Objective assessment of motor slowness in Huntington's disease: Clinical correlates and 2‐year follow‐up
Identifieur interne : 000542 ( Istex/Corpus ); précédent : 000541; suivant : 000543Objective assessment of motor slowness in Huntington's disease: Clinical correlates and 2‐year follow‐up
Auteurs : Jeroen P. P. Van Vugt ; Karlijne K. E. Piet ; Liesbeth J. Vink ; Sabine Siesling ; Aeilko H. Zwinderman ; Huub A. M. Middelkoop ; Raymund A. C. RoosSource :
- Movement Disorders [ 0885-3185 ] ; 2004-03.
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Abstract
Functional disability of patients with Huntington's disease (HD) is determined by impairment of voluntary motor function rather than the presence of chorea. However, only few attempts have been made to quantify this motor impairment. By using a simple reaction time paradigm, we measured the time needed for movement initiation (akinesia) and execution (bradykinesia) in 76 HD patients and 127 controls. Akinesia and bradykinesia were already evident in early stages and increased linearly with increasing disease stage. Quantified motor slowness correlated with clinical impairment of voluntary movements but also with cognitive impairment and medication use. In patients without severe cognitive impairment, quantified motor slowness reflected clinical motor impairment more purely. During 1.9 years follow‐up (range, 0.8–3.8 years), quantified akinesia and bradykinesia progressed concomitantly with progression of clinical impairment of voluntary movements, cognition, and functional capacity. However, rate of change in motor slowness did not discriminate between patients whose disease stage remained stable and those whose disease stage progressed. We conclude that the reaction time paradigm may be used to quantify akinesia and bradykinesia in HD, at least in patients without severe cognitive impairment. Although reaction and movement times increased in time, these measures failed to detect functionally important changes during our follow‐up period. © 2004 Movement Disorder Society
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DOI: 10.1002/mds.10718
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However, only few attempts have been made to quantify this motor impairment. By using a simple reaction time paradigm, we measured the time needed for movement initiation (akinesia) and execution (bradykinesia) in 76 HD patients and 127 controls. Akinesia and bradykinesia were already evident in early stages and increased linearly with increasing disease stage. Quantified motor slowness correlated with clinical impairment of voluntary movements but also with cognitive impairment and medication use. In patients without severe cognitive impairment, quantified motor slowness reflected clinical motor impairment more purely. During 1.9 years follow‐up (range, 0.8–3.8 years), quantified akinesia and bradykinesia progressed concomitantly with progression of clinical impairment of voluntary movements, cognition, and functional capacity. However, rate of change in motor slowness did not discriminate between patients whose disease stage remained stable and those whose disease stage progressed. We conclude that the reaction time paradigm may be used to quantify akinesia and bradykinesia in HD, at least in patients without severe cognitive impairment. Although reaction and movement times increased in time, these measures failed to detect functionally important changes during our follow‐up period. © 2004 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Jeroen P.P. van Vugt MD, PhD</name><affiliations><json:string>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Karlijne K.E. Piet MSc</name><affiliations><json:string>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Liesbeth J. Vink MSc</name><affiliations><json:string>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Sabine Siesling PhD</name><affiliations><json:string>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Aeilko H. Zwinderman PhD</name><affiliations><json:string>Department of Medical Statistics, Leiden University Medical Centre, Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Huub A.M. Middelkoop PhD</name><affiliations><json:string>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Raymund A.C. 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By using a simple reaction time paradigm, we measured the time needed for movement initiation (akinesia) and execution (bradykinesia) in 76 HD patients and 127 controls. Akinesia and bradykinesia were already evident in early stages and increased linearly with increasing disease stage. Quantified motor slowness correlated with clinical impairment of voluntary movements but also with cognitive impairment and medication use. In patients without severe cognitive impairment, quantified motor slowness reflected clinical motor impairment more purely. During 1.9 years follow‐up (range, 0.8–3.8 years), quantified akinesia and bradykinesia progressed concomitantly with progression of clinical impairment of voluntary movements, cognition, and functional capacity. However, rate of change in motor slowness did not discriminate between patients whose disease stage remained stable and those whose disease stage progressed. We conclude that the reaction time paradigm may be used to quantify akinesia and bradykinesia in HD, at least in patients without severe cognitive impairment. 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We conclude that the reaction time paradigm may be used to quantify akinesia and bradykinesia in HD, at least in patients without severe cognitive impairment. 