Milestones in research on the pathophysiology of Parkinson's disease
Identifieur interne : 001D21 ( Main/Corpus ); précédent : 001D20; suivant : 001D22Milestones in research on the pathophysiology of Parkinson's disease
Auteurs : Thomas Wichmann ; Mahlon R. Delong ; Jorge Guridi ; Jose A. ObesoSource :
- Movement Disorders [ 0885-3185 ] ; 2011-05.
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Abstract
Progress in our understanding of the mechanisms underlying the cardinal motor abnormalities of Parkinson's disease (PD), in particular akinesia and bradykinesia and their treatment, has been remarkable. Notable accomplishments include insights into the functional organization of the basal ganglia and their place in the motor system as components of a family of parallel cortico‐subcortical circuits that subserve motor and nonmotor functions and the development of models of the intrinsic organization of the basal ganglia, including delineation of the so‐called direct, indirect, and hyperdirect pathways. Studies in primate models of PD have provided insight into the alterations of neuronal activity that are responsible for the motor features of PD, revealing both altered tonic levels of discharge and significant disturbances of the patterns of discharge throughout the motor circuitry and have led to the formulation of circuit models of PD, providing testable hypotheses for research and stimulating the development of new therapies. Most importantly, the discovery that lesions of the subthalamic nucleus, a key node of the indirect pathway, abolish the cardinal features of PD contributed to the renaissance in the use of surgical approaches to treating patients with PD, including ablation and deep brain stimulation. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23695
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Notable accomplishments include insights into the functional organization of the basal ganglia and their place in the motor system as components of a family of parallel cortico‐subcortical circuits that subserve motor and nonmotor functions and the development of models of the intrinsic organization of the basal ganglia, including delineation of the so‐called direct, indirect, and hyperdirect pathways. Studies in primate models of PD have provided insight into the alterations of neuronal activity that are responsible for the motor features of PD, revealing both altered tonic levels of discharge and significant disturbances of the patterns of discharge throughout the motor circuitry and have led to the formulation of circuit models of PD, providing testable hypotheses for research and stimulating the development of new therapies. Most importantly, the discovery that lesions of the subthalamic nucleus, a key node of the indirect pathway, abolish the cardinal features of PD contributed to the renaissance in the use of surgical approaches to treating patients with PD, including ablation and deep brain stimulation. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Thomas Wichmann MD</name><affiliations><json:string>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia, USA</json:string><json:string>Yerkes National Primate Center at Emory University, Atlanta, Georgia, USA</json:string></affiliations></json:item><json:item><name>Mahlon R. 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Most importantly, the discovery that lesions of the subthalamic nucleus, a key node of the indirect pathway, abolish the cardinal features of PD contributed to the renaissance in the use of surgical approaches to treating patients with PD, including ablation and deep brain stimulation. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>basal ganglia</term></item><item><term>direct pathway</term></item><item><term>indirect pathway</term></item><item><term>dyskinesias</term></item><item><term>deep brain stimulation</term></item><item><term>pallidotomy</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Review</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-01-25">Received</change><change when="2011-02-06">Registration</change><change when="2011-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/C885A14D7CDB3C451FDD395E132E4C3059E9BCFF/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="60"><doi origin="wiley" registered="yes">10.1002/mds.v26.6</doi><titleGroup><title type="specialIssueTitle">25th Anniversary</title></titleGroup><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="2011-05">May 2011</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="120" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23695</doi><idGroup><id type="unit" value="MDS23695"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="articleCategory">Review</title><title type="tocHeading1">Reviews</title></titleGroup><copyright ownership="thirdParty">Copyright © 2011 <i>Movement</i> Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2011-01-25"></event><event type="manuscriptAccepted" date="2011-02-06"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.0.1 mode:FullText" date="2012-01-27"></event><event type="publishedOnlineFinalForm" date="2011-05-27"></event><event type="firstOnline" date="2011-05-27"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1032</numbering><numbering type="pageLast">1041</numbering></numberingGroup><correspondenceTo>Yerkes National Primate Center, Division of Neuropharmacology and Neurologic Diseases, 954 Gatewood Road, Atlanta, GA 30322, USA</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23695.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="115"></count><count type="wordTotal" number="7724"></count></countGroup><titleGroup><title type="main" xml:lang="en">Milestones in research on the pathophysiology of Parkinson's disease<link href="#fn1"></link><link href="#fn2"></link><link href="#fn3"></link></title><title type="short" xml:lang="en">Milestones in Research on PD Pathophysiology</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Thomas</givenNames><familyName>Wichmann</familyName><degrees>MD</degrees></personName><contactDetails><email>twichma@emory.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Mahlon R.</givenNames><familyName>DeLong</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3 #af4"><personName><givenNames>Jorge</givenNames><familyName>Guridi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3 #af4"><personName><givenNames>Jose A.