Gait and balance disorders in Parkinson's disease: Impaired active braking of the fall of centre of gravity
Identifieur interne : 000C99 ( Istex/Corpus ); précédent : 000C98; suivant : 000D00Gait and balance disorders in Parkinson's disease: Impaired active braking of the fall of centre of gravity
Auteurs : Nathalie Chastan ; Manh Cuong Do ; Fabrice Bonneville ; Frédéric Torny ; Frédéric Bloch ; G. W. Max Westby ; Didier Dormont ; Yves Agid ; Marie-Laure WelterSource :
- Movement Disorders [ 0885-3185 ] ; 2009-01-30.
English descriptors
Abstract
Gait and balance disorders are common in Parkinson's disease (PD), but its pathophysiology is still poorly understood. Step length, antero‐posterior, and vertical velocities of the center of gravity (CG) during gait initiation were analyzed in 32 controls and 32 PD patients, with and without levodopa, using a force platform. Brain volumes and mesencephalic surface area were measured in PD patients. During the swing limb period, controls showed a fall in the CG, which was reversed before foot‐contact indicating active braking of the CG fall. In PD patients, without levodopa, step length and velocity were significantly reduced and no braking occurred before foot‐contact in 22 patients. With levodopa, step length and velocity increased in all patients and 7 patients improved their braking capacity. PD patients with normal braking (n = 17) had significantly lower gait and balance disorder scores and higher normalized‐mesencephalic surface areas compared to patients with impaired braking (n = 15). The decreased step length and velocity, characteristic of PD, mainly result from degeneration of central dopaminergic systems. The markedly decreased braking capacity observed in half the PD patients contributes to their gait disorders and postural instability, perhaps as a result of nondopaminergic lesions, possibly at the mesencephalic level. © 2008 Movement Disorder Society
Url:
DOI: 10.1002/mds.22269
Links to Exploration step
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<front><div type="abstract" xml:lang="en">Gait and balance disorders are common in Parkinson's disease (PD), but its pathophysiology is still poorly understood. Step length, antero‐posterior, and vertical velocities of the center of gravity (CG) during gait initiation were analyzed in 32 controls and 32 PD patients, with and without levodopa, using a force platform. Brain volumes and mesencephalic surface area were measured in PD patients. During the swing limb period, controls showed a fall in the CG, which was reversed before foot‐contact indicating active braking of the CG fall. In PD patients, without levodopa, step length and velocity were significantly reduced and no braking occurred before foot‐contact in 22 patients. With levodopa, step length and velocity increased in all patients and 7 patients improved their braking capacity. PD patients with normal braking (n = 17) had significantly lower gait and balance disorder scores and higher normalized‐mesencephalic surface areas compared to patients with impaired braking (n = 15). The decreased step length and velocity, characteristic of PD, mainly result from degeneration of central dopaminergic systems. The markedly decreased braking capacity observed in half the PD patients contributes to their gait disorders and postural instability, perhaps as a result of nondopaminergic lesions, possibly at the mesencephalic level. © 2008 Movement Disorder Society</div>
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<abstract>Gait and balance disorders are common in Parkinson's disease (PD), but its pathophysiology is still poorly understood. Step length, antero‐posterior, and vertical velocities of the center of gravity (CG) during gait initiation were analyzed in 32 controls and 32 PD patients, with and without levodopa, using a force platform. Brain volumes and mesencephalic surface area were measured in PD patients. During the swing limb period, controls showed a fall in the CG, which was reversed before foot‐contact indicating active braking of the CG fall. In PD patients, without levodopa, step length and velocity were significantly reduced and no braking occurred before foot‐contact in 22 patients. With levodopa, step length and velocity increased in all patients and 7 patients improved their braking capacity. PD patients with normal braking (n = 17) had significantly lower gait and balance disorder scores and higher normalized‐mesencephalic surface areas compared to patients with impaired braking (n = 15). The decreased step length and velocity, characteristic of PD, mainly result from degeneration of central dopaminergic systems. The markedly decreased braking capacity observed in half the PD patients contributes to their gait disorders and postural instability, perhaps as a result of nondopaminergic lesions, possibly at the mesencephalic level. © 2008 Movement Disorder Society</abstract>
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</name>
<name type="personal"><namePart type="given">Didier</namePart>
