Movement Disorders (revue)

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Evidence for a disorder of locomotor timing in Huntington's disease

Identifieur interne : 003672 ( Main/Curation ); précédent : 003671; suivant : 003673

Evidence for a disorder of locomotor timing in Huntington's disease

Auteurs : Belinda Bilney [Australie] ; Meg E. Morris [Australie] ; Andrew Churchyard [Australie] ; Edmond Chiu [Australie] ; Nellie Georgiou-Karistianis [Australie]

Source :

RBID : ISTEX:89261A0123B121CF915296D0E819FA45F51E9963

Descripteurs français

English descriptors

Abstract

Disturbances of walking have been described in people with Huntington's disease (HD), although the nature of the deficits have not yet been well defined. The purpose of this investigation was to determine whether people with HD have a deficit in the regulation of footstep timing during walking. The footstep patterns of 30 people with HD and 30 matched comparisons were measured at self‐selected slow, preferred, and fast speeds. Subjects were also instructed to match their footsteps to auditory metronome cues set at 80 and 120 beats per minute. Gait speed, cadence, stride length, and double limb support as a percentage of the gait cycle were measured using a computerized foot‐switch system. People with HD demonstrated a disorder in their ability to regulate cadence, manifest as a reduced step frequency when walking at preferred speed and when required to increase their speed. For all walking conditions, people with HD had increased variability of footstep cadence. They also had difficulty synchronizing their footstep timing to an auditory cue. For all walking conditions, people with HD had reduced stride length. Thus, in HD, there is a disorder in the regulation of footstep timing, with increased variability, a restricted cadence range, difficulty synchronizing footsteps to an auditory cue and reduced stride length. The exact neural correlates of this timing disorder are yet to be determined. © 2004 Movement Disorder Society

DOI: 10.1002/mds.20294

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ISTEX:89261A0123B121CF915296D0E819FA45F51E9963

Le document en format XML

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<name sortKey="Churchyard, Andrew" sort="Churchyard, Andrew" uniqKey="Churchyard A" first="Andrew" last="Churchyard">Andrew Churchyard</name>
<affiliation wicri:level="1">
<country xml:lang="fr">Australie</country>
<wicri:regionArea>Movement Disorders Clinic, Kingston Centre, Cheltenham, Victoria</wicri:regionArea>
<wicri:noRegion>Victoria</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Chiu, Edmond" sort="Chiu, Edmond" uniqKey="Chiu E" first="Edmond" last="Chiu">Edmond Chiu</name>
<affiliation wicri:level="1">
<country xml:lang="fr">Australie</country>
<wicri:regionArea>Huntington's Disease Clinic, St. Georges Hospital, Kew, Victoria</wicri:regionArea>
<wicri:noRegion>Victoria</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Georgiou Aristianis, Nellie" sort="Georgiou Aristianis, Nellie" uniqKey="Georgiou Aristianis N" first="Nellie" last="Georgiou-Karistianis">Nellie Georgiou-Karistianis</name>
<affiliation wicri:level="1">
<country xml:lang="fr">Australie</country>
<wicri:regionArea>Experimental Neuropsychology Research Unit, Psychology Department, School of Psychology, Psychiatry and Psychological Medicine, Faculty of Medicine, Nursing and Health Sciences, Monash University</wicri:regionArea>
<wicri:noRegion>Monash University</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series>
<idno type="ISSN">0885-3185</idno>
</series>
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<idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Acoustic Stimulation</term>
<term>Adult</term>
<term>Analysis of Variance</term>
<term>Case-Control Studies</term>
<term>Cues</term>
<term>Female</term>
<term>Gait (physiology)</term>
<term>Gait Disorders, Neurologic (etiology)</term>
<term>Humans</term>
<term>Huntington Disease (physiopathology)</term>
<term>Male</term>
<term>Mental Status Schedule</term>
<term>Middle Aged</term>
<term>Neurologic Examination (methods)</term>
<term>Postural Balance (physiology)</term>
<term>Time Factors</term>
<term>Walking (physiology)</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en">
<term>Gait Disorders, Neurologic</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en">
<term>Neurologic Examination</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en">
<term>Gait</term>
<term>Postural Balance</term>
<term>Walking</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en">
<term>Huntington Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Acoustic Stimulation</term>
<term>Adult</term>
<term>Analysis of Variance</term>
<term>Case-Control Studies</term>
<term>Cues</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Mental Status Schedule</term>
<term>Middle Aged</term>
<term>Time Factors</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Disturbances of walking have been described in people with Huntington's disease (HD), although the nature of the deficits have not yet been well defined. The purpose of this investigation was to determine whether people with HD have a deficit in the regulation of footstep timing during walking. The footstep patterns of 30 people with HD and 30 matched comparisons were measured at self‐selected slow, preferred, and fast speeds. Subjects were also instructed to match their footsteps to auditory metronome cues set at 80 and 120 beats per minute. Gait speed, cadence, stride length, and double limb support as a percentage of the gait cycle were measured using a computerized foot‐switch system. People with HD demonstrated a disorder in their ability to regulate cadence, manifest as a reduced step frequency when walking at preferred speed and when required to increase their speed. For all walking conditions, people with HD had increased variability of footstep cadence. They also had difficulty synchronizing their footstep timing to an auditory cue. For all walking conditions, people with HD had reduced stride length. Thus, in HD, there is a disorder in the regulation of footstep timing, with increased variability, a restricted cadence range, difficulty synchronizing footsteps to an auditory cue and reduced stride length. The exact neural correlates of this timing disorder are yet to be determined. © 2004 Movement Disorder Society</div>
</front>
</TEI>
</ISTEX>
</double>
</record>

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