Spectrum of gait impairments in presymptomatic and symptomatic Huntington's disease
Identifieur interne : 000895 ( Istex/Corpus ); précédent : 000894; suivant : 000896Spectrum of gait impairments in presymptomatic and symptomatic Huntington's disease
Auteurs : Ashwini K. Rao ; Lisa Muratori ; Elan D. Louis ; Carol B. Moskowitz ; Karen S. MarderSource :
- Movement Disorders [ 0885-3185 ] ; 2008-06-15.
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- KwdEn :
Abstract
The purpose of this study was to quantify gait impairments in presymptomatic and symptomatic Huntington's disease (HD) subjects, and examine sensitivity of gait measures. Our sample (n = 65) included presymptomatic mutation carriers (PMC) (n = 15), symptomatic HD subjects (SHD) (n = 30) and healthy controls (n = 20). Participants were requested to walk at their preferred speed on a computerized walkway that recorded spatiotemporal variables. We administered the Unified HD Rating Scale (UHDRS) for PMC and SHD. PMC demonstrated decreased gait velocity (P < 0.01), stride length (P < 0.008), and increased time in double support (P < 0.001); and demonstrated higher variability in stride length (P < 0.01) and step time (P < 0.004) compared with controls. These impairments worsened with increasing disease severity for SHD. Gait impairments were correlated with predicted years to onset in PMC (velocity = −0.65; cadence = −0.70, step time = 0.71) and demonstrated high sensitivity and specificity in distinguishing between controls and mutation carriers. In contrast, UHDRS scores did not reveal impairments in gait and balance. Gait bradykinesia and dynamic balance impairments begin in the presymptomatic stage of HD and continue to worsen in the symptomatic stages. Gait measures are sensitive in differentiating between mutation positive and negative individuals even when impairments were not detected by clinical neurological examination. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.21987
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Rao</name><affiliation><mods:affiliation>Program in Physical Therapy, Department of Rehabilitation Medicine, Columbia University Medical Center, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</mods:affiliation></affiliation></author><author><name sortKey="Muratori, Lisa" sort="Muratori, Lisa" uniqKey="Muratori L" first="Lisa" last="Muratori">Lisa Muratori</name><affiliation><mods:affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Physical Therapy, School of Health Technology and Management, Stony Brook University, Stony Brook, NY, USA</mods:affiliation></affiliation></author><author><name sortKey="Louis, Elan D" sort="Louis, Elan D" uniqKey="Louis E" first="Elan D." last="Louis">Elan D. 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Louis</name><affiliation><mods:affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>G.H. Sergievsky Center, Columbia University Medical Center, New York, NY, USA</mods:affiliation></affiliation></author><author><name sortKey="Moskowitz, Carol B" sort="Moskowitz, Carol B" uniqKey="Moskowitz C" first="Carol B." last="Moskowitz">Carol B. Moskowitz</name><affiliation><mods:affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</mods:affiliation></affiliation></author><author><name sortKey="Marder, Karen S" sort="Marder, Karen S" uniqKey="Marder K" first="Karen S." last="Marder">Karen S. Marder</name><affiliation><mods:affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>G.H. 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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="2008-06-15">2008-06-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1100">1100</biblScope><biblScope unit="page" to="1107">1107</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">ED863BB5ED4591C7018328D8B7C760992C0DE1AA</idno><idno type="DOI">10.1002/mds.21987</idno><idno type="ArticleID">MDS21987</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Huntington's disease</term><term>gait</term><term>motor control</term><term>presymptomatic and symptomatic</term><term>sensitivity and specificity</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The purpose of this study was to quantify gait impairments in presymptomatic and symptomatic Huntington's disease (HD) subjects, and examine sensitivity of gait measures. Our sample (n = 65) included presymptomatic mutation carriers (PMC) (n = 15), symptomatic HD subjects (SHD) (n = 30) and healthy controls (n = 20). Participants were requested to walk at their preferred speed on a computerized walkway that recorded spatiotemporal variables. We administered the Unified HD Rating Scale (UHDRS) for PMC and SHD. PMC demonstrated decreased gait velocity (P < 0.01), stride length (P < 0.008), and increased time in double support (P < 0.001); and demonstrated higher variability in stride length (P < 0.01) and step time (P < 0.004) compared with controls. These impairments worsened with increasing disease severity for SHD. Gait impairments were correlated with predicted years to onset in PMC (velocity = −0.65; cadence = −0.70, step time = 0.71) and demonstrated high sensitivity and specificity in distinguishing between controls and mutation carriers. In contrast, UHDRS scores did not reveal impairments in gait and balance. Gait bradykinesia and dynamic balance impairments begin in the presymptomatic stage of HD and continue to worsen in the symptomatic stages. Gait measures are sensitive in differentiating between