Corticostriatal functional interactions in Parkinson's disease: a rTMS/[11C]raclopride PET study
Identifieur interne : 001495 ( Istex/Corpus ); précédent : 001494; suivant : 001496Corticostriatal functional interactions in Parkinson's disease: a rTMS/[11C]raclopride PET study
Auteurs : Antonio P. Strafella ; Ji Hyun Ko ; Joshua Grant ; Maria Fraraccio ; Oury MonchiSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2005-12.
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Abstract
Several animal studies have shown that striatal dopamine can be released under direct control of glutamatergic corticostriatal efferents. In Parkinson's disease (PD), abnormalities in corticostriatal interactions are believed to play an important role in the pathophysiology of the disease. Previously, we have reported that, in healthy subjects, repetitive transcranial magnetic stimulation (rTMS) of motor cortex (MC) induces focal dopamine release in the ipsilateral putamen. In the present study, using [11C]raclopride PET, we sought to investigate early PD patients with evidence of unilateral motor symptoms. We measured in the putamen changes in extracellular dopamine concentration following rTMS (intensity, 90% of the resting motor threshold; frequency, 10 Hz) of the left and right MC. The main objective was to identify potential differences in corticostriatal dopamine release between the hemisphere associated with clear contralateral motor symptoms (symptomatic hemisphere) and the presymptomatic stage of the other hemisphere (asymptomatic hemisphere). Repetitive TMS of MC caused a binding reduction in the ipsilateral putamen of both hemispheres. In the symptomatic hemisphere, while the amount of TMS‐induced dopamine release was, as expected, smaller, the size of the significant cluster of change in [11C]raclopride binding was, instead, 61.4% greater than in the asymptomatic hemisphere. This finding of a spatially enlarged area of dopamine release, following cortical stimulation, may represent a possible in vivo expression of a loss of functional segregation of cortical information to the striatum and an indirect evidence of abnormal corticostriatal transmission in early PD. This has potential implications for models of basal ganglia function in PD.
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DOI: 10.1111/j.1460-9568.2005.04476.x
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ISTEX:0F33C5B6FA15A84C75CAF06847B3E0B63CAEAEE6Le document en format XML
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In Parkinson's disease (PD), abnormalities in corticostriatal interactions are believed to play an important role in the pathophysiology of the disease. Previously, we have reported that, in healthy subjects, repetitive transcranial magnetic stimulation (rTMS) of motor cortex (MC) induces focal dopamine release in the ipsilateral putamen. In the present study, using [11C]raclopride PET, we sought to investigate early PD patients with evidence of unilateral motor symptoms. We measured in the putamen changes in extracellular dopamine concentration following rTMS (intensity, 90% of the resting motor threshold; frequency, 10 Hz) of the left and right MC. The main objective was to identify potential differences in corticostriatal dopamine release between the hemisphere associated with clear contralateral motor symptoms (symptomatic hemisphere) and the presymptomatic stage of the other hemisphere (asymptomatic hemisphere). Repetitive TMS of MC caused a binding reduction in the ipsilateral putamen of both hemispheres. In the symptomatic hemisphere, while the amount of TMS‐induced dopamine release was, as expected, smaller, the size of the significant cluster of change in [11C]raclopride binding was, instead, 61.4% greater than in the asymptomatic hemisphere. This finding of a spatially enlarged area of dopamine release, following cortical stimulation, may represent a possible in vivo expression of a loss of functional segregation of cortical information to the striatum and an indirect evidence of abnormal corticostriatal transmission in early PD. This has potential implications for models of basal ganglia function in PD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Antonio P. 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Repetitive TMS of MC caused a binding reduction in the ipsilateral putamen of both hemispheres. In the symptomatic hemisphere, while the amount of TMS‐induced dopamine release was, as expected, smaller, the size of the significant cluster of change in [11C]raclopride binding was, instead, 61.4% greater than in the asymptomatic hemisphere. This finding of a spatially enlarged area of dopamine release, following cortical stimulation, may represent a possible in vivo expression of a loss of functional segregation of cortical information to the striatum and an indirect evidence of abnormal corticostriatal transmission in early PD. 