On-line motor control in patients with Parkinson's disease
Identifieur interne : 000D70 ( PascalFrancis/Corpus ); précédent : 000D69; suivant : 000D71On-line motor control in patients with Parkinson's disease
Auteurs : M. Desmurget ; V. Gaveau ; P. Vindras ; R. S. Turner ; E. Broussolle ; S. ThoboisSource :
- Brain [ 0006-8950 ] ; 2004.
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- Pascal (Inist)
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Abstract
Recent models based, in part on a study of Huntington's disease, suggest that the basal ganglia are involved in on-line movement guidance. Two experiments were conducted to investigate this idea. First, we studied advanced Parkinson's disease patients performing a reaching task known to depend on on-line guidance. The task was to 'look and point' in the dark at visual targets displayed in the peripheral visual field. In some trials, the target location was slightly modified during saccadic gaze displacement (when vision is suppressed). In both patient and control groups, the target jump induced a gradual modification of the movement which diverged smoothly from its original path to reach the new target location. No deficit was found in the patients, except for an increased latency to respond to the target jump (Parkinson's disease: 243 ms; controls: 166 ms). A computational simulation indicated that this response slowing was likely to be a by-product of bradykinesia. The unexpected inconsistency between this result and previous reports was investigated in a second experiment. We hypothesized that the relevant factor was the characteristics of the corrections to be performed. To test this prediction, we investigated a task requiring corrections of the same type as investigated in Huntington's disease, namely large, consciously detected errors induced by large target jumps at hand movement onset. In contrast with the smooth adjustments observed in the first experiment, the subjects responded to the target jump by generating a discrete corrective sub-movement. While this iterative response was relatively rapid in the control subjects (220 ms), Parkinson's disease patients exhibited either dramatically late (>730 ms) or totally absent on-line corrections. When on-line corrections were absent, the initial motor response was completed before a second corrective response was initiated (the latency of the corrective response was the same as the latency of the initial response). Considered together, these results suggest that basal ganglia dependent circuits are not critical for feedback loops involving a smooth modulation of the ongoing command. These circuits may rather contribute to the generation of discrete corrective sub-movements. This deficit is in line with the general impairment of sequential and simultaneous actions in patients with basal ganglia disorders.
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Format Inist (serveur)
| NO : | PASCAL 04-0481650 INIST |
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| ET : | On-line motor control in patients with Parkinson's disease |
| AU : | DESMURGET (M.); GAVEAU (V.); VINDRAS (P.); TURNER (R. S.); BROUSSOLLE (E.); THOBOIS (S.) |
| AF : | Space and Action/Bron/France (1 aut., 2 aut.); Department of Neurology, Neurological Hospital Pierre Wertheimer/Lyon/France (3 aut.); FPSE, University of Geneva/Geneva/Suisse (4 aut.); Department of Neurosurgery, University of California, San Francisco/San Francisco, California/Etats-Unis (5 aut., 6 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Brain; ISSN 0006-8950; Royaume-Uni; Da. 2004; Vol. 127; No. p.8; Pp. 1755-1773; Bibl. 1 p.3/4 |
| LA : | Anglais |
| EA : | Recent models based, in part on a study of Huntington's disease, suggest that the basal ganglia are involved in on-line movement guidance. Two experiments were conducted to investigate this idea. First, we studied advanced Parkinson's disease patients performing a reaching task known to depend on on-line guidance. The task was to 'look and point' in the dark at visual targets displayed in the peripheral visual field. In some trials, the target location was slightly modified during saccadic gaze displacement (when vision is suppressed). In both patient and control groups, the target jump induced a gradual modification of the movement which diverged smoothly from its original path to reach the new target location. No deficit was found in the patients, except for an increased latency to respond to the target jump (Parkinson's disease: 243 ms; controls: 166 ms). A computational simulation indicated that this response slowing was likely to be a by-product of bradykinesia. The unexpected inconsistency between this result and previous reports was investigated in a second experiment. We hypothesized that the relevant factor was the characteristics of the corrections to be performed. To test this prediction, we investigated a task requiring corrections of the same type as investigated in Huntington's disease, namely large, consciously detected errors induced by large target jumps at hand movement onset. In contrast with the smooth adjustments observed in the first experiment, the subjects responded to the target jump by generating a discrete corrective sub-movement. While this iterative response was relatively rapid in the control subjects (220 ms), Parkinson's disease patients exhibited either dramatically late (>730 ms) or totally absent on-line corrections. When on-line corrections were absent, the initial motor response was completed before a second corrective response was initiated (the latency of the corrective response was the same as the latency of the initial response). Considered together, these results suggest that basal ganglia dependent circuits are not critical for feedback loops involving a smooth modulation of the ongoing command. These circuits may rather contribute to the generation of discrete corrective sub-movements. This deficit is in line with the general impairment of sequential and simultaneous actions in patients with basal ganglia disorders. |
