease may contribute to balance impairment in daily life.</p></abstract><textClass><keywords scheme="keyword"><list><head>Article category</head><item><term>Clinical section</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>Postural set</term></item><item><term>Reflex</term></item><item><term>Gain</term></item><item><term>Balance</term></item><item><term>Instability</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-10-18">Registration</change><change when="1994-10-11">Modified</change><change when="1994">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JNS</jid><aid>9400253K</aid><ce:pii>0022-510X(94)00253-K</ce:pii><ce:doi>10.1016/0022-510X(94)00253-K</ce:doi><ce:copyright type="unknown" year="1995"></ce:copyright><ce:doctopics><ce:doctopic><ce:text>Clinical section</ce:text></ce:doctopic></ce:doctopics></item-info><head><ce:dochead><ce:textfn>Research article</ce:textfn></ce:dochead><ce:title>Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks</ce:title><ce:author-group><ce:author><ce:given-name>Bastiaan R.</ce:given-name><ce:surname>Bloem</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Dennis J.</ce:given-name><ce:surname>Beckley</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Michael P.</ce:given-name><ce:surname>Remler</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Raymund A.C.</ce:given-name><ce:surname>Roos</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>J.Gert</ce:given-name><ce:surname>van Dijk</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Neurology, University Hospital Leiden, P.O. Box 9600, 2300 RC Leiden, The Netherlands</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Neurology, School of Medicine, University of California, Davis, CA, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Tel.: (071) 263920; Fax: (071) 248253.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="19" month="6" year="1994"></ce:date-received><ce:date-revised day="11" month="10" year="1994"></ce:date-revised><ce:date-accepted day="18" month="10" year="1994"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Postural reflexes in leg muscles appear to be set at a fixed gain in Parkinson's disease. To further investigate gain adaptation, we instructed 16 patients with idiopathic Parkinson's disease (studied during the ‘off’ phase) and 21 healthy controls to either ‘resist’ or ‘yield’ in response to 20 serial 4 ° toe-up perturbations of a supporting platform on which they were standing. We bilaterally recorded destabilizing medium latency (ML) reflexes from stretched gastrocnemius muscles and corrective long latency (LL) reflexes from shortened tibialis anterior muscles. We also assessed changes in center of foot pressure (CFP) and center of gravity (COG). During the ‘resist’ condition, patients had increased destabilizing ML reflexes, decreased corrective LL reflexes, increased backward displacement of the COG and increased forward (destabilizing) displacement of the CFP. In addition, the backward (corrective) displacement of CFP between 150 and 250 ms was delayed. During the ‘yield’ condition, reflex gains were modified in controls: LL reflexes were markedly attenuated, whereas ML reflexes were markedly increased. Although this reflex pattern resembled the ‘resist’ condition in patients, it was not associated with an increased forward displacement of the CFP, but only with a strongly delayed backward displacement of CFP which started after 150 ms. In patients, ML reflex amplitudes remained unchanged during the ‘yield’ condition, suggesting a fixed reflex gain. LL reflex amplitudes were reduced in patients but significantly less compared to controls, which again suggests a fixed reflex gain. This ‘inflexibility’ of postural reflexes was reflected by the CFP which showed much smaller changes between 0 and 250 ms in patients than controls. These results could not be ascribed to a different ability to yield because posterior displacement of the COG was identical in patients and controls during the ‘yield’ condition. We conclude that (1) patients with Parkinson's disease have abnormal and ‘inflexible’ postural reflexes, associated with delayed corrective movements about the ankle joint and increased body sway; and (2) the increased forward displacement of the CFP in patients likely reflects high stiffness in ankle muscles because reflex changes in controls only affected the CFP more than 150 ms after the perturbation. The increased muscle stiffness and inflexibility of postural reflexes in Parkinson's disease may contribute to balance impairment in daily life.