Movement Disorders (revue)

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Three-dimensional gait biomechanics in Parkinson's disease: Evidence for a centrally mediated amplitude regulation disorder

Identifieur interne : 001F55 ( PascalFrancis/Corpus ); précédent : 001F54; suivant : 001F56

Three-dimensional gait biomechanics in Parkinson's disease: Evidence for a centrally mediated amplitude regulation disorder

Auteurs : Meg Morris ; Robert Iansek ; Jennifer Mcginley ; Thomas Matyas ; Frances Huxham

Source :

RBID : Pascal:05-0172411

Descripteurs français

English descriptors

Abstract

We examined whether people with Parkinson's disease (PD) have a central amplitude regulation disorder using three-dimensional (3-D) gait analyses to compare the effects of medication and attentional strategies on gait in 12 PD subjects and 12 matched comparison subjects. Subjects with PD first performed several 10-m gait trials at preferred speed while off levodopa. They then walked at preferred speed on levodopa; off levodopa with cues; and on levodopa with cues. Control subjects walked at preferred speed and then with visual cues to match their stride length to PD values. As well as spatiotemporal footstep data, pelvic and lower limb kinematic profiles and angle-angle diagrams were produced for sagittal, coronal, and transverse plane movements using a 3-D motion analysis system. In people with PD, decreased step length was accompanied by reduced movement amplitude across all lower limb joints, in all movement planes. When control subjects were required to walk with short steps matched to the size of PD comparisons, they displayed a similar multijoint reduction in amplitude. For PD subjects, both levodopa and visual cues increased movement amplitude across all lower limb joints. Amplitude increased further when levodopa and visual cues were combined, resulting in normalization of step length. This finding suggested that reduced step length is due to a mismatch between cortically selected movement amplitude and basal ganglia maintenance mechanisms. Levodopa and cues normalized amplitude across all joints by altering motor set and bypassing defective basal ganglia mechanisms.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A06       @2 1
A08 01  1  ENG  @1 Three-dimensional gait biomechanics in Parkinson's disease: Evidence for a centrally mediated amplitude regulation disorder
A11 01  1    @1 MORRIS (Meg)
A11 02  1    @1 IANSEK (Robert)
A11 03  1    @1 MCGINLEY (Jennifer)
A11 04  1    @1 MATYAS (Thomas)
A11 05  1    @1 HUXHAM (Frances)
A14 01      @1 School of Physiotherapy, Faculty of Health Sciences, La Trobe University @2 Melbourne, Victoria @3 AUS @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 5 aut.
A14 02      @1 Geriatric Research Unit, Kingston Centre, Southern Health @2 Cheltenham, Victoria @3 AUS @Z 2 aut. @Z 3 aut. @Z 5 aut.
A14 03      @1 School of Psychology, Faculty of Science and Technology, La Trobe University @2 Melbourne, Victoria @3 AUS @Z 4 aut.
A20       @1 40-50
A21       @1 2005
A23 01      @0 ENG
A43 01      @1 INIST @2 20953 @5 354000125001470050
A44       @0 0000 @1 © 2005 INIST-CNRS. All rights reserved.
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A47 01  1    @0 05-0172411
A60       @1 P
A61       @0 A
A64 01  1    @0 Movement disorders
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C01 01    ENG  @0 We examined whether people with Parkinson's disease (PD) have a central amplitude regulation disorder using three-dimensional (3-D) gait analyses to compare the effects of medication and attentional strategies on gait in 12 PD subjects and 12 matched comparison subjects. Subjects with PD first performed several 10-m gait trials at preferred speed while off levodopa. They then walked at preferred speed on levodopa; off levodopa with cues; and on levodopa with cues. Control subjects walked at preferred speed and then with visual cues to match their stride length to PD values. As well as spatiotemporal footstep data, pelvic and lower limb kinematic profiles and angle-angle diagrams were produced for sagittal, coronal, and transverse plane movements using a 3-D motion analysis system. In people with PD, decreased step length was accompanied by reduced movement amplitude across all lower limb joints, in all movement planes. When control subjects were required to walk with short steps matched to the size of PD comparisons, they displayed a similar multijoint reduction in amplitude. For PD subjects, both levodopa and visual cues increased movement amplitude across all lower limb joints. Amplitude increased further when levodopa and visual cues were combined, resulting in normalization of step length. This finding suggested that reduced step length is due to a mismatch between cortically selected movement amplitude and basal ganglia maintenance mechanisms. Levodopa and cues normalized amplitude across all joints by altering motor set and bypassing defective basal ganglia mechanisms.
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C03 02  X  FRE  @0 Biomécanique @5 02
C03 02  X  ENG  @0 Biomechanics @5 02
C03 02  X  SPA  @0 Biomecánica @5 02
C03 03  X  FRE  @0 Amplitude @5 03
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C03 03  X  SPA  @0 Amplitud @5 03
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C03 06  X  FRE  @0 Traitement @5 06
C03 06  X  ENG  @0 Treatment @5 06
C03 06  X  SPA  @0 Tratamiento @5 06
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C07 01  X  SPA  @0 Encéfalo patología @5 37
C07 02  X  FRE  @0 Extrapyramidal syndrome @5 38
C07 02  X  ENG  @0 Extrapyramidal syndrome @5 38
C07 02  X  SPA  @0 Extrapiramidal síndrome @5 38
C07 03  X  FRE  @0 Maladie dégénérative @5 39
C07 03  X  ENG  @0 Degenerative disease @5 39
C07 03  X  SPA  @0 Enfermedad degenerativa @5 39
C07 04  X  FRE  @0 Système nerveux central pathologie @5 40
C07 04  X  ENG  @0 Central nervous system disease @5 40
C07 04  X  SPA  @0 Sistema nervosio central patología @5 40
C07 05  X  FRE  @0 Antiparkinsonien @5 41
C07 05  X  ENG  @0 Antiparkinson agent @5 41
C07 05  X  SPA  @0 Antiparkinsoniano @5 41
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Format Inist (serveur)