| CC : | 002B17 |
| FD : | Parkinson maladie; Contrôle moteur; Homme; Chorée Huntington; Noyau gris central; Guidage; Système nerveux pathologie; Stade avancé; Champ visuel; Regard; Vision; Simulation; Correction; Latence réponse; Boucle réaction |
| FG : | Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Maladie héréditaire; Système nerveux central |
| ED : | Parkinson disease; Motor control; Human; Huntington disease; Basal ganglion; Guidance; Nervous system diseases; Advanced stage; Visual field; Gaze; Vision; Simulation; Corrections; Response latency; Feedback |
| EG : | Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Genetic disease; Central nervous system |
| SD : | Parkinson enfermedad; Control motor; Hombre; Corea Huntington; Núcleo basal; Guiado; Sistema nervioso patología; Estadio avanzado; Campo visual; Mirada; Visión; Simulación; Corrección; Latencia respuesta; Retroalimentación |
| LO : | INIST-998.354000116304080090 |
| ID : | 04-0481650 |
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Thobois</name><affiliation><inist:fA14 i1="04"><s1>Department of Neurosurgery, University of California, San Francisco</s1><s2>San Francisco, California</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">04-0481650</idno><date when="2004">2004</date><idno type="stanalyst">PASCAL 04-0481650 INIST</idno><idno type="RBID">Pascal:04-0481650</idno><idno type="wicri:Area/PascalFrancis/Corpus">000D70</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">On-line motor control in patients with Parkinson's disease</title><author><name sortKey="Desmurget, M" sort="Desmurget, M" uniqKey="Desmurget M" first="M." last="Desmurget">M. Desmurget</name><affiliation><inist:fA14 i1="01"><s1>Space and Action</s1><s2>Bron</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Gaveau, V" sort="Gaveau, V" uniqKey="Gaveau V" first="V." last="Gaveau">V. Gaveau</name><affiliation><inist:fA14 i1="01"><s1>Space and Action</s1><s2>Bron</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Vindras, P" sort="Vindras, P" uniqKey="Vindras P" first="P." last="Vindras">P. Vindras</name><affiliation><inist:fA14 i1="02"><s1>Department of Neurology, Neurological Hospital Pierre Wertheimer</s1><s2>Lyon</s2><s3>FRA</s3><sZ>3 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Turner, R S" sort="Turner, R S" uniqKey="Turner R" first="R. S." last="Turner">R. S. Turner</name><affiliation><inist:fA14 i1="03"><s1>FPSE, University of Geneva</s1><s2>Geneva</s2><s3>CHE</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Broussolle, E" sort="Broussolle, E" uniqKey="Broussolle E" first="E." last="Broussolle">E. Broussolle</name><affiliation><inist:fA14 i1="04"><s1>Department of Neurosurgery, University of California, San Francisco</s1><s2>San Francisco, California</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Thobois, S" sort="Thobois, S" uniqKey="Thobois S" first="S." last="Thobois">S. Thobois</name><affiliation><inist:fA14 i1="04"><s1>Department of Neurosurgery, University of California, San Francisco</s1><s2>San Francisco, California</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno><imprint><date when="2004">2004</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Advanced stage</term><term>Basal ganglion</term><term>Corrections</term><term>Feedback</term><term>Gaze</term><term>Guidance</term><term>Human</term><term>Huntington disease</term><term>Motor control</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Response latency</term><term>Simulation</term><term>Vision</term><term>Visual field</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Parkinson maladie</term><term>Contrôle moteur</term><term>Homme</term><term>Chorée Huntington</term><term>Noyau gris central</term><term>Guidage</term><term>Système nerveux pathologie</term><term>Stade avancé</term><term>Champ visuel</term><term>Regard</term><term>Vision</term><term>Simulation</term><term>Correction</term><term>Latence réponse</term><term>Boucle réaction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent models based, in part on a study of Huntington's disease, suggest that the basal ganglia are involved in on-line movement guidance. Two experiments were conducted to investigate this idea. First, we studied advanced Parkinson's disease patients performing a reaching task known to depend on on-line guidance. The task was to 'look and point' in the dark at visual targets displayed in the peripheral visual field. In some trials, the target location was slightly modified during saccadic gaze displacement (when vision is suppressed). In both patient and control groups, the target jump induced a gradual modification of the movement which diverged smoothly from its original path to reach the new target location. No deficit was found in the patients, except for an increased latency to respond to the target jump (Parkinson's disease: 243 ms; controls: 166 ms). A computational simulation indicated that this response slowing was likely to be a by-product of bradykinesia. The unexpected inconsistency between this result and previous reports was investigated in a second experiment. We hypothesized that the relevant factor was the characteristics of the corrections to be performed. To test this prediction, we investigated a task requiring corrections of the same type as investigated in Huntington's disease, namely large, consciously detected errors induced by large target jumps at hand movement onset. In contrast with the smooth adjustments observed in the first experiment, the subjects responded to the target jump by generating a discrete corrective sub-movement. While this iterative response was relatively rapid in the control subjects (220 ms), Parkinson's disease patients exhibited either dramatically late (>730 ms) or totally absent on-line corrections. When on-line corrections were absent, the initial motor response was completed before a second corrective response was initiated (the latency of the corrective response was the same as the latency of the initial response). Considered together, these results suggest that basal ganglia dependent circuits are not critical for feedback loops involving a smooth modulation of the ongoing command. These circuits may rather contribute to the generation of discrete corrective sub-movements. This deficit is in line with the general impairment of sequential and simultaneous actions in patients with basal ganglia disorders.