Dopaminergic modulation of timing control and variability in the gait of Parkinson's disease
Identifieur interne : 002589 ( Main/Exploration ); précédent : 002588; suivant : 002590Dopaminergic modulation of timing control and variability in the gait of Parkinson's disease
Auteurs : Quincy J. Almeida [Canada] ; James S. Frank [Canada] ; Eric A. Roy [Canada] ; Aftab E. Patla [Canada] ; Mandar S. Jog [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2007-09-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Aged, Analysis of Variance, Antiparkinson Agents (administration & dosage), Basal ganglion, Dopamine Agents (administration & dosage), Female, Gait (drug effects), Humans, Male, Middle Aged, Modulation, Nervous system diseases, Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Space Perception (drug effects), Time Perception (drug effects), Timing, Variability, basal ganglia, gait, timing, variability.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Dopamine Agents.
- drug effects : Gait, Space Perception, Time Perception.
- drug therapy : Parkinson Disease.
- physiopathology : Parkinson Disease.
- Aged, Analysis of Variance, Female, Humans, Male, Middle Aged.
Abstract
The basal ganglia have been implicated in timing control, yet the nature of timing disturbances in Parkinson's disease (PD) is poorly understood. We evaluated the influence of timing cues on spatiotemporal aspects of gait control and its variability, and the impact of dopaminergic treatment on timing. Three separate groups: 19 PD (OFF state); 24 PD (ON state); and 30 control participants were tested. Participants walked on a computerized carpet at four randomized and metronome‐controlled rates: self‐paced, 60, 80, or 100 steps/min. To our knowledge, this is the first study to demonstrate that medicated PD patients had poorer timing control than patients withdrawn from medication and healthy participants when modulating timing to an external stimulus. Increased step‐to‐step timing variability and deficits in mean temporal gait characteristics revealed that the medicated PD group (in contrast to nonmedicated PD group) performed least like healthy participants. This was observable in externally‐cued conditions, but not during self‐paced gait. Similar to previous research, step length contributed to overall slowness in PD, while temporal characteristics of gait did not. Interestingly, healthy participants increased stride length with each increase in cue rate, whereas both PD groups locked their step length regardless of temporal demand. Step‐to‐step variability differences between PD and healthy (e.g. step and double‐support time measurements) may be indicative of specific basal ganglia involvement in temporal control of gait. © 2007 Movement Disorder Society
Url:
DOI: 10.1002/mds.21603
Affiliations:
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Le document en format XML
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Almeida</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Movement Disorders Research & Rehabilitation Centre, Department of Kinesiology & Physical Education, Faculty of Science, Wilfrid Laurier University, Waterloo, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation><affiliation wicri:level="1"><country>Canada</country><wicri:regionArea>Movement Disorders Research & Rehabilitation Centre, Department of Kinesiology & Physical Education, Faculty of Science, Wilfrid Laurier University, Rm BA‐515, 75 University Ave. W., Waterloo, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Frank, James S" sort="Frank, James S" uniqKey="Frank J" first="James S." last="Frank">James S. Frank</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Graduate Studies & Research, University of Windsor, Windsor, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Roy, Eric A" sort="Roy, Eric A" uniqKey="Roy E" first="Eric A." last="Roy">Eric A. Roy</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Kinesiology, University of Waterloo, Waterloo, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Patla, Aftab E" sort="Patla, Aftab E" uniqKey="Patla A" first="Aftab E." last="Patla">Aftab E. 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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-09-15">2007-09-15</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1735">1735</biblScope><biblScope unit="page" to="1742">1742</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">65CE09EF200BDDA9FD213FE41C7902860C1CCFC5</idno><idno type="DOI">10.1002/mds.21603</idno><idno type="ArticleID">MDS21603</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Antiparkinson Agents (administration & dosage)</term><term>Basal ganglion</term><term>Dopamine Agents (administration & dosage)</term><term>Female</term><term>Gait (drug effects)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Modulation</term><term>Nervous system diseases</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Space Perception (drug effects)</term><term>Time Perception (drug effects)</term><term>Timing</term><term>Variability</term><term>basal ganglia</term><term>gait</term><term>timing</term><term>variability</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gait</term><term>Space Perception</term><term>Time Perception</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Modulation</term><term>Noyau gris central</term><term>Parkinson maladie</term><term>Système nerveux pathologie</term><term>Timing</term><term>Variabilité</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The basal ganglia have been implicated in timing control, yet the nature of timing disturbances in Parkinson's disease (PD) is poorly understood. We evaluated the influence of timing cues on spatiotemporal aspects of gait control and its variability, and the impact of dopaminergic treatment on timing. Three separate groups: 19 PD (OFF state); 24 PD (ON state); and 30 control participants were tested. Participants walked on a computerized carpet at four randomized and metronome‐controlled rates: self‐paced, 60, 80, or 100 steps/min. To our knowledge, this is the first study to demonstrate that medicated PD patients had poorer timing control than patients withdrawn from medication and healthy participants when modulating timing to an external stimulus. Increased step‐to‐step timing variability and deficits in mean temporal gait characteristics revealed that the medicated PD group (in contrast to nonmedicated PD group) performed least like healthy participants. This was observable in externally‐cued conditions, but not during self‐paced gait. Similar to previous research, step length contributed to overall slowness in PD, while temporal characteristics of gait did not. Interestingly, healthy participants increased stride length with each increase in cue rate, whereas both PD groups locked their step length regardless of temporal demand. Step‐to‐step variability differences between PD and healthy (e.g. step and double‐support time measurements) may be indicative of specific basal ganglia involvement in temporal control of gait. © 2007 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Almeida, Quincy J" sort="Almeida, Quincy J" uniqKey="Almeida Q" first="Quincy J." last="Almeida">Quincy J. Almeida</name></noRegion><name sortKey="Almeida, Quincy J" sort="Almeida, Quincy J" uniqKey="Almeida Q" first="Quincy J." last="Almeida">Quincy J. Almeida</name><name sortKey="Frank, James S" sort="Frank, James S" uniqKey="Frank J" first="James S." last="Frank">James S. Frank</name><name sortKey="Jog, Mandar S" sort="Jog, Mandar S" uniqKey="Jog M" first="Mandar S." last="Jog">Mandar S. Jog</name><name sortKey="Patla, Aftab E" sort="Patla, Aftab E" uniqKey="Patla A" first="Aftab E." last="Patla">Aftab E. Patla</name><name sortKey="Roy, Eric A" sort="Roy, Eric A" uniqKey="Roy E" first="Eric A." last="Roy">Eric A. Roy</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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