Gait and balance disorders in Parkinson's disease: Impaired active braking of the fall of centre of gravity
Identifieur interne : 002295 ( Main/Curation ); précédent : 002294; suivant : 002296Gait 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 [France] ; Frédéric Torny [France] ; Frédéric Bloch [France] ; G. W. Max Westby [France] ; Didier Dormont [France] ; Yves Agid [France] ; Marie-Laure Welter [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-01-30.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Basal Ganglia (pathology), Basal Ganglia (physiopathology), Biomechanical Phenomena, Brain (pathology), Brain (physiopathology), Case-Control Studies, Dopamine (physiology), Equilibrium disorder, Female, Gait Apraxia (etiology), Gait Apraxia (pathology), Gait Apraxia (physiopathology), Gait disorder, Gravitation, Humans, Instability, Levodopa (pharmacology), Levodopa (therapeutic use), Magnetic Resonance Imaging, Male, Mesencephalon (pathology), Mesencephalon (physiopathology), Middle Aged, Nervous system diseases, Nuclear magnetic resonance imaging, Organ Size, Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Postural Balance (drug effects), Postural Balance (physiology), Sensation Disorders (etiology), Sensation Disorders (pathology), Sensation Disorders (physiopathology), Walking (physiology), gait initiation, magnetic resonance imaging, postural instability.
- MESH :
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- chemical , physiology : Dopamine.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- complications : Parkinson Disease.
- drug effects : Postural Balance.
- drug therapy : Parkinson Disease.
- etiology : Gait Apraxia, Sensation Disorders.
- pathology : Basal Ganglia, Brain, Gait Apraxia, Mesencephalon, Parkinson Disease, Sensation Disorders.
- physiology : Postural Balance, Walking.
- physiopathology : Basal Ganglia, Brain, Gait Apraxia, Mesencephalon, Parkinson Disease, Sensation Disorders.
- Biomechanical Phenomena, Case-Control Studies, Female, Gravitation, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Organ Size.
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:
- https://api.istex.fr/document/0ED61862F7ABEEF5D1BF780D12CC96A8747C1EFE/fulltext/pdf
- https://hal.inria.fr/hal-00805424
- https://hal.archives-ouvertes.fr/hal-00583632
DOI: 10.1002/mds.22269
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<term>Basal Ganglia (pathology)</term>
<term>Basal Ganglia (physiopathology)</term>
<term>Biomechanical Phenomena</term>
<term>Brain (pathology)</term>
<term>Brain (physiopathology)</term>
<term>Case-Control Studies</term>
<term>Dopamine (physiology)</term>
<term>Equilibrium disorder</term>
<term>Female</term>
<term>Gait Apraxia (etiology)</term>
<term>Gait Apraxia (pathology)</term>
<term>Gait Apraxia (physiopathology)</term>
<term>Gait disorder</term>
<term>Gravitation</term>
<term>Humans</term>
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<term>Levodopa (therapeutic use)</term>
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<term>Mesencephalon (pathology)</term>
<term>Mesencephalon (physiopathology)</term>
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<term>Nervous system diseases</term>
<term>Nuclear magnetic resonance imaging</term>
<term>Organ Size</term>
<term>Parkinson Disease (complications)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Parkinson disease</term>
<term>Parkinson's disease</term>
<term>Postural Balance (drug effects)</term>
<term>Postural Balance (physiology)</term>
<term>Sensation Disorders (etiology)</term>
<term>Sensation Disorders (pathology)</term>
<term>Sensation Disorders (physiopathology)</term>
<term>Walking (physiology)</term>
<term>gait initiation</term>
<term>magnetic resonance imaging</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term>
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</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Postural Balance</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Apraxia</term>
<term>Sensation Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term>
<term>Brain</term>
<term>Gait Apraxia</term>
<term>Mesencephalon</term>
<term>Parkinson Disease</term>
<term>Sensation Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Postural Balance</term>
<term>Walking</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term>
<term>Brain</term>
<term>Gait Apraxia</term>
<term>Mesencephalon</term>
<term>Parkinson Disease</term>
<term>Sensation Disorders</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Biomechanical Phenomena</term>
<term>Case-Control Studies</term>
<term>Female</term>
<term>Gravitation</term>
<term>Humans</term>
<term>Magnetic Resonance Imaging</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Organ Size</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Imagerie RMN</term>
<term>Instabilité</term>
<term>Maladie de Parkinson</term>
<term>Pathologie du système nerveux</term>
<term>Trouble de l'équilibre</term>
<term>Trouble de la marche</term>
</keywords>
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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>
</front>
</TEI>