</givenNames><familyName>Obeso</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Yerkes National Primate Center at Emory University, Atlanta, Georgia, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Clinica Universidad de Navarra and Medical School, Neuroscience Area, CIMA, University of Navarra, Pamplona, Spain</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Centros de Investigació Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Santander, Spain</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">basal ganglia</keyword><keyword xml:id="kwd2">direct pathway</keyword><keyword xml:id="kwd3">indirect pathway</keyword><keyword xml:id="kwd4">dyskinesias</keyword><keyword xml:id="kwd5">deep brain stimulation</keyword><keyword xml:id="kwd6">pallidotomy</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Progress in our understanding of the mechanisms underlying the cardinal motor abnormalities of Parkinson's disease (PD), in particular akinesia and bradykinesia and their treatment, has been remarkable. Notable accomplishments include insights into the functional organization of the basal ganglia and their place in the motor system as components of a family of parallel cortico‐subcortical circuits that subserve motor and nonmotor functions and the development of models of the intrinsic organization of the basal ganglia, including delineation of the so‐called direct, indirect, and hyperdirect pathways. Studies in primate models of PD have provided insight into the alterations of neuronal activity that are responsible for the motor features of PD, revealing both altered tonic levels of discharge and significant disturbances of the patterns of discharge throughout the motor circuitry and have led to the formulation of circuit models of PD, providing testable hypotheses for research and stimulating the development of new therapies. Most importantly, the discovery that lesions of the subthalamic nucleus, a key node of the indirect pathway, abolish the cardinal features of PD contributed to the renaissance in the use of surgical approaches to treating patients with PD, including ablation and deep brain stimulation. © 2011 <i>Movement</i> Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="fn2"><p>Writing this article was supported in part by NIH/NINDS grants R01NS054976 and P50NS071669 (to T.W.) and an infrastructure grant to the Yerkes National Primate Research Center (NIH/NCRR grant RR‐000165).</p></note><note xml:id="fn3"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Milestones in research on the pathophysiology of Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Milestones in Research on PD Pathophysiology</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Milestones in research on the pathophysiology of Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Wichmann</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia, USA</affiliation><affiliation>Yerkes National Primate Center at Emory University, Atlanta, Georgia, USA</affiliation><description>Correspondence: Yerkes National Primate Center, Division of Neuropharmacology and Neurologic Diseases, 954 Gatewood Road, Atlanta, GA 30322, USA</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mahlon R.</namePart><namePart type="family">DeLong</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, School of Medicine, Emory University, Atlanta, Georgia, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jorge</namePart><namePart type="family">Guridi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Clinica Universidad de Navarra and Medical School, Neuroscience Area, CIMA, University of Navarra, Pamplona, Spain</affiliation><affiliation>Centros de Investigació Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Santander, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jose A.</namePart><namePart type="family">Obeso</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Clinica Universidad de Navarra and Medical School, Neuroscience Area, CIMA, University of Navarra, Pamplona, Spain</affiliation><affiliation>Centros de Investigació Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Santander, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-05</dateIssued><dateCaptured encoding="w3cdtf">2011-01-25</dateCaptured><dateValid encoding="w3cdtf">2011-02-06</dateValid><copyrightDate encoding="w3cdtf">2011</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">4</extent><extent unit="references">115</extent><extent unit="words">7724</extent></physicalDescription><abstract lang="en">Progress in our understanding of the mechanisms underlying the cardinal motor abnormalities of Parkinson's disease (PD), in particular akinesia and bradykinesia and their treatment, has been remarkable. Notable accomplishments include insights into the functional organization of the basal ganglia and their place in the motor system as components of a family of parallel cortico‐subcortical circuits that subserve motor and nonmotor functions and the development of models of the intrinsic organization of the basal ganglia, including delineation of the so‐called direct, indirect, and hyperdirect pathways. Studies in primate models of PD have provided insight into the alterations of neuronal activity that are responsible for the motor features of PD, revealing both altered tonic levels of discharge and significant disturbances of the patterns of discharge throughout the motor circuitry and have led to the formulation of circuit models of PD, providing testable hypotheses for research and stimulating the development of new therapies. Most importantly, the discovery that lesions of the subthalamic nucleus, a key node of the indirect pathway, abolish the cardinal features of PD contributed to the renaissance in the use of surgical approaches to treating patients with PD, including ablation and deep brain stimulation. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Writing this article was supported in part by NIH/NINDS grants R01NS054976 and P50NS071669 (to T.W.) and an infrastructure grant to the Yerkes National Primate Research Center (NIH/NCRR grant RR‐000165).</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>basal ganglia</topic><topic>direct pathway</topic><topic>indirect pathway</topic><topic>dyskinesias</topic><topic>deep brain stimulation</topic><topic>pallidotomy</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Review</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2011</date><detail type="title"><title>25th Anniversary</title></detail><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1032</start><end>1041</end><total>10</total></extent></part></relatedItem><identifier type="istex">C885A14D7CDB3C451FDD395E132E4C3059E9BCFF</identifier><identifier type="DOI">10.1002/mds.23695</identifier><identifier type="ArticleID">MDS23695</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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