Examination of central gait control mechanisms in Parkinson's disease using movement-related potentials.
Identifieur interne : 003343 ( Ncbi/Checkpoint ); précédent : 003342; suivant : 003344Examination of central gait control mechanisms in Parkinson's disease using movement-related potentials.
Auteurs : Mehrnaz Shoushtarian [Australie] ; Anna Murphy ; Robert IansekSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- Adult, Aged, Basal Ganglia (physiopathology), Electroencephalography, Electromyography, Evoked Potentials (physiology), Eye Movements (physiology), Female, Gait (physiology), Humans, Hypokinesia (physiopathology), Male, Middle Aged, Motor Cortex (physiopathology), Movement (physiology), Parkinson Disease (physiopathology), Severity of Illness Index, Young Adult.
- MESH :
- physiology : Evoked Potentials, Eye Movements, Gait, Movement.
- physiopathology : Basal Ganglia, Hypokinesia, Motor Cortex, Parkinson Disease.
- Adult, Aged, Electroencephalography, Electromyography, Female, Humans, Male, Middle Aged, Severity of Illness Index, Young Adult.
Abstract
Gait disorders are common in people with Parkinson's disease. The pathophysiology of these disorders is not fully understood. Movement-related potentials reflect supplementary motor area activity associated with the preparation and execution of voluntary movement. Our aim was to investigate movement-related potentials associated with gait disturbances in patients with Parkinson's disease, as reflected by gait hypokinesia and initiation difficulties, in order to better understand the role of the basal ganglia in the pathogenesis of these conditions. Movement-related potentials were back-averaged from electroencephalography recordings performed on 11 participants with Parkinson's disease with no gait initiation difficulties, 9 participants with Parkinson's disease who suffered from gait initiation difficulties, 12 young healthy adults, and 8 healthy older adults. Participants took 3 steps forward, stepping off a force plate. Trigger signals from the force plate and electromyographic activity of the tibialis anterior muscle were used to identify gait initiation time. Participants' stride length was also measured using a 3-dimensional motion analysis system. Movement-related potentials showed significant group differences between the healthy young adults and the 2 Parkinson's disease groups as well as the Parkinson's disease group as a whole. No significant difference was found between the participants with Parkinson's disease and age-matched controls. A significant inverse relationship between movement-related potentials and stride length was found in patients with Parkinson's disease who did not experience gait initiation difficulties but not in those who did have this symptom. Gait-generated movement-related potentials appear to show electrical evidence of cortical disturbances correlated with stride length reduction in patients with Parkinson's disease without gait initiation difficulties.
DOI: 10.1002/mds.23844
PubMed: 21739471
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Examination of central gait control mechanisms in Parkinson's disease using movement-related potentials.</title><author><name sortKey="Shoushtarian, Mehrnaz" sort="Shoushtarian, Mehrnaz" uniqKey="Shoushtarian M" first="Mehrnaz" last="Shoushtarian">Mehrnaz Shoushtarian</name><affiliation wicri:level="1"><nlm:affiliation>Clinical Research Centre for Movement Disorders and Gait, Kingston Centre, Southern Health, Melbourne, Australia. mehrnaz.shoushtarian@southernhealth.org.au</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Clinical Research Centre for Movement Disorders and Gait, Kingston Centre, Southern Health, Melbourne</wicri:regionArea><wicri:noRegion>Melbourne</wicri:noRegion></affiliation></author><author><name sortKey="Murphy, Anna" sort="Murphy, Anna" uniqKey="Murphy A" first="Anna" last="Murphy">Anna Murphy</name></author><author><name sortKey="Iansek, Robert" sort="Iansek, Robert" uniqKey="Iansek R" first="Robert" last="Iansek">Robert Iansek</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="doi">10.1002/mds.23844</idno><idno type="RBID">pubmed:21739471</idno><idno type="pmid">21739471</idno><idno type="wicri:Area/PubMed/Corpus">001086</idno><idno type="wicri:Area/PubMed/Curation">001086</idno><idno type="wicri:Area/PubMed/Checkpoint">001349</idno><idno type="wicri:Area/Ncbi/Merge">003343</idno><idno type="wicri:Area/Ncbi/Curation">003343</idno><idno type="wicri:Area/Ncbi/Checkpoint">003343</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Examination of central gait control mechanisms in Parkinson's disease using movement-related potentials.