NO : PASCAL 05-0172411 INIST
ET : Three-dimensional gait biomechanics in Parkinson's disease: Evidence for a centrally mediated amplitude regulation disorder
AU : MORRIS (Meg); IANSEK (Robert); MCGINLEY (Jennifer); MATYAS (Thomas); HUXHAM (Frances)
AF : School of Physiotherapy, Faculty of Health Sciences, La Trobe University/Melbourne, Victoria/Australie (1 aut., 2 aut., 3 aut., 5 aut.); Geriatric Research Unit, Kingston Centre, Southern Health/Cheltenham, Victoria/Australie (2 aut., 3 aut., 5 aut.); School of Psychology, Faculty of Science and Technology, La Trobe University/Melbourne, Victoria/Australie (4 aut.)
DT : Publication en série; Niveau analytique
SO : Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2005; Vol. 20; No. 1; Pp. 40-50; Bibl. 44 ref.
LA : Anglais
EA : We examined whether people with Parkinson's disease (PD) have a central amplitude regulation disorder using three-dimensional (3-D) gait analyses to compare the effects of medication and attentional strategies on gait in 12 PD subjects and 12 matched comparison subjects. Subjects with PD first performed several 10-m gait trials at preferred speed while off levodopa. They then walked at preferred speed on levodopa; off levodopa with cues; and on levodopa with cues. Control subjects walked at preferred speed and then with visual cues to match their stride length to PD values. As well as spatiotemporal footstep data, pelvic and lower limb kinematic profiles and angle-angle diagrams were produced for sagittal, coronal, and transverse plane movements using a 3-D motion analysis system. In people with PD, decreased step length was accompanied by reduced movement amplitude across all lower limb joints, in all movement planes. When control subjects were required to walk with short steps matched to the size of PD comparisons, they displayed a similar multijoint reduction in amplitude. For PD subjects, both levodopa and visual cues increased movement amplitude across all lower limb joints. Amplitude increased further when levodopa and visual cues were combined, resulting in normalization of step length. This finding suggested that reduced step length is due to a mismatch between cortically selected movement amplitude and basal ganglia maintenance mechanisms. Levodopa and cues normalized amplitude across all joints by altering motor set and bypassing defective basal ganglia mechanisms.
CC : 002B17; 002B17G; 002B17A03
FD : Système nerveux pathologie; Biomécanique; Amplitude; Parkinson maladie; Lévodopa; Traitement
FG : Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Antiparkinsonien
ED : Nervous system diseases; Biomechanics; Amplitude; Parkinson disease; Levodopa; Treatment
EG : Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Antiparkinson agent
SD : Sistema nervioso patología; Biomecánica; Amplitud; Parkinson enfermedad; Levodopa; Tratamiento
LO : INIST-20953.354000125001470050
ID : 05-0172411