mutation positive and negative individuals even when impairments were not detected by clinical neurological examination. © 2008 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ashwini K. Rao Otr, EdD</name><affiliations><json:string>Program in Physical Therapy, Department of Rehabilitation Medicine, Columbia University Medical Center, New York, NY, USA</json:string><json:string>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</json:string></affiliations></json:item><json:item><name>Lisa Muratori PT, EdD</name><affiliations><json:string>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</json:string><json:string>Department of Physical Therapy, School of Health Technology and Management, Stony Brook University, Stony Brook, NY, USA</json:string></affiliations></json:item><json:item><name>Elan D. Louis MD, MSc</name><affiliations><json:string>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</json:string><json:string>Department of Neurology, Columbia University Medical Center, New York, NY, USA</json:string><json:string>G.H. Sergievsky Center, Columbia University Medical Center, New York, NY, USA</json:string></affiliations></json:item><json:item><name>Carol B. Moskowitz MS, Aprn‐C, CNRN</name><affiliations><json:string>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</json:string><json:string>Department of Neurology, Columbia University Medical Center, New York, NY, USA</json:string></affiliations></json:item><json:item><name>Karen S. Marder MD, MPH</name><affiliations><json:string>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</json:string><json:string>Department of Neurology, Columbia University Medical Center, New York, NY, USA</json:string><json:string>G.H. Sergievsky Center, Columbia University Medical Center, New York, NY, USA</json:string><json:string>Departments of Psychiatry, Columbia University Medical Center, New York, NY, USA</json:string><json:string>Taub Institute for Alzheimer's Disease and the Aging Brain, Columbia University Medical Center, New York, NY, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Huntington's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gait</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>presymptomatic and symptomatic</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sensitivity and specificity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor control</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The purpose of this study was to quantify gait impairments in presymptomatic and symptomatic Huntington's disease (HD) subjects, and examine sensitivity of gait measures. Our sample (n = 65) included presymptomatic mutation carriers (PMC) (n = 15), symptomatic HD subjects (SHD) (n = 30) and healthy controls (n = 20). Participants were requested to walk at their preferred speed on a computerized walkway that recorded spatiotemporal variables. We administered the Unified HD Rating Scale (UHDRS) for PMC and SHD. PMC demonstrated decreased gait velocity (P > 0.01), stride length (P > 0.008), and increased time in double support (P > 0.001); and demonstrated higher variability in stride length (P > 0.01) and step time (P > 0.004) compared with controls. These impairments worsened with increasing disease severity for SHD. Gait impairments were correlated with predicted years to onset in PMC (velocity = −0.65; cadence = −0.70, step time = 0.71) and demonstrated high sensitivity and specificity in distinguishing between controls and mutation carriers. In contrast, UHDRS scores did not reveal impairments in gait and balance. Gait bradykinesia and dynamic balance impairments begin in the presymptomatic stage of HD and continue to worsen in the symptomatic stages. 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Sergievsky Center, Columbia University Medical Center, New York, NY, USA</affiliation></author><author><persName><forename type="first">Carol B.</forename><surname>Moskowitz</surname><roleName type="degree">MS, Aprn‐C, CNRN</roleName></persName><affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</affiliation><affiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</affiliation></author><author><persName><forename type="first">Karen S.</forename><surname>Marder</surname><roleName type="degree">MD, MPH</roleName></persName><affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</affiliation><affiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</affiliation><affiliation>G.H. 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Our sample (n = 65) included presymptomatic mutation carriers (PMC) (n = 15), symptomatic HD subjects (SHD) (n = 30) and healthy controls (n = 20). Participants were requested to walk at their preferred speed on a computerized walkway that recorded spatiotemporal variables. We administered the Unified HD Rating Scale (UHDRS) for PMC and SHD. PMC demonstrated decreased gait velocity (P < 0.01), stride length (P < 0.008), and increased time in double support (P < 0.001); and demonstrated higher variability in stride length (P < 0.01) and step time (P < 0.004) compared with controls. These impairments worsened with increasing disease severity for SHD. Gait impairments were correlated with predicted years to onset in PMC (velocity = −0.65; cadence = −0.70, step time = 0.71) and demonstrated high sensitivity and specificity in distinguishing between controls and mutation carriers. In contrast, UHDRS scores did not reveal impairments in gait and balance. Gait