On-line motor control in patients with Parkinson's disease
Identifieur interne : 000865 ( Main/Corpus ); précédent : 000864; suivant : 000866On-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 ] ; 2004-08.
English descriptors
- KwdEn :
- EOG = electro-oculography, Huntington's disease, LED = light emitting diode, MD = movement duration, MRT = motor reaction time, PL = path linearity, PV = peak velocity, Parkinson's disease, RT = reaction time, TC = time constant, UPDRS = Unified Parkinson's Disease Rating Score., basal ganglia, on-line movement control.
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.
Url:
DOI: 10.1093/brain/awh206
Links to Exploration step
ISTEX:660BDB06640F1CDB259B0C52D69187301BA506F2Le document en format XML
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Thobois</name><affiliation><mods:affiliation>Department of Neurosurgery, University of California San Francisco, San Francisco, California, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Space and Action, Bron, and</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2004-08">2004-08</date><biblScope unit="volume">127</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1755">1755</biblScope><biblScope unit="page" to="1773">1773</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">660BDB06640F1CDB259B0C52D69187301BA506F2</idno><idno type="DOI">10.1093/brain/awh206</idno><idno type="local">awh206</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>EOG = electro-oculography</term><term>Huntington's disease</term><term>LED = light emitting diode</term><term>MD = movement duration</term><term>MRT = motor reaction time</term><term>PL = path linearity</term><term>PV = peak velocity</term><term>Parkinson's disease</term><term>RT = reaction time</term><term>TC = time constant</term><term>UPDRS = Unified Parkinson's Disease Rating Score.</term><term>basal ganglia</term><term>on-line movement control</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></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><istex><corpusName>oup</corpusName><author><json:item><name>M. Desmurget</name><affiliations><json:string>Space and Action, Bron, and</json:string><json:string>Space and Action, Bron, and</json:string></affiliations></json:item><json:item><name>V. Gaveau</name><affiliations><json:string>Space and Action, Bron, and</json:string><json:string>Space and Action, Bron, and</json:string></affiliations></json:item><json:item><name>P. 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Thobois</name><affiliations><json:string>Department of Neurosurgery, University of California San Francisco, San Francisco, California, USA</json:string><json:string>Space and Action, Bron, and</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Articles</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>basal ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>on-line movement control</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Huntington's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>EOG = electro-oculography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LED = light emitting diode</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MD = movement duration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MRT = motor reaction time</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PL = path linearity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PV = peak velocity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>RT = reaction time</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>TC = time constant</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>UPDRS = Unified Parkinson's Disease Rating Score.</value></json:item></subject><language><json:string>eng</json:string></language><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.</abstract><qualityIndicators><score>8.5</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>14</keywordCount><abstractCharCount>2401</abstractCharCount><pdfWordCount>12885</pdfWordCount><pdfCharCount>76943</pdfCharCount><pdfPageCount>19</pdfPageCount><abstractWordCount>357</abstractWordCount></qualityIndicators><title>On-line motor control in patients with Parkinson's disease</title><genre><json:string>research-article</json:string></genre><host><volume>127</volume><pages><last>1773</last><first>1755</first></pages><issn><json:string>0006-8950</json:string></issn><issue>8</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2156</json:string></eissn><title>Brain</title></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>2004</publicationDate><copyrightDate>2004</copyrightDate><doi><json:string>10.1093/brain/awh206</json:string></doi><id>660BDB06640F1CDB259B0C52D69187301BA506F2</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/660BDB06640F1CDB259B0C52D69187301BA506F2/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/660BDB06640F1CDB259B0C52D69187301BA506F2/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/660BDB06640F1CDB259B0C52D69187301BA506F2/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">On-line motor control in patients with Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>2004-06-23</date></publicationStmt><notesStmt><note>Correspondence to: Michel Desmurget, INSERM, U 534. Space and Action, 16 avenue du doyen Lépine, 69500 Bron, France E-mail: Desmurget@lyon.inserm.fr</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">On-line motor control in patients with Parkinson's disease</title><author><persName><forename type="first">M.