Links to Exploration step

Pascal:05-0172411

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<s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Biomécanique</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Biomechanics</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Biomecánica</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Amplitude</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Amplitude</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Amplitud</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Lévodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Traitement</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Treatment</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Tratamiento</s0>
<s5>06</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Antiparkinsonien</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Antiparkinson agent</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Antiparkinsoniano</s0>
<s5>41</s5>
</fC07>
<fN21>
<s1>115</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
<server>
<NO>PASCAL 05-0172411 INIST</NO>
<ET>Three-dimensional gait biomechanics in Parkinson's disease: Evidence for a centrally mediated amplitude regulation disorder</ET>
<AU>MORRIS (Meg); IANSEK (Robert); MCGINLEY (Jennifer); MATYAS (Thomas); HUXHAM (Frances)</AU>
<AF>School of Physiotherapy, Faculty of Health Sciences, La Trobe University/Melbourne, Victoria/Australie (1 aut., 2 aut., 3 aut., 5 aut.); Geriatric Research Unit, Kingston Centre, Southern Health/Cheltenham, Victoria/Australie (2 aut., 3 aut., 5 aut.); School of Psychology, Faculty of Science and Technology, La Trobe University/Melbourne, Victoria/Australie (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2005; Vol. 20; No. 1; Pp. 40-50; Bibl. 44 ref.</SO>
<LA>Anglais</LA>
<EA>We examined whether people with Parkinson's disease (PD) have a central amplitude regulation disorder using three-dimensional (3-D) gait analyses to compare the effects of medication and attentional strategies on gait in 12 PD subjects and 12 matched comparison subjects. Subjects with PD first performed several 10-m gait trials at preferred speed while off levodopa. They then walked at preferred speed on levodopa; off levodopa with cues; and on levodopa with cues. Control subjects walked at preferred speed and then with visual cues to match their stride length to PD values. As well as spatiotemporal footstep data, pelvic and lower limb kinematic profiles and angle-angle diagrams were produced for sagittal, coronal, and transverse plane movements using a 3-D motion analysis system. In people with PD, decreased step length was accompanied by reduced movement amplitude across all lower limb joints, in all movement planes. When control subjects were required to walk with short steps matched to the size of PD comparisons, they displayed a similar multijoint reduction in amplitude. For PD subjects, both levodopa and visual cues increased movement amplitude across all lower limb joints. Amplitude increased further when levodopa and visual cues were combined, resulting in normalization of step length. This finding suggested that reduced step length is due to a mismatch between cortically selected movement amplitude and basal ganglia maintenance mechanisms. Levodopa and cues normalized amplitude across all joints by altering motor set and bypassing defective basal ganglia mechanisms.</EA>
<CC>002B17; 002B17G; 002B17A03</CC>
<FD>Système nerveux pathologie; Biomécanique; Amplitude; Parkinson maladie; Lévodopa; Traitement</FD>
<FG>Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Antiparkinsonien</FG>
<ED>Nervous system diseases; Biomechanics; Amplitude; Parkinson disease; Levodopa; Treatment</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Antiparkinson agent</EG>
<SD>Sistema nervioso patología; Biomecánica; Amplitud; Parkinson enfermedad; Levodopa; Tratamiento</SD>
<LO>INIST-20953.354000125001470050</LO>
<ID>05-0172411</ID>
</server>
</inist>
</record>

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