Impact of deep brain stimulation on upper limb akinesia in Parkinson's disease
Identifieur interne : 001775 ( Istex/Corpus ); précédent : 001774; suivant : 001776Impact of deep brain stimulation on upper limb akinesia in Parkinson's disease
Auteurs : R. G. Brown ; P. Limousin Dowsey ; P. Brown ; M. Jahanshahi ; P. Pollak ; A. L. Benabid ; M. C. Rodriguez-Oroz ; J. Obeso ; J. C. RothwellSource :
- Annals of Neurology [ 0364-5134 ] ; 1999-04.
Abstract
Recent pathophysiological models of Parkinson's disease have led to new surgical approaches to treatment including deep brain stimulation (DBS) and lesioning of basal ganglia structures. Various measures of upper limb akinesia were assessed in 6 patients with bilateral DBS of the internal pallidum and 6 with DBS of the subthalamic nucleus. Stimulation improved a number of aspects of motor function, and particularly movement time, and force production. Time to initiate movements, and to perform repetitive movements also improved but less dramatically. Processes indicating preparatory motor processes showed no significant change. Few significant differences were found between the internal pallidum and subthalamic nucleus groups. In general, the effects of DBS closely parallel previous reports of the effects of dopaminergic medication. It is suggested that disrupted pallidal output in Parkinson's disease interferes with the rate, level, and coordination of force production but has little effect on preparatory processes. The similarity of the effects of subthalamic nucleus and internal pallidum stimulation suggests this disrupted outflow is the most important determinant of upper limb akinesia in Parkinson's disease. The effects of DBS were similar to the effects of unilateral pallidal lesions reported elsewhere. Ann Neurol 1999;45:473–488
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DOI: 10.1002/1531-8249(199904)45:4<473::AID-ANA9>3.0.CO;2-V
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Pollak</name><affiliation><mods:affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Benabid, A L" sort="Benabid, A L" uniqKey="Benabid A" first="A. L." last="Benabid">A. L. Benabid</name><affiliation><mods:affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Rodriguez Roz, M C" sort="Rodriguez Roz, M C" uniqKey="Rodriguez Roz M" first="M. C." last="Rodriguez-Oroz">M. C. Rodriguez-Oroz</name><affiliation><mods:affiliation>Clinica Quiron, San Sebastian, Spain</mods:affiliation></affiliation></author><author><name sortKey="Obeso, J" sort="Obeso, J" uniqKey="Obeso J" first="J." last="Obeso">J. 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Brown</name><affiliation><mods:affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychology, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK</mods:affiliation></affiliation></author><author><name sortKey="Limousin Dowsey, P" sort="Limousin Dowsey, P" uniqKey="Limousin Dowsey P" first="P." last="Limousin Dowsey">P. Limousin Dowsey</name><affiliation><mods:affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Brown, P" sort="Brown, P" uniqKey="Brown P" first="P." last="Brown">P. Brown</name><affiliation><mods:affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Jahanshahi, M" sort="Jahanshahi, M" uniqKey="Jahanshahi M" first="M." last="Jahanshahi">M. Jahanshahi</name><affiliation><mods:affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Pollak, P" sort="Pollak, P" uniqKey="Pollak P" first="P." last="Pollak">P. Pollak</name><affiliation><mods:affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Benabid, A L" sort="Benabid, A L" uniqKey="Benabid A" first="A. L." last="Benabid">A. L. Benabid</name><affiliation><mods:affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Rodriguez Roz, M C" sort="Rodriguez Roz, M C" uniqKey="Rodriguez Roz M" first="M. C." last="Rodriguez-Oroz">M. C. Rodriguez-Oroz</name><affiliation><mods:affiliation>Clinica Quiron, San Sebastian, Spain</mods:affiliation></affiliation></author><author><name sortKey="Obeso, J" sort="Obeso, J" uniqKey="Obeso J" first="J." last="Obeso">J. Obeso</name><affiliation><mods:affiliation>Clinica Quiron, San Sebastian, Spain</mods:affiliation></affiliation></author><author><name sortKey="Rothwell, J C" sort="Rothwell, J C" uniqKey="Rothwell J" first="J. C." last="Rothwell">J. C. Rothwell</name><affiliation><mods:affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="1999-04">1999-04</date><biblScope unit="volume">45</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="473">473</biblScope><biblScope unit="page" to="488">488</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">6BCAC4DB9C96BA0B9E9CC4B7E4AE2645210E9C51</idno><idno type="DOI">10.1002/1531-8249(199904)45:4<473::AID-ANA9>3.0.CO;2-V</idno><idno type="ArticleID">ANA9</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent pathophysiological models of Parkinson's disease have led to new surgical approaches to treatment including deep brain stimulation (DBS) and lesioning of basal ganglia structures. Various measures of upper limb akinesia were assessed in 6 patients with bilateral DBS of the internal pallidum and 6 with DBS of the subthalamic nucleus. Stimulation improved a number of aspects of motor function, and particularly movement time, and force production. Time to initiate movements, and to perform repetitive movements also improved but less dramatically. Processes indicating preparatory motor processes showed no significant change. Few significant differences were found between the internal pallidum and subthalamic nucleus groups. In general, the effects of DBS closely parallel previous reports of the effects of dopaminergic medication. It is suggested that disrupted pallidal output in Parkinson's disease interferes with the rate, level, and coordination of force production but has little effect on preparatory processes. The similarity of the effects of subthalamic nucleus and internal pallidum stimulation suggests this disrupted outflow is the most important determinant of upper limb akinesia in Parkinson's disease. The effects of DBS were similar to the effects of unilateral pallidal lesions reported elsewhere. Ann Neurol 1999;45:473–488</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>R. G. Brown PhD</name><affiliations><json:string>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</json:string><json:string>Department of Psychology, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK</json:string></affiliations></json:item><json:item><name>P. Limousin Dowsey MD</name><affiliations><json:string>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</json:string><json:string>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</json:string></affiliations></json:item><json:item><name>P. Brown PhD</name><affiliations><json:string>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>M. Jahanshahi PhD</name><affiliations><json:string>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>P. Pollak MD</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</json:string></affiliations></json:item><json:item><name>A. L. Benabid MD</name><affiliations><json:string>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</json:string></affiliations></json:item><json:item><name>M. C. Rodriguez‐Oroz MD</name><affiliations><json:string>Clinica Quiron, San Sebastian, Spain</json:string></affiliations></json:item><json:item><name>J. Obeso MD</name><affiliations><json:string>Clinica Quiron, San Sebastian, Spain</json:string></affiliations></json:item><json:item><name>J. C. Rothwell PhD</name><affiliations><json:string>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</json:string></affiliations></json:item></author><articleId><json:string>ANA9</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Recent pathophysiological models of Parkinson's disease have led to new surgical approaches to treatment including deep brain stimulation (DBS) and lesioning of basal ganglia structures. Various measures of upper limb akinesia were assessed in 6 patients with bilateral DBS of the internal pallidum and 6 with DBS of the subthalamic nucleus. Stimulation improved a number of aspects of motor function, and particularly movement time, and force production. Time to initiate movements, and to perform repetitive movements also improved but less dramatically. Processes indicating preparatory motor processes showed no significant change. Few significant differences were found between the internal pallidum and subthalamic nucleus groups. In general, the effects of DBS closely parallel previous reports of the effects of dopaminergic medication. It is suggested that disrupted pallidal output in Parkinson's disease interferes with the rate, level, and coordination of force production but has little effect on preparatory processes. The similarity of the effects of subthalamic nucleus and internal pallidum stimulation suggests this disrupted outflow is the most important determinant of upper limb akinesia in Parkinson's disease. The effects of DBS were similar to the effects of unilateral pallidal lesions reported elsewhere. Ann Neurol 1999;45:473–488</abstract><qualityIndicators><score>7.304</score><pdfVersion>1.2</pdfVersion><pdfPageSize>605 x 786 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1357</abstractCharCount><pdfWordCount>10459</pdfWordCount><pdfCharCount>65422</pdfCharCount><pdfPageCount>16</pdfPageCount><abstractWordCount>192</abstractWordCount></qualityIndicators><title>Impact of deep brain stimulation on upper limb akinesia in Parkinson's disease</title><refBibs><json:item><author><json:item><name>R Benecke</name></json:item><json:item><name>JC Rothwell</name></json:item><json:item><name>JP Dick</name></json:item></author><host><volume>109</volume><pages><last>757</last><first>739</first></pages><author></author><title>Brain</title></host><title>Performance of simultaneous movements in patients with Parkinson's disease</title></json:item><json:item><author><json:item><name>R Benecke</name></json:item><json:item><name>JC Rothwell</name></json:item><json:item><name>JP Dick</name></json:item></author><host><volume>110</volume><pages><last>379</last><first>361</first></pages><author></author><title>Brain</title></host><title>Disturbance of sequential movements in patients with Parkinson's disease</title></json:item><json:item><author><json:item><name>N Yanagisawa</name></json:item><json:item><name>S Fujimoto</name></json:item><json:item><name>F Tamaru</name></json:item></author><host><volume>29</volume><pages><last>28</last><first>19</first></pages><issue>Suppl 1</issue><author></author><title>Eur Neurol</title></host><title>Bradykinesia in Parkinson's disease: disorders of onset and execution of fast movement</title></json:item><json:item><author><json:item><name>CA Bloxham</name></json:item><json:item><name>DJ Dick</name></json:item><json:item><name>M Moore</name></json:item></author><host><volume>50</volume><pages><last>1183</last><first>1178</first></pages><author></author><title>J Neurol Neurosurg Psychiatry</title></host><title>Reaction times and attention in Parkinson's disease</title></json:item><json:item><author><json:item><name>M Jahanshahi</name></json:item><json:item><name>RG Brown</name></json:item><json:item><name>CD Marsden</name></json:item></author><host><volume>115</volume><pages><last>564</last><first>539</first></pages><author></author><title>Brain</title></host><title>Simple and choice reaction time and the use of advance information for motor preparation in Parkinson's disease</title></json:item><json:item><author><json:item><name>RG Brown</name></json:item><json:item><name>M Jahanshahi</name></json:item><json:item><name>CD Marsden</name></json:item></author><host><volume>116</volume><pages><last>885</last><first>869</first></pages><author></author><title>Brain</title></host><title>Response choice in Parkinson's disease. 