<double idat="0885-3185:2009:Chastan N:gait:and:balance"><INIST><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Gait and Balance Disorders in Parkinson's Disease : Impaired Active Braking of the Fall of Centre of Gravity</title>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Gait and Balance Disorders in Parkinson's Disease : Impaired Active Braking of the Fall of Centre of Gravity</title>
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</analytic>
<series><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="2009">2009</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Equilibrium disorder</term>
<term>Gait disorder</term>
<term>Instability</term>
<term>Nervous system diseases</term>
<term>Nuclear magnetic resonance imaging</term>
<term>Parkinson disease</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Trouble de la marche</term>
<term>Trouble de l'équilibre</term>
<term>Maladie de Parkinson</term>
<term>Pathologie du système nerveux</term>
<term>Instabilité</term>
<term>Imagerie RMN</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Gait and balance disorders are common in Parkinson 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.</div>
</front>
</TEI>
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<author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name>
<affiliation><country>France</country>
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<author><name sortKey="Torny, Frederic" sort="Torny, Frederic" uniqKey="Torny F" first="Frédéric" last="Torny">Frédéric Torny</name>
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<author><name sortKey="Bloch, Frederic" sort="Bloch, Frederic" uniqKey="Bloch F" first="Frédéric" last="Bloch">Frédéric Bloch</name>
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<author><name sortKey="Westby, G W Max" sort="Westby, G W Max" uniqKey="Westby G" first="G. W. Max" last="Westby">G. W. Max Westby</name>
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<placeName><settlement type="city">Paris</settlement>
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<author><name sortKey="Dormont, Didier" sort="Dormont, Didier" uniqKey="Dormont D" first="Didier" last="Dormont">Didier Dormont</name>
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<placeName><settlement type="city">Paris</settlement>
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<orgName type="university">Université Pierre-et-Marie-Curie</orgName>
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<author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name>
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<placeName><settlement type="city">Paris</settlement>
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<author><name sortKey="Welter, Marie Aure" sort="Welter, Marie Aure" uniqKey="Welter M" first="Marie-Laure" last="Welter">Marie-Laure Welter</name>
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<monogr></monogr>
<series><title level="j">Movement Disorders</title>
<title level="j" type="sub">Official Journal of the Movement Disorder Society</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="ISSN">0885-3185</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (pharmacology)</term>
<term>Antiparkinson Agents (therapeutic use)</term>
<term>Basal Ganglia (pathology)</term>
<term>Basal Ganglia (physiopathology)</term>
<term>Biomechanical Phenomena</term>
<term>Brain (pathology)</term>
<term>Brain (physiopathology)</term>
<term>Case-Control Studies</term>
<term>Dopamine (physiology)</term>
<term>Female</term>
<term>Gait Apraxia (etiology)</term>
<term>Gait Apraxia (pathology)</term>
<term>Gait Apraxia (physiopathology)</term>
<term>Gravitation</term>
<term>Humans</term>
<term>Levodopa (pharmacology)</term>
<term>Levodopa (therapeutic use)</term>
<term>Magnetic Resonance Imaging</term>
<term>Male</term>
<term>Mesencephalon (pathology)</term>
<term>Mesencephalon (physiopathology)</term>
<term>Middle Aged</term>
<term>Organ Size</term>
<term>Parkinson Disease (complications)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Parkinson's disease</term>
<term>Postural Balance (drug effects)</term>
<term>Postural Balance (physiology)</term>
<term>Sensation Disorders (etiology)</term>
<term>Sensation Disorders (pathology)</term>
<term>Sensation Disorders (physiopathology)</term>
<term>Walking (physiology)</term>
<term>gait initiation</term>
<term>magnetic resonance imaging</term>
<term>postural instability</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Postural Balance</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Apraxia</term>
<term>Sensation Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term>
<term>Brain</term>
<term>Gait Apraxia</term>
<term>Mesencephalon</term>
<term>Parkinson Disease</term>
<term>Sensation Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Postural Balance</term>
<term>Walking</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term>
<term>Brain</term>
<term>Gait Apraxia</term>
<term>Mesencephalon</term>
<term>Parkinson Disease</term>
<term>Sensation Disorders</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Biomechanical Phenomena</term>
<term>Case-Control Studies</term>
<term>Female</term>
<term>Gravitation</term>
<term>Humans</term>
<term>Magnetic Resonance Imaging</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Organ Size</term>
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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>
</front>
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