Dopaminergic modulation of timing control and variability in the gait of Parkinson's disease.
Identifieur interne : 002854 ( PubMed/Checkpoint ); précédent : 002853; suivant : 002855Dopaminergic modulation of timing control and variability in the gait of Parkinson's disease.
Auteurs : Quincy J. Almeida [Canada] ; James S. Frank ; Eric A. Roy ; Aftab E. Patla ; Mandar S. JogSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Aged, Analysis of Variance, Antiparkinson Agents (administration & dosage), Dopamine Agents (administration & dosage), Female, Gait (drug effects), Humans, Male, Middle Aged, Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Space Perception (drug effects), Time Perception (drug effects).
- 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knowledge, this is the first study to demonstrate that medicated PD patients had poorer timing control than patients withdrawn from medication and healthy participants when modulating timing to an external stimulus.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.
DOI: 10.1002/mds.21603
PubMed: 17557356
Affiliations:
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Frank</name></author><author><name sortKey="Roy, Eric A" sort="Roy, Eric A" uniqKey="Roy E" first="Eric A" last="Roy">Eric A. Roy</name></author><author><name sortKey="Patla, Aftab E" sort="Patla, Aftab E" uniqKey="Patla A" first="Aftab E" last="Patla">Aftab E. Patla</name></author><author><name sortKey="Jog, Mandar S" sort="Jog, Mandar S" uniqKey="Jog M" first="Mandar S" last="Jog">Mandar S. Jog</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="doi">10.1002/mds.21603</idno><idno type="RBID">pubmed:17557356</idno><idno type="pmid">17557356</idno><idno type="wicri:Area/PubMed/Corpus">002641</idno><idno type="wicri:Area/PubMed/Curation">002641</idno><idno type="wicri:Area/PubMed/Checkpoint">002854</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dopaminergic modulation of timing control and variability in the gait of Parkinson's disease.</title><author><name sortKey="Almeida, Quincy J" sort="Almeida, Quincy J" uniqKey="Almeida Q" first="Quincy J" last="Almeida">Quincy J. Almeida</name><affiliation wicri:level="1"><nlm:affiliation>Movement Disorders Research & Rehabilitation Centre, Department of Kinesiology & Physical Education, Faculty of Science, Wilfrid Laurier University, Waterloo, Ontario, Canada. qalmeida@wlu.ca</nlm:affiliation><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></author><author><name sortKey="Frank, James S" sort="Frank, James S" uniqKey="Frank J" first="James S" last="Frank">James S. Frank</name></author><author><name sortKey="Roy, Eric A" sort="Roy, Eric A" uniqKey="Roy E" first="Eric A" last="Roy">Eric A. Roy</name></author><author><name sortKey="Patla, Aftab E" sort="Patla, Aftab E" uniqKey="Patla A" first="Aftab E" last="Patla">Aftab E. Patla</name></author><author><name sortKey="Jog, Mandar S" sort="Jog, Mandar S" uniqKey="Jog M" first="Mandar S" last="Jog">Mandar S. Jog</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Antiparkinson Agents (administration & dosage)</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>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Space Perception (drug effects)</term><term>Time Perception (drug effects)</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></textClass></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.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">17557356</PMID><DateCreated><Year>2007</Year><Month>10</Month><Day>01</Day></DateCreated><DateCompleted><Year>2008</Year><Month>01</Month><Day>09</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>22</Volume><Issue>12</Issue><PubDate><Year>2007</Year><Month>Sep</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Dopaminergic modulation of timing control and variability in the gait of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1735-42</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>(c) 2007 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Almeida</LastName><ForeName>Quincy J</ForeName><Initials>QJ</Initials><AffiliationInfo><Affiliation>Movement Disorders Research & Rehabilitation Centre, Department of Kinesiology & Physical Education, Faculty of Science, Wilfrid Laurier University, Waterloo, Ontario, Canada. qalmeida@wlu.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frank</LastName><ForeName>James S</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Roy</LastName><ForeName>Eric A</ForeName><Initials>EA</Initials></Author><Author ValidYN="Y"><LastName>Patla</LastName><ForeName>Aftab E</ForeName><Initials>AE</Initials></Author><Author ValidYN="Y"><LastName>Jog</LastName><ForeName>Mandar S</ForeName><Initials>MS</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D023362">Evaluation Studies</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000704">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000008">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015259">Dopamine Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000008">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005684">Gait</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013028">Space Perception</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013998">Time Perception</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>6</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>1</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>6</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.21603</ArticleId><ArticleId IdType="pubmed">17557356</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><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></noCountry><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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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