Gait and balance disorders in Parkinson's disease: impaired active braking of the fall of centre of gravity.
Identifieur interne : 000030 ( Hal/Checkpoint ); précédent : 000029; suivant : 000031Gait and balance disorders in Parkinson's disease: impaired active braking of the fall of centre of gravity.
Auteurs : Nathalie Chastan [France] ; Manh-Cuong Do [France] ; Fabrice Bonneville ; Frédéric Torny ; Frédéric Bloch ; G W Max Westby ; Didier Dormont [France] ; Yves Agid [France] ; Marie-Laure Welter [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-01-30.
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.
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DOI: 10.1002/mds.22269
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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.</div></front></TEI><hal api="V3"><titleStmt><title xml:lang="en">Gait and balance disorders in Parkinson's disease: impaired active braking of the fall of centre of gravity.</title><author role="aut"><persName><forename type="first">Nathalie</forename><surname>Chastan</surname></persName><email></email><idno type="halauthor">479008</idno><affiliation ref="#struct-115097"></affiliation></author><author role="aut"><persName><forename type="first">Manh-Cuong</forename><surname>Do</surname></persName><email>manh-cuong.do@u-psud.fr</email><idno type="halauthor">595322</idno><affiliation ref="#struct-148375"></affiliation></author><author role="aut"><persName><forename type="first">Fabrice</forename><surname>Bonneville</surname></persName><email></email><idno type="halauthor">301219</idno></author><author role="aut"><persName><forename type="first">Frédéric</forename><surname>Torny</surname></persName><email></email><idno type="halauthor">598334</idno></author><author role="aut"><persName><forename type="first">Frédéric</forename><surname>Bloch</surname></persName><email></email><idno type="halauthor">380942</idno></author><author role="aut"><persName><forename type="first">G W Max</forename><surname>Westby</surname></persName><email></email><idno type="halauthor">598335</idno></author><author role="aut"><persName><forename type="first">Didier</forename><surname>Dormont</surname></persName><email></email><idno type="halauthor">98507</idno><affiliation ref="#struct-81470"></affiliation></author><author role="aut"><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><email></email><idno type="halauthor">217013</idno><affiliation ref="#struct-43171"></affiliation></author><author role="aut"><persName><forename type="first">Marie-Laure</forename><surname>Welter</surname></persName><email></email><idno type="halauthor">214475</idno><affiliation ref="#struct-81470"></affiliation><affiliation ref="#struct-95919"></affiliation></author><editor role="depositor"><persName><forename>Jeuvrey</forename><surname>Jean</surname></persName><email>jean.jeuvrey@u-psud.fr</email></editor></titleStmt><editionStmt><edition n="v1" type="current"><date type="whenSubmitted">2011-04-06 10:35:55</date><date type="whenModified">2011-04-06 10:35:55</date><date type="whenReleased">2011-04-06 10:35:55</date><date type="whenProduced">2009-01-30</date></edition><respStmt><resp>contributor</resp><name key="159855"><persName><forename>Jeuvrey</forename><surname>Jean</surname></persName><email>jean.jeuvrey@u-psud.fr</email></name></respStmt></editionStmt><publicationStmt><distributor>CCSD</distributor><idno type="halId">hal-00583632</idno><idno type="halUri">https://hal.archives-ouvertes.fr/hal-00583632</idno><idno type="halBibtex">chastan:hal-00583632</idno><idno type="halRefHtml">Movement Disorders, Wiley, 2009, 24 (2), pp.188-95. <10.1002/mds.22269></idno><idno type="halRef">Movement Disorders, Wiley, 2009, 24 (2), pp.188-95. <10.1002/mds.22269></idno></publicationStmt><seriesStmt><idno type="stamp" n="CIAMS">Complexité, Innovation, Activités Motrices et Sportives</idno><idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno><idno type="stamp" n="UNIV-PARIS6">Université Pierre et Marie Curie - Paris VI</idno><idno type="stamp" n="UNIV-PSUD">Université Paris Sud - Paris XI</idno><idno type="stamp" n="UNIV-PARIS11">Université Paris-Sud 11</idno><idno type="stamp" n="UPMC">Université Pierre et Marie Curie</idno><idno type="stamp" n="ICM" p="UPMC">Institut du Cerveau et de la Moëlle Epinière</idno></seriesStmt><notesStmt><note type="audience" n="2">International</note><note type="popular" n="0">No</note><note type="peer" n="1">Yes</note></notesStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Gait and balance disorders in Parkinson's disease: impaired active braking of the fall of centre of gravity.</title><author role="aut"><persName><forename type="first">Nathalie</forename><surname>Chastan</surname></persName><idno type="halAuthorId">479008</idno><affiliation ref="#struct-115097"></affiliation></author><author role="aut"><persName><forename type="first">Manh-Cuong</forename><surname>Do</surname></persName><email>manh-cuong.do@u-psud.fr</email><idno type="halAuthorId">595322</idno><affiliation ref="#struct-148375"></affiliation></author><author role="aut"><persName><forename type="first">Fabrice</forename><surname>Bonneville</surname></persName><idno type="halAuthorId">301219</idno></author><author role="aut"><persName><forename type="first">Frédéric</forename><surname>Torny</surname></persName><idno type="halAuthorId">598334</idno></author><author role="aut"><persName><forename type="first">Frédéric</forename><surname>Bloch</surname></persName><idno type="halAuthorId">380942</idno></author><author role="aut"><persName><forename type="first">G W Max</forename><surname>Westby</surname></persName><idno type="halAuthorId">598335</idno></author><author role="aut"><persName><forename type="first">Didier</forename><surname>Dormont</surname></persName><idno type="halAuthorId">98507</idno><affiliation ref="#struct-81470"></affiliation></author><author role="aut"><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><idno type="halAuthorId">217013</idno><affiliation ref="#struct-43171"></affiliation></author><author role="aut"><persName><forename type="first">Marie-Laure</forename><surname>Welter</surname></persName><idno type="halAuthorId">214475</idno><affiliation ref="#struct-81470"></affiliation><affiliation ref="#struct-95919"></affiliation></author></analytic><monogr><idno type="halJournalId" status="VALID">17211</idno><idno type="issn">0885-3185</idno><idno type="eissn">1531-8257</idno><title level="j">Movement Disorders</title><imprint><publisher>Wiley</publisher><biblScope unit="volume">24</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="pp">188-95</biblScope><date type="datePub">2009-01-30</date></imprint></monogr><idno type="doi">10.1002/mds.22269</idno><idno type="pubmed">18973252</idno></biblStruct></sourceDesc><profileDesc><langUsage><language ident="en">English</language></langUsage><textClass><classCode scheme="halDomain" n="spi.meca.biom">Engineering Sciences [physics]/Mechanics [physics.med-ph]/Biomechanics [physics.med-ph]</classCode><classCode scheme="halDomain" n="phys.meca.biom">Physics [physics]/Mechanics [physics]/Biomechanics [physics.med-ph]</classCode><classCode scheme="halDomain" n="scco.neur">Cognitive science/Neuroscience</classCode><classCode scheme="halTypology" n="ART">Journal articles</classCode></textClass><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.</abstract></profileDesc></hal></record>Pour manipuler ce document sous Unix (Dilib)
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