MovDisordV3, Main, Merge, bibRecord, 002B56

Gait and balance disorders in Parkinson's disease: Impaired active braking of the fall of centre of gravity

Identifieur interne : 002B56 ( Main/Merge ); précédent : 002B55; suivant : 002B57

Gait 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.

RBID : ISTEX:0ED61862F7ABEEF5D1BF780D12CC96A8747C1EFE

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), Female, Gait Apraxia (etiology), Gait Apraxia (pathology), Gait Apraxia (physiopathology), Gravitation, Humans, Levodopa (pharmacology), Levodopa (therapeutic use), Magnetic Resonance Imaging, Male, Mesencephalon (pathology), Mesencephalon (physiopathology), Middle Aged, Organ Size, Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson Disease (physiopathology), 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:

DOI: 10.1002/mds.22269

Links to Exploration step

ISTEX:0ED61862F7ABEEF5D1BF780D12CC96A8747C1EFE

Le document en format XML

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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>
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<term>Levodopa</term>
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<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
</keywords>
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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>
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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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<author><name sortKey="Do, Manh Cuong" sort="Do, Manh Cuong" uniqKey="Do M" first="Manh-Cuong" last="Do">Manh-Cuong Do</name>
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<author><name sortKey="Welter, Marie Laure" sort="Welter, Marie Laure" uniqKey="Welter M" first="Marie-Laure" last="Welter">Marie-Laure Welter</name>
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<idno type="DOI">10.1002/mds.22269</idno>
<series><title level="j">Movement Disorders</title>
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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.</div>
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<series><title level="j">Movement Disorders</title>
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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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<author><name sortKey="Do, Manh Cuong" sort="Do, Manh Cuong" uniqKey="Do M" first="Manh Cuong" last="Do">Manh Cuong Do</name>
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<author><name sortKey="Bonneville, Fabrice" sort="Bonneville, Fabrice" uniqKey="Bonneville F" first="Fabrice" last="Bonneville">Fabrice Bonneville</name>
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<term>Basal Ganglia (physiopathology)</term>
<term>Biomechanical Phenomena</term>
<term>Brain (pathology)</term>
<term>Brain (physiopathology)</term>
<term>Case-Control Studies</term>
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<term>Female</term>
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<term>Gait Apraxia (pathology)</term>
<term>Gait Apraxia (physiopathology)</term>
<term>Gravitation</term>
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<term>Levodopa (pharmacology)</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.</div>
</front>
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Movement Disorders (revue)

Gait and balance disorders in Parkinson's disease: Impaired active braking of the fall of centre of gravity

Gait and balance disorders in Parkinson's disease: Impaired active braking of the fall of centre of gravity

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	Movement Disorders (revue)
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