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study</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2005</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Corticostriatal functional interactions in Parkinson's disease: a rTMS/[11C]raclopride PET study</title><author xml:id="author-1"><persName><forename type="first">Antonio P.</forename><surname>Strafella</surname></persName><affiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</affiliation></author><author xml:id="author-2"><persName><forename type="first">Ji Hyun</forename><surname>Ko</surname></persName><affiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</affiliation></author><author xml:id="author-3"><persName><forename type="first">Joshua</forename><surname>Grant</surname></persName><affiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</affiliation></author><author xml:id="author-4"><persName><forename type="first">Maria</forename><surname>Fraraccio</surname></persName><affiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</affiliation></author><author xml:id="author-5"><persName><forename type="first">Oury</forename><surname>Monchi</surname></persName><affiliation>Functional Neuroimaging Unit, Geriatric's Institute, University of Montréal, Montréal, Québec, Canada</affiliation></author></analytic><monogr><title level="j">European Journal of Neuroscience</title><idno type="pISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><idno type="DOI">10.1111/(ISSN)1460-9568</idno><imprint><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-12"></date><biblScope unit="volume">22</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="2946">2946</biblScope><biblScope unit="page" to="2952">2952</biblScope></imprint></monogr><idno type="istex">0F33C5B6FA15A84C75CAF06847B3E0B63CAEAEE6</idno><idno type="DOI">10.1111/j.1460-9568.2005.04476.x</idno><idno type="ArticleID">EJN4476</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Several animal studies have shown that striatal dopamine can be released under direct control of glutamatergic corticostriatal efferents. In Parkinson's disease (PD), abnormalities in corticostriatal interactions are believed to play an important role in the pathophysiology of the disease. Previously, we have reported that, in healthy subjects, repetitive transcranial magnetic stimulation (rTMS) of motor cortex (MC) induces focal dopamine release in the ipsilateral putamen. In the present study, using [11C]raclopride PET, we sought to investigate early PD patients with evidence of unilateral motor symptoms. We measured in the putamen changes in extracellular dopamine concentration following rTMS (intensity, 90% of the resting motor threshold; frequency, 10 Hz) of the left and right MC. The main objective was to identify potential differences in corticostriatal dopamine release between the hemisphere associated with clear contralateral motor symptoms (symptomatic hemisphere) and the presymptomatic stage of the other hemisphere (asymptomatic hemisphere). Repetitive TMS of MC caused a binding reduction in the ipsilateral putamen of both hemispheres. In the symptomatic hemisphere, while the amount of TMS‐induced dopamine release was, as expected, smaller, the size of the significant cluster of change in [11C]raclopride binding was, instead, 61.4% greater than in the asymptomatic hemisphere. This finding of a spatially enlarged area of dopamine release, following cortical stimulation, may represent a possible in vivo expression of a loss of functional segregation of cortical information to the striatum and an indirect evidence of abnormal corticostriatal transmission in early PD. This has potential implications for models of basal ganglia function in PD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>Parkinson's disease</term></item><item><term>positron emission tomography</term></item><item><term>raclopride</term></item><item><term>motor cortex stimulation</term></item><item><term>transcranial magnetic stimulation</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/0F33C5B6FA15A84C75CAF06847B3E0B63CAEAEE6/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>Blackwell Science Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="12011"><doi origin="wiley">10.1111/ejn.2005.22.issue-11</doi><numberingGroup><numbering type="journalVolume" number="22">22</numbering><numbering type="journalIssue" number="11">11</numbering></numberingGroup><coverDate startDate="2005-12">December 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="28" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2005.04476.x</doi><idGroup><id type="unit" value="EJN4476"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2005-11-25"></event><event type="publishedOnlineFinalForm" date="2005-11-25"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.4 mode:FullText source:FullText result:FullText" date="2010-03-29"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="2946">2946</numbering><numbering type="pageLast" number="2952">2952</numbering></numberingGroup><correspondenceTo>Dr A. P. Strafella, as above.
