Gait and balance disorders in Parkinson's disease: impaired active braking of the fall of centre of gravity.
Identifieur interne : 002416 ( Ncbi/Checkpoint ); précédent : 002415; suivant : 002417Gait and balance disorders in Parkinson's disease: impaired active braking of the fall of centre of gravity.
Auteurs : Nathalie Chastan [France] ; Manh Cuong Do ; Fabrice Bonneville ; Frédéric Torny ; Frédéric Bloch ; G W Max Westby ; Didier Dormont ; Yves Agid [France] ; Marie-Laure WelterSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2009.
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), Postural Balance (drug effects), Postural Balance (physiology), Sensation Disorders (etiology), Sensation Disorders (pathology), Sensation Disorders (physiopathology), Walking (physiology).
- 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.
DOI: 10.1002/mds.22269
PubMed: 18973252
Affiliations:
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Do</name></author><author><name sortKey="Bonneville, Fabrice" sort="Bonneville, Fabrice" uniqKey="Bonneville F" first="Fabrice" last="Bonneville">Fabrice Bonneville</name></author><author><name sortKey="Torny, Frederic" sort="Torny, Frederic" uniqKey="Torny F" first="Frédéric" last="Torny">Frédéric Torny</name></author><author><name sortKey="Bloch, Frederic" sort="Bloch, Frederic" uniqKey="Bloch F" first="Frédéric" last="Bloch">Frédéric Bloch</name></author><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></author><author><name sortKey="Dormont, Didier" sort="Dormont, Didier" uniqKey="Dormont D" first="Didier" last="Dormont">Didier Dormont</name></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><affiliation><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" 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sortKey="Torny, Frederic" sort="Torny, Frederic" uniqKey="Torny F" first="Frédéric" last="Torny">Frédéric Torny</name></author><author><name sortKey="Bloch, Frederic" sort="Bloch, Frederic" uniqKey="Bloch F" first="Frédéric" last="Bloch">Frédéric Bloch</name></author><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></author><author><name sortKey="Dormont, Didier" sort="Dormont, Didier" uniqKey="Dormont D" first="Didier" last="Dormont">Didier Dormont</name></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><affiliation><country>France</country><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author><author><name sortKey="Welter, Marie Laure" sort="Welter, Marie Laure" uniqKey="Welter M" first="Marie-Laure" last="Welter">Marie-Laure Welter</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><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>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></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></keywords></textClass></profileDesc></teiHeader><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></TEI><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement><orgName><li>Hôpital de la Salpêtrière</li></orgName></list><tree><noCountry><name sortKey="Bloch, Frederic" sort="Bloch, Frederic" uniqKey="Bloch F" first="Frédéric" last="Bloch">Frédéric Bloch</name><name sortKey="Bonneville, Fabrice" sort="Bonneville, Fabrice" uniqKey="Bonneville F" first="Fabrice" last="Bonneville">Fabrice Bonneville</name><name sortKey="Do, Manh Cuong" sort="Do, Manh Cuong" uniqKey="Do M" first="Manh Cuong" last="Do">Manh Cuong Do</name><name sortKey="Dormont, Didier" sort="Dormont, Didier" uniqKey="Dormont D" first="Didier" last="Dormont">Didier Dormont</name><name sortKey="Torny, Frederic" sort="Torny, Frederic" uniqKey="Torny F" first="Frédéric" last="Torny">Frédéric Torny</name><name sortKey="Welter, Marie Laure" sort="Welter, Marie Laure" uniqKey="Welter M" first="Marie-Laure" last="Welter">Marie-Laure Welter</name><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></noCountry><country name="France"><noRegion><name sortKey="Chastan, Nathalie" sort="Chastan, Nathalie" uniqKey="Chastan N" first="Nathalie" last="Chastan">Nathalie Chastan</name></noRegion><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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