Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy
Identifieur interne : 002134 ( Main/Corpus ); précédent : 002133; suivant : 002135Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy
Auteurs : G. Ebersbach ; M. Sojer ; F. Valldeoriola ; J. Wissel ; J. Mu Ller ; E. Tolosa ; W. PoeweSource :
- Brain [ 0006-8950 ] ; 1999-07.
English descriptors
Abstract
Quantitative gait analysis has been used to elucidate characteristic features of neurological gait disturbances. Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson's disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy. In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson's disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.
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DOI: 10.1093/brain/122.7.1349
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Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson's disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy. In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson's disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>G. Ebersbach</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>M. Sojer</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>F. Valldeoriola</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>J. Wissel</name><affiliations><json:string>Department of Neurology, University Hospital Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>J. 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In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. 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Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson's disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy. In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson's disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>gait</term></item><item><term>Parkinson's disease</term></item><item><term>ataxia</term></item><item><term>subcortical arteriosclerotic encephalopathy</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1999-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/133B6685FA819C72B929CC40E449D1AACD8B9446/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="nlm-ta">Brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><abbrev-journal-title abbrev-type="publisher">Brain</abbrev-journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">1221349</article-id><article-id pub-id-type="doi">10.1093/brain/122.7.1349</article-id><title-group><article-title>Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Ebersbach</surname><given-names>G.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Sojer</surname><given-names>M.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Valldeoriola</surname><given-names>F.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Wissel</surname><given-names>J.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Müller</surname><given-names>J.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Tolosa</surname><given-names>E.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Poewe</surname><given-names>W.</given-names></name></contrib><aff>Department of Neurology, University Hospital Innsbruck, Austria</aff></contrib-group><author-notes><corresp>Professor Dr W. Poewe, Department of Neurology, Unversity Hospital Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria</corresp></author-notes><pub-date pub-type="ppub"><month>7</month><year>1999</year></pub-date><volume>122</volume><issue>7</issue><fpage>1349</fpage><lpage>1355</lpage><history><date date-type="accepted"><day>25</day><month>02</month><year>1999</year></date><date date-type="received"><day>05</day><month>02</month><year>1999</year></date></history><copyright-statement>© Oxford University Press 1999</copyright-statement><copyright-year>1999</copyright-year><abstract xml:lang="en"><p>Quantitative gait analysis has been used to elucidate characteristic features of neurological gait disturbances. Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson's disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy. In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson's disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.</p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>gait</kwd><kwd>Parkinson's disease</kwd><kwd>ataxia</kwd><kwd>subcortical arteriosclerotic encephalopathy</kwd></kwd-group><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>1349</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>Article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy</title></titleInfo><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Ebersbach</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Sojer</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Valldeoriola</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Wissel</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Müller</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Tolosa</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="family">Poewe</namePart><affiliation>Department of Neurology, University Hospital Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">1999-07</dateIssued><copyrightDate encoding="w3cdtf">1999</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">Quantitative gait analysis has been used to elucidate characteristic features of neurological gait disturbances. Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson's disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy. In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson's disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.</abstract><note type="author-notes">Professor Dr W. Poewe, Department of Neurology, Unversity Hospital Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria</note><subject lang="en"><genre>KWD</genre><topic>gait</topic><topic>Parkinson's disease</topic><topic>ataxia</topic><topic>subcortical arteriosclerotic encephalopathy</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><titleInfo type="abbreviated"><title>Brain</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><identifier type="PublisherID-nlm-ta">Brain</identifier><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>122</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>1349</start><end>1355</end></extent></part></relatedItem><identifier type="istex">133B6685FA819C72B929CC40E449D1AACD8B9446</identifier><identifier type="DOI">10.1093/brain/122.7.1349</identifier><identifier type="local">1221349</identifier><accessCondition type="use and reproduction" contentType="copyright">© Oxford University Press 1999</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/133B6685FA819C72B929CC40E449D1AACD8B9446/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</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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