<namePart type="family">Dormont</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
<affiliation>Université Pierre et Marie Curie‐Paris 6, Institut Fédératif de Recherche (IFR‐70), Paris, France</affiliation>
<affiliation>Service de Neuroradiologie, Assistance Publique‐Hôpitaux de Paris, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation>
<affiliation>Centre National de la Recherche et de la Santé, UPR640, Paris, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Yves</namePart>
<namePart type="family">Agid</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
<affiliation>Fédération des Maladies du Système Nerveux, Centre d'Investigation Clinique, Assistance Publique‐Hôpitaux de Paris, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation>
<affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 679, Paris, France</affiliation>
<affiliation>Université Pierre et Marie Curie‐Paris 6, Institut Fédératif de Recherche (IFR‐70), Paris, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Marie‐Laure</namePart>
<namePart type="family">Welter</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
<affiliation>Fédération des Maladies du Système Nerveux, Centre d'Investigation Clinique, Assistance Publique‐Hôpitaux de Paris, Hôpital Pitié‐Salpêtrière, Paris, France</affiliation>
<affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 679, Paris, France</affiliation>
<affiliation>Université Pierre et Marie Curie‐Paris 6, Institut Fédératif de Recherche (IFR‐70), Paris, France</affiliation>
<affiliation>Groupe AVENIR‐IFR 70, Institut National de la Santé et de la Recherche Médicale, Paris, France</affiliation>
<description>Correspondence: Centre d'Investigation Clinique, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75013 Paris, France</description>
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<originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<place><placeTerm type="text">Hoboken</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2009-01-30</dateIssued>
<dateCaptured encoding="w3cdtf">2008-04-04</dateCaptured>
<dateValid encoding="w3cdtf">2008-07-13</dateValid>
<copyrightDate encoding="w3cdtf">2009</copyrightDate>
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<language><languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="figures">3</extent>
<extent unit="tables">2</extent>
<extent unit="references">32</extent>
<extent unit="words">5438</extent>
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<abstract lang="en">Gait and balance disorders are common in Parkinson's disease (PD), but its pathophysiology is still poorly understood. Step length, antero‐posterior, and vertical velocities of the center of gravity (CG) during gait initiation were analyzed in 32 controls and 32 PD patients, with and without levodopa, using a force platform. Brain volumes and mesencephalic surface area were measured in PD patients. During the swing limb period, controls showed a fall in the CG, which was reversed before foot‐contact indicating active braking of the CG fall. In PD patients, without levodopa, step length and velocity were significantly reduced and no braking occurred before foot‐contact in 22 patients. With levodopa, step length and velocity increased in all patients and 7 patients improved their braking capacity. PD patients with normal braking (n = 17) had significantly lower gait and balance disorder scores and higher normalized‐mesencephalic surface areas compared to patients with impaired braking (n = 15). The decreased step length and velocity, characteristic of PD, mainly result from degeneration of central dopaminergic systems. The markedly decreased braking capacity observed in half the PD patients contributes to their gait disorders and postural instability, perhaps as a result of nondopaminergic lesions, possibly at the mesencephalic level. © 2008 Movement Disorder Society</abstract>
<note type="content">*Potential conflict of interest: None reported.</note>
<note type="funding">Institut National de la Santé et de la Recherche Médicale</note>
<note type="funding">Pierre et Marie Curie University Paris 6</note>
<note type="funding">Assistance Publique‐Hôpitaux de Paris</note>
<subject lang="en"><genre>Keywords</genre>
<topic>Parkinson's disease</topic>
<topic>gait initiation</topic>
<topic>postural instability</topic>
<topic>magnetic resonance imaging</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>2009</date>
<detail type="volume"><caption>vol.</caption>
<number>24</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>2</number>
</detail>
<extent unit="pages"><start>188</start>
<end>195</end>
<total>8</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">0ED61862F7ABEEF5D1BF780D12CC96A8747C1EFE</identifier>
<identifier type="DOI">10.1002/mds.22269</identifier>
<identifier type="ArticleID">MDS22269</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Movement Disorder Society</accessCondition>
<recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
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