</title><author><name sortKey="Shoushtarian, Mehrnaz" sort="Shoushtarian, Mehrnaz" uniqKey="Shoushtarian M" first="Mehrnaz" last="Shoushtarian">Mehrnaz Shoushtarian</name><affiliation wicri:level="1"><nlm:affiliation>Clinical Research Centre for Movement Disorders and Gait, Kingston Centre, Southern Health, Melbourne, Australia. mehrnaz.shoushtarian@southernhealth.org.au</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Clinical Research Centre for Movement Disorders and Gait, Kingston Centre, Southern Health, Melbourne</wicri:regionArea><wicri:noRegion>Melbourne</wicri:noRegion></affiliation></author><author><name sortKey="Murphy, Anna" sort="Murphy, Anna" uniqKey="Murphy A" first="Anna" last="Murphy">Anna Murphy</name></author><author><name sortKey="Iansek, Robert" sort="Iansek, Robert" uniqKey="Iansek R" first="Robert" last="Iansek">Robert Iansek</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="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Basal Ganglia (physiopathology)</term><term>Electroencephalography</term><term>Electromyography</term><term>Evoked Potentials (physiology)</term><term>Eye Movements (physiology)</term><term>Female</term><term>Gait (physiology)</term><term>Humans</term><term>Hypokinesia (physiopathology)</term><term>Male</term><term>Middle Aged</term><term>Motor Cortex (physiopathology)</term><term>Movement (physiology)</term><term>Parkinson Disease (physiopathology)</term><term>Severity of Illness Index</term><term>Young Adult</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Evoked Potentials</term><term>Eye Movements</term><term>Gait</term><term>Movement</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Hypokinesia</term><term>Motor Cortex</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Electroencephalography</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Severity of Illness Index</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Gait disorders are common in people with Parkinson's disease. The pathophysiology of these disorders is not fully understood. Movement-related potentials reflect supplementary motor area activity associated with the preparation and execution of voluntary movement. Our aim was to investigate movement-related potentials associated with gait disturbances in patients with Parkinson's disease, as reflected by gait hypokinesia and initiation difficulties, in order to better understand the role of the basal ganglia in the pathogenesis of these conditions. Movement-related potentials were back-averaged from electroencephalography recordings performed on 11 participants with Parkinson's disease with no gait initiation difficulties, 9 participants with Parkinson's disease who suffered from gait initiation difficulties, 12 young healthy adults, and 8 healthy older adults. Participants took 3 steps forward, stepping off a force plate. Trigger signals from the force plate and electromyographic activity of the tibialis anterior muscle were used to identify gait initiation time. Participants' stride length was also measured using a 3-dimensional motion analysis system. Movement-related potentials showed significant group differences between the healthy young adults and the 2 Parkinson's disease groups as well as the Parkinson's disease group as a whole. No significant difference was found between the participants with Parkinson's disease and age-matched controls. A significant inverse relationship between movement-related potentials and stride length was found in patients with Parkinson's disease who did not experience gait initiation difficulties but not in those who did have this symptom. Gait-generated movement-related potentials appear to show electrical evidence of cortical disturbances correlated with stride length reduction in patients with Parkinson's disease without gait initiation difficulties.</div></front></TEI><affiliations><list><country><li>Australie</li></country></list><tree><noCountry><name sortKey="Iansek, Robert" sort="Iansek, Robert" uniqKey="Iansek R" first="Robert" last="Iansek">Robert Iansek</name><name sortKey="Murphy, Anna" sort="Murphy, Anna" uniqKey="Murphy A" first="Anna" last="Murphy">Anna Murphy</name></noCountry><country name="Australie"><noRegion><name sortKey="Shoushtarian, Mehrnaz" sort="Shoushtarian, Mehrnaz" uniqKey="Shoushtarian M" first="Mehrnaz" last="Shoushtarian">Mehrnaz Shoushtarian</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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