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However, only few attempts have been made to quantify this motor impairment. By using a simple reaction time paradigm, we measured the time needed for movement initiation (akinesia) and execution (bradykinesia) in 76 HD patients and 127 controls. Akinesia and bradykinesia were already evident in early stages and increased linearly with increasing disease stage. Quantified motor slowness correlated with clinical impairment of voluntary movements but also with cognitive impairment and medication use. In patients without severe cognitive impairment, quantified motor slowness reflected clinical motor impairment more purely. During 1.9 years follow‐up (range, 0.8–3.8 years), quantified akinesia and bradykinesia progressed concomitantly with progression of clinical impairment of voluntary movements, cognition, and functional capacity. However, rate of change in motor slowness did not discriminate between patients whose disease stage remained stable and those whose disease stage progressed. We conclude that the reaction time paradigm may be used to quantify akinesia and bradykinesia in HD, at least in patients without severe cognitive impairment. Although reaction and movement times increased in time, these measures failed to detect functionally important changes during our follow‐up period. © 2004 Movement Disorder Society</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>Objective assessment of motor slowness in Huntington's disease: Clinical correlates and 2‐year follow‐up</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Motor Slowness in Huntington's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Objective assessment of motor slowness in Huntington's disease: Clinical correlates and 2‐year follow‐up</title></titleInfo><name type="personal"><namePart type="given">Jeroen P.P.</namePart><namePart type="family">van Vugt</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</affiliation><description>Correspondence: Department of Neurology, Leiden University Medical Centre, PO Box 9600, 2300 RC Leiden, The Netherlands</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karlijne K.E.</namePart><namePart type="family">Piet</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Liesbeth J.</namePart><namePart type="family">Vink</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sabine</namePart><namePart type="family">Siesling</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Aeilko H.</namePart><namePart type="family">Zwinderman</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Medical Statistics, Leiden University Medical Centre, Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Huub A.M.</namePart><namePart type="family">Middelkoop</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Raymund A.C.</namePart><namePart type="family">Roos</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Leiden University Medical Centre, 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">2004-03</dateIssued><dateCaptured encoding="w3cdtf">2003-05-17</dateCaptured><dateValid encoding="w3cdtf">2003-10-17</dateValid><copyrightDate encoding="w3cdtf">2004</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">5</extent><extent unit="tables">4</extent><extent unit="references">88</extent><extent unit="words">9130</extent></physicalDescription><abstract lang="en">Functional disability of patients with Huntington's disease (HD) is determined by impairment of voluntary motor function rather than the presence of chorea. However, only few attempts have been made to quantify this motor impairment. By using a simple reaction time paradigm, we measured the time needed for movement initiation (akinesia) and execution (bradykinesia) in 76 HD patients and 127 controls. Akinesia and bradykinesia were already evident in early stages and increased linearly with increasing disease stage. Quantified motor slowness correlated with clinical impairment of voluntary movements but also with cognitive impairment and medication use. In patients without severe cognitive impairment, quantified motor slowness reflected clinical motor impairment more purely. During 1.9 years follow‐up (range, 0.8–3.8 years), quantified akinesia and bradykinesia progressed concomitantly with progression of clinical impairment of voluntary movements, cognition, and functional capacity. However, rate of change in motor slowness did not discriminate between patients whose disease stage remained stable and those whose disease stage progressed. We conclude that the reaction time paradigm may be used to quantify akinesia and bradykinesia in HD, at least in patients without severe cognitive impairment. Although reaction and movement times increased in time, these measures failed to detect functionally important changes during our follow‐up period. © 2004 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Huntington's disease</topic><topic>akinesia</topic><topic>bradykinesia</topic><topic>reaction time</topic><topic>follow‐up</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>Research 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>2004</date><detail type="volume"><caption>vol.</caption><number>19</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>285</start><end>297</end><total>13</total></extent></part></relatedItem><identifier type="istex">ADF3EDB4726CA2D3868BDB8ECF9F79BD46F0782D</identifier><identifier type="DOI">10.1002/mds.10718</identifier><identifier type="ArticleID">MDS10718</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2004 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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