</forename><surname>Desmurget</surname></persName><affiliation>Space and Action, Bron, and</affiliation><affiliation>Space and Action, Bron, and</affiliation></author><author><persName><forename type="first">V.</forename><surname>Gaveau</surname></persName><affiliation>Space and Action, Bron, and</affiliation><affiliation>Space and Action, Bron, and</affiliation></author><author><persName><forename type="first">P.</forename><surname>Vindras</surname></persName><affiliation>Department of Neurology, Neurological Hospital Pierre Wertheimer, Lyon, France,</affiliation><affiliation>Space and Action, Bron, and</affiliation></author><author><persName><forename type="first">R. S.</forename><surname>Turner</surname></persName><affiliation>FPSE, University of Geneva, Geneva, Switzerland, and</affiliation><affiliation>Space and Action, Bron, and</affiliation></author><author><persName><forename type="first">E.</forename><surname>Broussolle</surname></persName><affiliation>Department of Neurosurgery, University of California San Francisco, San Francisco, California, USA</affiliation><affiliation>Space and Action, Bron, and</affiliation></author><author><persName><forename type="first">S.</forename><surname>Thobois</surname></persName><affiliation>Department of Neurosurgery, University of California San Francisco, San Francisco, California, USA</affiliation><affiliation>Space and Action, Bron, and</affiliation></author></analytic><monogr><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="pISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2004-08"></date><biblScope unit="volume">127</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1755">1755</biblScope><biblScope unit="page" to="1773">1773</biblScope></imprint></monogr><idno type="istex">660BDB06640F1CDB259B0C52D69187301BA506F2</idno><idno type="DOI">10.1093/brain/awh206</idno><idno type="local">awh206</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004-06-23</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>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.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>basal ganglia</term></item><item><term>Parkinson's disease</term></item><item><term>on-line movement control</term></item><item><term>Huntington's disease</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>EOG = electro-oculography</term></item><item><term>LED = light emitting diode</term></item><item><term>MD = movement duration</term></item><item><term>MRT = motor reaction time</term></item><item><term>PL = path linearity</term></item><item><term>PV = peak velocity</term></item><item><term>RT = reaction time</term></item><item><term>TC = time constant</term></item><item><term>UPDRS = Unified Parkinson's Disease Rating Score.</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2004-06-23">Created</change><change when="2004-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/660BDB06640F1CDB259B0C52D69187301BA506F2/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="nlm-ta">Brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><abbrev-journal-title abbrev-type="publisher">Brain</abbrev-journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">awh206</article-id><article-id pub-id-type="doi">10.1093/brain/awh206</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>On-line motor control in patients with Parkinson's disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Desmurget</surname><given-names>M.</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Gaveau</surname><given-names>V.</given-names></name><xref rid="AFF1">1</xref></contrib><contrib contrib-type="author"><name><surname>Vindras</surname><given-names>P.</given-names></name><xref rid="AFF2">2</xref></contrib><contrib contrib-type="author"><name><surname>Turner</surname><given-names>R. S.</given-names></name><xref rid="AFF3">3</xref></contrib><contrib contrib-type="author"><name><surname>Broussolle</surname><given-names>E.</given-names></name><xref rid="AFF4">4</xref></contrib><contrib contrib-type="author"><name><surname>Thobois</surname><given-names>S.