ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000703

Dopaminergic modulation of timing control and variability in the gait of parkinson's disease

Identifieur interne : 000703 ( PascalFrancis/Corpus ); précédent : 000702; suivant : 000704

Dopaminergic modulation of timing control and variability in the gait of parkinson's disease

Auteurs : Quincy J. Almeida ; James S. Frank ; Eric A. Roy ; Aftab E. Patla ; Mandar S. Jog

Source :

Movement disorders [ 0885-3185 ] ; 2007.

RBID : Pascal:07-0491120

Descripteurs français

Pascal (Inist)
- Système nerveux pathologie, Parkinson maladie, Modulation, Timing, Variabilité, Noyau gris central.

English descriptors

KwdEn :
- Basal ganglion, Modulation, Nervous system diseases, Parkinson disease, Timing, Variability.

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knowledge, this is the first study to demonstrate that medicated PD patients had poorer timing control than patients withdrawn from medication and healthy participants when modulating timing to an external stimulus.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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`01`	`1`		`@1 ALMEIDA (Quincy J.)`
A11	`02`	`1`		`@1 FRANK (James S.)`
A11	`03`	`1`		`@1 ROY (Eric A.)`
A11	`04`	`1`		`@1 PATLA (Aftab E.)`
A11	`05`	`1`		`@1 JOG (Mandar S.)`
A14	`01`			`@1 Movement Disorders Research & Rehabilitation Centre, Department of Kinesiology & Physical Education, Faculty of Science, Wilfrid Laurier University @2 Waterloo, Ontario @3 CAN @Z 1 aut.`
A14	`02`			`@1 Faculty of Graduate Studies & Research, University of Windsor @2 Windsor, Ontario @3 CAN @Z 2 aut.`
A14	`03`			`@1 Department of Kinesiology, University of Waterloo @2 Waterloo, Ontario @3 CAN @Z 3 aut. @Z 4 aut.`
A14	`04`			`@1 Clinical Neurological Science, London Health Sciences Centre-UC @2 Ontario @3 CAN @Z 5 aut.`
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A21				`@1 2007`
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A44				`@0 0000 @1 © 2007 INIST-CNRS. All rights reserved.`
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C01	`01`		`ENG`	@0 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.
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C03	`05`	`X`	`FRE`	`@0 Variabilité @5 11`
C03	`05`	`X`	`ENG`	`@0 Variability @5 11`
C03	`05`	`X`	`SPA`	`@0 Variabilidad @5 11`
C03	`06`	`X`	`FRE`	`@0 Noyau gris central @5 12`
C03	`06`	`X`	`ENG`	`@0 Basal ganglion @5 12`
C03	`06`	`X`	`SPA`	`@0 Núcleo basal @5 12`
C07	`01`	`X`	`FRE`	`@0 Encéphale pathologie @5 37`
C07	`01`	`X`	`ENG`	`@0 Cerebral disorder @5 37`
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C07	`02`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 38`
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N21				`@1 323`
N44	`01`			`@1 OTO`
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Format Inist (serveur)

NO :	PASCAL 07-0491120 INIST
ET :	Dopaminergic modulation of timing control and variability in the gait of parkinson's disease
AU :	ALMEIDA (Quincy J.); FRANK (James S.); ROY (Eric A.); PATLA (Aftab E.); JOG (Mandar S.)
AF :	Movement Disorders Research & Rehabilitation Centre, Department of Kinesiology & Physical Education, Faculty of Science, Wilfrid Laurier University/Waterloo, Ontario/Canada (1 aut.); Faculty of Graduate Studies & Research, University of Windsor/Windsor, Ontario/Canada (2 aut.); Department of Kinesiology, University of Waterloo/Waterloo, Ontario/Canada (3 aut., 4 aut.); Clinical Neurological Science, London Health Sciences Centre-UC/Ontario/Canada (5 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2007; Vol. 22; No. 12; Pp. 1735-1742; Bibl. 29 ref.
LA :	Anglais
EA :	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.
CC :	002B17; 002B17G; 002B17A03
FD :	Système nerveux pathologie; Parkinson maladie; Modulation; Timing; Variabilité; Noyau gris central
FG :	Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux central
ED :	Nervous system diseases; Parkinson disease; Modulation; Timing; Variability; Basal ganglion
EG :	Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Central nervous system
SD :	Sistema nervioso patología; Parkinson enfermedad; Modulación; Timing; Variabilidad; Núcleo basal
LO :	INIST-20953.354000143464810070
ID :	07-0491120

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Pascal:07-0491120

Le document en format XML

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<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.</div>
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<server><NO>PASCAL 07-0491120 INIST</NO>
<ET>Dopaminergic modulation of timing control and variability in the gait of parkinson's disease</ET>
<AU>ALMEIDA (Quincy J.); FRANK (James S.); ROY (Eric A.); PATLA (Aftab E.); JOG (Mandar S.)</AU>
<AF>Movement Disorders Research & Rehabilitation Centre, Department of Kinesiology & Physical Education, Faculty of Science, Wilfrid Laurier University/Waterloo, Ontario/Canada (1 aut.); Faculty of Graduate Studies & Research, University of Windsor/Windsor, Ontario/Canada (2 aut.); Department of Kinesiology, University of Waterloo/Waterloo, Ontario/Canada (3 aut., 4 aut.); Clinical Neurological Science, London Health Sciences Centre-UC/Ontario/Canada (5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2007; Vol. 22; No. 12; Pp. 1735-1742; Bibl. 29 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17; 002B17G; 002B17A03</CC>
<FD>Système nerveux pathologie; Parkinson maladie; Modulation; Timing; Variabilité; Noyau gris central</FD>
<FG>Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux central</FG>
<ED>Nervous system diseases; Parkinson disease; Modulation; Timing; Variability; Basal ganglion</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Central nervous system</EG>
<SD>Sistema nervioso patología; Parkinson enfermedad; Modulación; Timing; Variabilidad; Núcleo basal</SD>
<LO>INIST-20953.354000143464810070</LO>
<ID>07-0491120</ID>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Dopaminergic modulation of timing control and variability in the gait of parkinson's disease

Dopaminergic modulation of timing control and variability in the gait of parkinson's disease

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