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-8950</s0></fA01><fA03 i2="1"><s0>Brain</s0></fA03><fA05><s2>127</s2></fA05><fA06><s3>p.8</s3></fA06><fA08 i1="01" i2="1" l="ENG"><s1>On-line motor control in patients with Parkinson's disease</s1></fA08><fA11 i1="01" i2="1"><s1>DESMURGET (M.)</s1></fA11><fA11 i1="02" i2="1"><s1>GAVEAU (V.)</s1></fA11><fA11 i1="03" i2="1"><s1>VINDRAS (P.)</s1></fA11><fA11 i1="04" i2="1"><s1>TURNER (R. S.)</s1></fA11><fA11 i1="05" i2="1"><s1>BROUSSOLLE (E.)</s1></fA11><fA11 i1="06" i2="1"><s1>THOBOIS (S.)</s1></fA11><fA14 i1="01"><s1>Space and Action</s1><s2>Bron</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Neurology, Neurological Hospital Pierre Wertheimer</s1><s2>Lyon</s2><s3>FRA</s3><sZ>3 aut.</sZ></fA14><fA14 i1="03"><s1>FPSE, University of Geneva</s1><s2>Geneva</s2><s3>CHE</s3><sZ>4 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Neurosurgery, University of California, San Francisco</s1><s2>San Francisco, California</s2><s3>USA</s3><sZ>5 aut.</sZ><sZ>6 aut.</sZ></fA14><fA20><s1>1755-1773</s1></fA20><fA21><s1>2004</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>998</s2><s5>354000116304080090</s5></fA43><fA44><s0>0000</s0><s1>© 2004 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.3/4</s0></fA45><fA47 i1="01" i2="1"><s0>04-0481650</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Brain</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Recent models based, in part on a study of Huntington's disease, suggest that the basal ganglia are involved in on-line movement guidance. Two experiments were conducted to investigate this idea. First, we studied advanced Parkinson's disease patients performing a reaching task known to depend on on-line guidance. The task was to 'look and point' in the dark at visual targets displayed in the peripheral visual field. In some trials, the target location was slightly modified during saccadic gaze displacement (when vision is suppressed). In both patient and control groups, the target jump induced a gradual modification of the movement which diverged smoothly from its original path to reach the new target location. No deficit was found in the patients, except for an increased latency to respond to the target jump (Parkinson's disease: 243 ms; controls: 166 ms). A computational simulation indicated that this response slowing was likely to be a by-product of bradykinesia. The unexpected inconsistency between this result and previous reports was investigated in a second experiment. We hypothesized that the relevant factor was the characteristics of the corrections to be performed. To test this prediction, we investigated a task requiring corrections of the same type as investigated in Huntington's disease, namely large, consciously detected errors induced by large target jumps at hand movement onset. In contrast with the smooth adjustments observed in the first experiment, the subjects responded to the target jump by generating a discrete corrective sub-movement. While this iterative response was relatively rapid in the control subjects (220 ms), Parkinson's disease patients exhibited either dramatically late (>730 ms) or totally absent on-line corrections. When on-line corrections were absent, the initial motor response was completed before a second corrective response was initiated (the latency of the corrective response was the same as the latency of the initial response). Considered together, these results suggest that basal ganglia dependent circuits are not critical for feedback loops involving a smooth modulation of the ongoing command. These circuits may rather contribute to the generation of discrete corrective sub-movements. This deficit is in line with the general impairment of sequential and simultaneous actions in patients with basal ganglia disorders.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Contrôle moteur</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Motor control</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Control motor</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Homme</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Human</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Hombre</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Chorée Huntington</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Huntington disease</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Corea Huntington</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Noyau gris central</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Basal ganglion</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Núcleo basal</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Guidage</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Guidance</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Guiado</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Stade avancé</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Advanced stage</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Estadio avanzado</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Champ visuel</s0><s5>09</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Visual field</s0><s5>09</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Campo visual</s0><s5>09</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Regard</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Gaze</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Mirada</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Vision</s0><s5>12</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Vision</s0><s5>12</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Visión</s0><s5>12</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Simulation</s0><s5>14</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Simulation</s0><s5>14</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Simulación</s0><s5>14</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Correction</s0><s5>15</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Corrections</s0><s5>15</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Corrección</s0><s5>15</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Latence réponse</s0><s5>17</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>Response latency</s0><s5>17</s5></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Latencia respuesta</s0><s5>17</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>Boucle réaction</s0><s5>18</s5></fC03><fC03 i1="15" i2="X" l="ENG"><s0>Feedback</s0><s5>18</s5></fC03><fC03 i1="15" i2="X" l="SPA"><s0>Retroalimentación</s0><s5>18</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>Maladie héréditaire</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Genetic disease</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>42</s5></fC07><fN21><s1>271</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 04-0481650 INIST</NO><ET>On-line motor control in patients with Parkinson's disease</ET><AU>DESMURGET (M.); GAVEAU (V.); VINDRAS (P.); TURNER (R. S.); BROUSSOLLE (E.); THOBOIS (S.)</AU><AF>Space and Action/Bron/France (1 aut., 2 aut.); Department of Neurology, Neurological Hospital Pierre Wertheimer/Lyon/France (3 aut.); FPSE, University of Geneva/Geneva/Suisse (4 aut.); Department of Neurosurgery, University of California, San Francisco/San Francisco, California/Etats-Unis (5 aut., 6 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Brain; ISSN 0006-8950; Royaume-Uni; Da. 2004; Vol. 127; No. p.8; Pp. 1755-1773; Bibl. 1 p.3/4</SO><LA>Anglais</LA><EA>Recent models based, in part on a study of Huntington's disease, suggest that the basal ganglia are involved in on-line movement guidance. Two experiments were conducted to investigate this idea. First, we studied advanced Parkinson's disease patients performing a reaching task known to depend on on-line guidance. The task was to 'look and point' in the dark at visual targets displayed in the peripheral visual field. In some trials, the target location was slightly modified during saccadic gaze displacement (when vision is suppressed). In both patient and control groups, the target jump induced a gradual modification of the movement which diverged smoothly from its original path to reach the new target location. No deficit was found in the patients, except for an increased latency to respond to the target jump (Parkinson's disease: 243 ms; controls: 166 ms). A computational simulation indicated that this response slowing was likely to be a by-product of bradykinesia. The unexpected inconsistency between this result and previous reports was investigated in a second experiment. We hypothesized that the relevant factor was the characteristics of the corrections to be performed. To test this prediction, we investigated a task requiring corrections of the same type as investigated in Huntington's disease, namely large, consciously detected errors induced by large target jumps at hand movement onset. In contrast with the smooth adjustments observed in the first experiment, the subjects responded to the target jump by generating a discrete corrective sub-movement. While this iterative response was relatively rapid in the control subjects (220 ms), Parkinson's disease patients exhibited either dramatically late (>730 ms) or totally absent on-line corrections. When on-line corrections were absent, the initial motor response was completed before a second corrective response was initiated (the latency of the corrective response was the same as the latency of the initial response). Considered together, these results suggest that basal ganglia dependent circuits are not critical for feedback loops involving a smooth modulation of the ongoing command. These circuits may rather contribute to the generation of discrete corrective sub-movements. This deficit is in line with the general impairment of sequential and simultaneous actions in patients with basal ganglia disorders.</EA><CC>002B17</CC><FD>Parkinson maladie; Contrôle moteur; Homme; Chorée Huntington; Noyau gris central; Guidage; Système nerveux pathologie; Stade avancé; Champ visuel; Regard; Vision; Simulation; Correction; Latence réponse; Boucle réaction</FD><FG>Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Maladie héréditaire; Système nerveux central</FG><ED>Parkinson disease; Motor control; Human; Huntington disease; Basal ganglion; Guidance; Nervous system diseases; Advanced stage; Visual field; Gaze; Vision; Simulation; Corrections; Response latency; Feedback</ED><EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Genetic disease; Central nervous system</EG><SD>Parkinson enfermedad; Control motor; Hombre; Corea Huntington; Núcleo basal; Guiado; Sistema nervioso patología; Estadio avanzado; Campo visual; Mirada; Visión; Simulación; Corrección; Latencia respuesta; Retroalimentación</SD><LO>INIST-998.354000116304080090</LO><ID>04-0481650</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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