</given-names></name><xref rid="AFF4">4</xref></contrib><aff><target target-type="aff" id="AFF1"></target><label>1</label>Space and Action, Bron, and <target target-type="aff" id="AFF2"></target><label>2</label>Department of Neurology, Neurological Hospital Pierre Wertheimer, Lyon, France, <target target-type="aff" id="AFF3"></target><label>3</label>FPSE, University of Geneva, Geneva, Switzerland, and <target target-type="aff" id="AFF4"></target><label>4</label>Department of Neurosurgery, University of California San Francisco, San Francisco, California, USA</aff></contrib-group><author-notes><corresp>Correspondence to: Michel Desmurget, INSERM, U 534. Space and Action, 16 avenue du doyen Lépine, 69500 Bron, France E-mail: <ext-link xlink:href="Desmurget@lyon.inserm.fr" ext-link-type="email">Desmurget@lyon.inserm.fr</ext-link></corresp></author-notes><pub-date pub-type="epub"><day>23</day><month>6</month><year>2004</year></pub-date><pub-date pub-type="ppub"><month>8</month><year>2004</year></pub-date><volume>127</volume><issue>8</issue><fpage>1755</fpage><lpage>1773</lpage><history><date date-type="accepted"><day>24</day><month>3</month><year>2004</year></date><date date-type="received"><day>1</day><month>12</month><year>2003</year></date><date date-type="rev-recd"><day>23</day><month>3</month><year>2004</year></date></history><copyright-statement><italic>Brain Vol. 127 No. 8 © Guarantors of Brain 2004; all rights reserved</italic></copyright-statement><copyright-year>2004</copyright-year><abstract xml:lang="en"><p>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.</p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>basal ganglia</kwd><kwd>Parkinson's disease</kwd><kwd>on-line movement control</kwd><kwd>Huntington's disease</kwd></kwd-group><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd>EOG = electro-oculography</kwd><kwd>LED = light emitting diode</kwd><kwd>MD = movement duration</kwd><kwd>MRT = motor reaction time</kwd><kwd>PL = path linearity</kwd><kwd>PV = peak velocity</kwd><kwd>RT = reaction time</kwd><kwd>TC = time constant</kwd><kwd>UPDRS = Unified Parkinson's Disease Rating Score.</kwd></kwd-group><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>1755</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>Article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>On-line motor control in patients with Parkinson's disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>On-line motor control in patients with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Desmurget</namePart><affiliation>Space and Action, Bron, and</affiliation><affiliation>Space and Action, Bron, and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V.</namePart><namePart type="family">Gaveau</namePart><affiliation>Space and Action, Bron, and</affiliation><affiliation>Space and Action, Bron, and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Vindras</namePart><affiliation>Department of Neurology, Neurological Hospital Pierre Wertheimer, Lyon, France,</affiliation><affiliation>Space and Action, Bron, and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. S.</namePart><namePart type="family">Turner</namePart><affiliation>FPSE, University of Geneva, Geneva, Switzerland, and</affiliation><affiliation>Space and Action, Bron, and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Broussolle</namePart><affiliation>Department of Neurosurgery, University of California San Francisco, San Francisco, California, USA</affiliation><affiliation>Space and Action, Bron, and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Thobois</namePart><affiliation>Department of Neurosurgery, University of California San Francisco, San Francisco, California, USA</affiliation><affiliation>Space and Action, Bron, and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2004-08</dateIssued><dateCreated encoding="w3cdtf">2004-06-23</dateCreated><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract 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.</abstract><note type="author-notes">Correspondence to: Michel Desmurget, INSERM, U 534. Space and Action, 16 avenue du doyen Lépine, 69500 Bron, France E-mail: Desmurget@lyon.inserm.fr</note><subject lang="en"><genre>KWD</genre><topic>basal ganglia</topic><topic>Parkinson's disease</topic><topic>on-line movement control</topic><topic>Huntington's disease</topic></subject><subject lang="en"><genre>ABR</genre><topic>EOG = electro-oculography</topic><topic>LED = light emitting diode</topic><topic>MD = movement duration</topic><topic>MRT = motor reaction time</topic><topic>PL = path linearity</topic><topic>PV = peak velocity</topic><topic>RT = reaction time</topic><topic>TC = time constant</topic><topic>UPDRS = Unified Parkinson's Disease Rating Score.</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><titleInfo type="abbreviated"><title>Brain</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><identifier type="PublisherID-nlm-ta">Brain</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>127</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>1755</start><end>1773</end></extent></part></relatedItem><identifier type="istex">660BDB06640F1CDB259B0C52D69187301BA506F2</identifier><identifier type="DOI">10.1093/brain/awh206</identifier><identifier type="local">awh206</identifier><accessCondition type="use and reproduction" contentType="copyright">Brain Vol. 127 No. 8 © Guarantors of Brain 2004; all rights reserved</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/660BDB06640F1CDB259B0C52D69187301BA506F2/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/660BDB06640F1CDB259B0C52D69187301BA506F2/annexes/gif</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/660BDB06640F1CDB259B0C52D69187301BA506F2/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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