bradykinesia and dynamic balance impairments begin in the presymptomatic stage of HD and continue to worsen in the symptomatic stages. Gait measures are sensitive in differentiating between mutation positive and negative individuals even when impairments were not detected by clinical neurological examination. © 2008 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Huntington's disease</term></item><item><term>gait</term></item><item><term>presymptomatic and symptomatic</term></item><item><term>sensitivity and specificity</term></item><item><term>motor control</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-08-29">Received</change><change when="2008-01-22">Registration</change><change when="2008-06-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/ED863BB5ED4591C7018328D8B7C760992C0DE1AA/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. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="80"><doi origin="wiley" registered="yes">10.1002/mds.v23:8</doi><numberingGroup><numbering type="journalVolume" number="23">23</numbering><numbering type="journalIssue">8</numbering></numberingGroup><coverDate startDate="2008-06-15">15 June 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="50" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.21987</doi><idGroup><id type="unit" value="MDS21987"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2008 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2007-08-29"></event><event type="manuscriptRevised" date="2007-11-07"></event><event type="manuscriptAccepted" date="2008-01-22"></event><event type="publishedOnlineEarlyUnpaginated" date="2008-04-15"></event><event type="firstOnline" date="2008-04-15"></event><event type="publishedOnlineFinalForm" date="2008-06-24"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1100</numbering><numbering type="pageLast">1107</numbering></numberingGroup><correspondenceTo>Program in Physical Therapy, Columbia University Medical Center, Room 823B, 710 West 168th Street, New York, NY 10032</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS21987.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="34"></count><count type="wordTotal" number="5577"></count></countGroup><titleGroup><title type="main" xml:lang="en">Spectrum of gait impairments in presymptomatic and symptomatic Huntington's disease</title><title type="short" xml:lang="en">Gait Impairments in PRE‐HD and Symptomatic HD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Ashwini K.</givenNames><familyName>Rao</familyName><degrees>Otr, EdD</degrees></personName><contactDetails><email>akr7@columbia.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2 #af3"><personName><givenNames>Lisa</givenNames><familyName>Muratori</familyName><degrees>PT, EdD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2 #af4 #af5"><personName><givenNames>Elan D.</givenNames><familyName>Louis</familyName><degrees>MD, MSc</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2 #af4"><personName><givenNames>Carol B.</givenNames><familyName>Moskowitz</familyName><degrees>MS, Aprn‐C, CNRN</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2 #af4 #af5 #af6 #af7"><personName><givenNames>Karen S.</givenNames><familyName>Marder</familyName><degrees>MD, MPH</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Program in Physical Therapy, Department of Rehabilitation Medicine, Columbia University Medical Center, New York, NY, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Physical Therapy, School of Health Technology and Management, Stony Brook University, Stony Brook, NY, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>G.H. Sergievsky Center, Columbia University Medical Center, New York, NY, USA</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="US" type="organization"><unparsedAffiliation>Departments of Psychiatry, Columbia University Medical Center, New York, NY, USA</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="US" type="organization"><unparsedAffiliation>Taub Institute for Alzheimer's Disease and the Aging Brain, Columbia University Medical Center, New York, NY, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Huntington's disease</keyword><keyword xml:id="kwd2">gait</keyword><keyword xml:id="kwd3">presymptomatic and symptomatic</keyword><keyword xml:id="kwd4">sensitivity and specificity</keyword><keyword xml:id="kwd5">motor control</keyword></keywordGroup><fundingInfo><fundingAgency>Huntington's Disease Society of America (AKR)</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The purpose of this study was to quantify gait impairments in presymptomatic and symptomatic Huntington's disease (HD) subjects, and examine sensitivity of gait measures. Our sample (n = 65) included presymptomatic mutation carriers (PMC) (n = 15), symptomatic HD subjects (SHD) (n = 30) and healthy controls (n = 20). Participants were requested to walk at their preferred speed on a computerized walkway that recorded spatiotemporal variables. We administered the Unified HD Rating Scale (UHDRS) for PMC and SHD. PMC demonstrated decreased gait velocity (<i>P</i> < 0.01), stride length (<i>P</i> < 0.008), and increased time in double support (<i>P</i> < 0.001); and demonstrated higher variability in stride length (<i>P</i> < 0.01) and step time (<i>P</i> < 0.004) compared with controls. These impairments worsened with increasing disease severity for SHD. Gait impairments were correlated with predicted years to onset in PMC (velocity = −0.65; cadence = −0.70, step time = 0.71) and demonstrated high sensitivity and specificity in distinguishing between controls and mutation carriers. In contrast, UHDRS scores did not reveal impairments in gait and balance. Gait bradykinesia and dynamic balance impairments begin in the presymptomatic stage of HD and continue to worsen in the symptomatic stages. Gait measures are sensitive in differentiating between mutation positive and negative individuals even when impairments were not detected by clinical neurological examination. © 2008 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Spectrum of gait impairments in presymptomatic and symptomatic Huntington's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Gait Impairments in PRE‐HD and Symptomatic HD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Spectrum of gait impairments in presymptomatic and symptomatic Huntington's disease</title></titleInfo><name type="personal"><namePart type="given">Ashwini K.</namePart><namePart type="family">Rao</namePart><namePart type="termsOfAddress">Otr, EdD</namePart><affiliation>Program in Physical Therapy, Department of Rehabilitation Medicine, Columbia University Medical Center, New York, NY, USA</affiliation><affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</affiliation><description>Correspondence: Program in Physical Therapy, Columbia University Medical Center, Room 823B, 710 West 168th Street, New York, NY 10032</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lisa</namePart><namePart type="family">Muratori</namePart><namePart type="termsOfAddress">PT, EdD</namePart><affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</affiliation><affiliation>Department of Physical Therapy, School of Health Technology and Management, Stony Brook University, Stony Brook, NY, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elan D.</namePart><namePart type="family">Louis</namePart><namePart type="termsOfAddress">MD, MSc</namePart><affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</affiliation><affiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</affiliation><affiliation>G.H. Sergievsky Center, Columbia University Medical Center, New York, NY, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carol B.</namePart><namePart type="family">Moskowitz</namePart><namePart type="termsOfAddress">MS, Aprn‐C, CNRN</namePart><affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</affiliation><affiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karen S.</namePart><namePart type="family">Marder</namePart><namePart type="termsOfAddress">MD, MPH</namePart><affiliation>Huntington's Disease Center of Excellence, New York State Psychiatric Institute, New York, NY, USA</affiliation><affiliation>Department of Neurology, Columbia University Medical Center, New York, NY, USA</affiliation><affiliation>G.H. Sergievsky Center, Columbia University Medical Center, New York, NY, USA</affiliation><affiliation>Departments of Psychiatry, Columbia University Medical Center, New York, NY, USA</affiliation><affiliation>Taub Institute for Alzheimer's Disease and the Aging Brain, Columbia University Medical Center, New York, NY, USA</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">2008-06-15</dateIssued><dateCaptured encoding="w3cdtf">2007-08-29</dateCaptured><dateValid encoding="w3cdtf">2008-01-22</dateValid><copyrightDate encoding="w3cdtf">2008</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">1</extent><extent unit="tables">3</extent><extent unit="references">34</extent><extent unit="words">5577</extent></physicalDescription><abstract lang="en">The purpose of this study was to quantify gait impairments in presymptomatic and symptomatic Huntington's disease (HD) subjects, and examine sensitivity of gait measures. Our sample (n = 65) included presymptomatic mutation carriers (PMC) (n = 15), symptomatic HD subjects (SHD) (n = 30) and healthy controls (n = 20). Participants were requested to walk at their preferred speed on a computerized walkway that recorded spatiotemporal variables. We administered the Unified HD Rating Scale (UHDRS) for PMC and SHD. PMC demonstrated decreased gait velocity (P < 0.01), stride length (P < 0.008), and increased time in double support (P < 0.001); and demonstrated higher variability in stride length (P < 0.01) and step time (P < 0.004) compared with controls. These impairments worsened with increasing disease severity for SHD. Gait impairments were correlated with predicted years to onset in PMC (velocity = −0.65; cadence = −0.70, step time = 0.71) and demonstrated high sensitivity and specificity in distinguishing between controls and mutation carriers. In contrast, UHDRS scores did not reveal impairments in gait and balance. Gait bradykinesia and dynamic balance impairments begin in the presymptomatic stage of HD and continue to worsen in the symptomatic stages. Gait measures are sensitive in differentiating between mutation positive and negative individuals even when impairments were not detected by clinical neurological examination. © 2008 Movement Disorder Society</abstract><note type="funding">Huntington's Disease Society of America (AKR)</note><subject lang="en"><genre>Keywords</genre><topic>Huntington's disease</topic><topic>gait</topic><topic>presymptomatic and symptomatic</topic><topic>sensitivity and specificity</topic><topic>motor control</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. 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