Impact of deep brain stimulation on upper limb akinesia in Parkinson's disease
Identifieur interne : 002060 ( Main/Corpus ); précédent : 002059; suivant : 002061Impact 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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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></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. 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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><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. 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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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L.</givenNames><familyName>Benabid</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>M. C.</givenNames><familyName>Rodriguez‐Oroz</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>J.</givenNames><familyName>Obeso</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>J. C.</givenNames><familyName>Rothwell</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="ES" type="organization"><unparsedAffiliation>Clinica Quiron, San Sebastian, Spain</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>Fondation Gustave Prévot (France)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Medtronic</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Parkinson Foundation (Miami, FL)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Wellcome Trust (UK)</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>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</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Impact of deep brain stimulation on upper limb akinesia in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Deep Brain Stimulation and Akinesia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Impact of deep brain stimulation on upper limb akinesia in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">R. G.</namePart><namePart type="family">Brown</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>MRC Human Movement and Balance Unit, Institute of Neurology, London, UK</affiliation><description>Correspondence: Department of Psychology, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Limousin Dowsey</namePart><namePart type="termsOfAddress">MD</namePart><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><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Brown</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><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Jahanshahi</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><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Pollak</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. L.</namePart><namePart type="family">Benabid</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. C.</namePart><namePart type="family">Rodriguez‐Oroz</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Clinica Quiron, San Sebastian, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Obeso</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Clinica Quiron, San Sebastian, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. 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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