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>Postural set</ce:text></ce:keyword><ce:keyword><ce:text>Reflex</ce:text></ce:keyword><ce:keyword><ce:text>Gain</ce:text></ce:keyword><ce:keyword><ce:text>Balance</ce:text></ce:keyword><ce:keyword><ce:text>Instability</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Postural reflexes in Parkinson's disease during ‘resist’ and ‘yield’ tasks</title></titleInfo><name type="personal"><namePart type="given">Bastiaan R.</namePart><namePart type="family">Bloem</namePart><affiliation>Department of Neurology, University Hospital Leiden, P.O. Box 9600, 2300 RC Leiden, The Netherlands</affiliation><description>Corresponding author. Tel.: (071) 263920; Fax: (071) 248253.</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, CA, USA</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, CA, USA</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, P.O. Box 9600, 2300 RC 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, P.O. Box 9600, 2300 RC Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1994</dateIssued><dateValid encoding="w3cdtf">1994-10-18</dateValid><dateModified encoding="w3cdtf">1994-10-11</dateModified><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Postural reflexes in leg muscles appear to be set at a fixed gain in Parkinson's disease. To further investigate gain adaptation, we instructed 16 patients with idiopathic Parkinson's disease (studied during the ‘off’ phase) and 21 healthy controls to either ‘resist’ or ‘yield’ in response to 20 serial 4 ° toe-up perturbations of a supporting platform on which they were standing. We bilaterally recorded destabilizing medium latency (ML) reflexes from stretched gastrocnemius muscles and corrective long latency (LL) reflexes from shortened tibialis anterior muscles. We also assessed changes in center of foot pressure (CFP) and center of gravity (COG). During the ‘resist’ condition, patients had increased destabilizing ML reflexes, decreased corrective LL reflexes, increased backward displacement of the COG and increased forward (destabilizing) displacement of the CFP. In addition, the backward (corrective) displacement of CFP between 150 and 250 ms was delayed. During the ‘yield’ condition, reflex gains were modified in controls: LL reflexes were markedly attenuated, whereas ML reflexes were markedly increased. Although this reflex pattern resembled the ‘resist’ condition in patients, it was not associated with an increased forward displacement of the CFP, but only with a strongly delayed backward displacement of CFP which started after 150 ms. In patients, ML reflex amplitudes remained unchanged during the ‘yield’ condition, suggesting a fixed reflex gain. LL reflex amplitudes were reduced in patients but significantly less compared to controls, which again suggests a fixed reflex gain. This ‘inflexibility’ of postural reflexes was reflected by the CFP which showed much smaller changes between 0 and 250 ms in patients than controls. These results could not be ascribed to a different ability to yield because posterior displacement of the COG was identical in patients and controls during the ‘yield’ condition. We conclude that (1) patients with Parkinson's disease have abnormal and ‘inflexible’ postural reflexes, associated with delayed corrective movements about the ankle joint and increased body sway; and (2) the increased forward displacement of the CFP in patients likely reflects high stiffness in ankle muscles because reflex changes in controls only affected the CFP more than 150 ms after the perturbation. The increased muscle stiffness and inflexibility of postural reflexes in Parkinson's disease may contribute to balance impairment in daily life.</abstract><note type="content">Section title: Research article</note><subject><genre>Article category</genre><topic>Clinical section</topic></subject><subject><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>Postural set</topic><topic>Reflex</topic><topic>Gain</topic><topic>Balance</topic><topic>Instability</topic></subject><relatedItem type="host"><titleInfo><title>Journal of the Neurological Sciences</title></titleInfo><titleInfo type="abbreviated"><title>JNS</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199504</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0021-4</identifier><part><date>199504</date><detail type="volume"><number>129</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>81</start><end>238</end></extent><extent unit="pages"><start>109</start><end>119</end></extent></part></relatedItem><identifier type="istex">6560A3FE3BDD72B060C79289995F00758AB4B920</identifier><identifier type="DOI">10.1016/0022-510X(94)00253-K</identifier><identifier type="PII">0022-510X(94)00253-K</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/6560A3FE3BDD72B060C79289995F00758AB4B920/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROIMAGING</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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