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disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><availability><p>Copyright © 1999 American Neurological Association</p></availability><date>1999</date></publicationStmt><notesStmt><note>Fondation Gustave Prévot (France)</note><note>Medtronic</note><note>National Parkinson Foundation (Miami, FL)</note><note>Wellcome Trust (UK)</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Impact of deep brain stimulation on upper limb akinesia in Parkinson's disease</title><author xml:id="author-1"><persName><forename type="first">R. G.</forename><surname>Brown</surname></persName><roleName type="degree">PhD</roleName><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</affiliation><affiliation>Department of Psychology, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK</affiliation></author><author xml:id="author-2"><persName><forename type="first">P.</forename><surname>Limousin Dowsey</surname></persName><roleName type="degree">MD</roleName><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</affiliation><affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">P.</forename><surname>Brown</surname></persName><roleName type="degree">PhD</roleName><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</affiliation></author><author xml:id="author-4"><persName><forename type="first">M.</forename><surname>Jahanshahi</surname></persName><roleName type="degree">PhD</roleName><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</affiliation></author><author xml:id="author-5"><persName><forename type="first">P.</forename><surname>Pollak</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</affiliation></author><author xml:id="author-6"><persName><forename type="first">A. L.</forename><surname>Benabid</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</affiliation></author><author xml:id="author-7"><persName><forename type="first">M. C.</forename><surname>Rodriguez‐Oroz</surname></persName><roleName type="degree">MD</roleName><affiliation>Clinica Quiron, San Sebastian, Spain</affiliation></author><author xml:id="author-8"><persName><forename type="first">J.</forename><surname>Obeso</surname></persName><roleName type="degree">MD</roleName><affiliation>Clinica Quiron, San Sebastian, Spain</affiliation></author><author xml:id="author-9"><persName><forename type="first">J. 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The similarity of the effects of subthalamic nucleus and internal pallidum stimulation suggests this disrupted outflow is the most important determinant of upper limb akinesia in Parkinson's disease. The effects of DBS were similar to the effects of unilateral pallidal lesions reported elsewhere. 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C.</namePart><namePart type="family">Rothwell</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">1999-04</dateIssued><dateCaptured encoding="w3cdtf">1998-10-13</dateCaptured><dateValid encoding="w3cdtf">1998-12-09</dateValid><copyrightDate encoding="w3cdtf">1999</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="tables">7</extent><extent unit="references">81</extent><extent unit="words">12607</extent></physicalDescription><abstract lang="en">Recent pathophysiological models of Parkinson's disease have led to new surgical approaches to treatment including deep brain stimulation (DBS) and lesioning of basal ganglia structures. Various measures of upper limb akinesia were assessed in 6 patients with bilateral DBS of the internal pallidum and 6 with DBS of the subthalamic nucleus. Stimulation improved a number of aspects of motor function, and particularly movement time, and force production. Time to initiate movements, and to perform repetitive movements also improved but less dramatically. Processes indicating preparatory motor processes showed no significant change. Few significant differences were found between the internal pallidum and subthalamic nucleus groups. In general, the effects of DBS closely parallel previous reports of the effects of dopaminergic medication. It is suggested that disrupted pallidal output in Parkinson's disease interferes with the rate, level, and coordination of force production but has little effect on preparatory processes. The similarity of the effects of subthalamic nucleus and internal pallidum stimulation suggests this disrupted outflow is the most important determinant of upper limb akinesia in Parkinson's disease. The effects of DBS were similar to the effects of unilateral pallidal lesions reported elsewhere. Ann Neurol 1999;45:473–488</abstract><note type="funding">Fondation Gustave Prévot (France)</note><note type="funding">Medtronic</note><note type="funding">National Parkinson Foundation (Miami, FL)</note><note type="funding">Wellcome Trust (UK)</note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>45</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>473</start><end>488</end><total>16</total></extent></part></relatedItem><identifier type="istex">6BCAC4DB9C96BA0B9E9CC4B7E4AE2645210E9C51</identifier><identifier type="DOI">10.1002/1531-8249(199904)45:4<473::AID-ANA9>3.0.CO;2-V</identifier><identifier type="ArticleID">ANA9</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1999 American Neurological Association</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Inc.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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