E‐mail: <email>antonio@bic.mni.mcgill.ca</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN4476.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 7 August 2005, revised 20 September 2005, accepted 28 September 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="64"></count><count type="wordTotal" number="4174"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Corticostriatal functional interactions in Parkinson's disease: a rTMS/[<sup>11</sup>C]raclopride PET study</title><title type="shortAuthors">A. P. Strafella <i>et al.</i></title><title type="short">Dopamine release and transcranial magnetic stimulation</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Antonio P.</givenNames><familyName>Strafella</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Ji Hyun</givenNames><familyName>Ko</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Joshua</givenNames><familyName>Grant</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Maria</givenNames><familyName>Fraraccio</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a2"><personName><givenNames>Oury</givenNames><familyName>Monchi</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CA"><unparsedAffiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="CA"><unparsedAffiliation>Functional Neuroimaging Unit, Geriatric's Institute, University of Montréal, Montréal, Québec, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinson's disease</keyword><keyword xml:id="k2">positron emission tomography</keyword><keyword xml:id="k3">raclopride</keyword><keyword xml:id="k4">motor cortex stimulation</keyword><keyword xml:id="k5">transcranial magnetic stimulation</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Several animal studies have shown that striatal dopamine can be released under direct control of glutamatergic corticostriatal efferents. In Parkinson's disease (PD), abnormalities in corticostriatal interactions are believed to play an important role in the pathophysiology of the disease. Previously, we have reported that, in healthy subjects, repetitive transcranial magnetic stimulation (rTMS) of motor cortex (MC) induces focal dopamine release in the ipsilateral putamen. In the present study, using [<sup>11</sup>C]raclopride PET, we sought to investigate early PD patients with evidence of unilateral motor symptoms. We measured in the putamen changes in extracellular dopamine concentration following rTMS (intensity, 90% of the resting motor threshold; frequency, 10 Hz) of the left and right MC. The main objective was to identify potential differences in corticostriatal dopamine release between the hemisphere associated with clear contralateral motor symptoms (symptomatic hemisphere) and the presymptomatic stage of the other hemisphere (asymptomatic hemisphere). Repetitive TMS of MC caused a binding reduction in the ipsilateral putamen of both hemispheres. In the symptomatic hemisphere, while the amount of TMS‐induced dopamine release was, as expected, smaller, the size of the significant cluster of change in [<sup>11</sup>C]raclopride binding was, instead, 61.4% greater than in the asymptomatic hemisphere. This finding of a spatially enlarged area of dopamine release, following cortical stimulation, may represent a possible <i>in vivo</i> expression of a loss of functional segregation of cortical information to the striatum and an indirect evidence of abnormal corticostriatal transmission in early PD. This has potential implications for models of basal ganglia function in PD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Corticostriatal functional interactions in Parkinson's disease: a rTMS/[11C]raclopride PET study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dopamine release and transcranial magnetic stimulation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Corticostriatal functional interactions in Parkinson's disease: a rTMS/[11C]raclopride PET study</title></titleInfo><name type="personal"><namePart type="given">Antonio P.</namePart><namePart type="family">Strafella</namePart><affiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ji Hyun</namePart><namePart type="family">Ko</namePart><affiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joshua</namePart><namePart type="family">Grant</namePart><affiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maria</namePart><namePart type="family">Fraraccio</namePart><affiliation>Montreal Neurological Institute, Neurology & Neurosurgery Department, McGill University, 3801 University St., Montréal, QC H3A 2B4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Oury</namePart><namePart type="family">Monchi</namePart><affiliation>Functional Neuroimaging Unit, Geriatric's Institute, University of Montréal, Montréal, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2005-12</dateIssued><edition>Received 7 August 2005, revised 20 September 2005, accepted 28 September 2005</edition><copyrightDate encoding="w3cdtf">2005</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">2</extent><extent unit="tables">3</extent><extent unit="references">64</extent><extent unit="words">4174</extent></physicalDescription><abstract lang="en">Several animal studies have shown that striatal dopamine can be released under direct control of glutamatergic corticostriatal efferents. In Parkinson's disease (PD), abnormalities in corticostriatal interactions are believed to play an important role in the pathophysiology of the disease. Previously, we have reported that, in healthy subjects, repetitive transcranial magnetic stimulation (rTMS) of motor cortex (MC) induces focal dopamine release in the ipsilateral putamen. In the present study, using [11C]raclopride PET, we sought to investigate early PD patients with evidence of unilateral motor symptoms. We measured in the putamen changes in extracellular dopamine concentration following rTMS (intensity, 90% of the resting motor threshold; frequency, 10 Hz) of the left and right MC. The main objective was to identify potential differences in corticostriatal dopamine release between the hemisphere associated with clear contralateral motor symptoms (symptomatic hemisphere) and the presymptomatic stage of the other hemisphere (asymptomatic hemisphere). Repetitive TMS of MC caused a binding reduction in the ipsilateral putamen of both hemispheres. In the symptomatic hemisphere, while the amount of TMS‐induced dopamine release was, as expected, smaller, the size of the significant cluster of change in [11C]raclopride binding was, instead, 61.4% greater than in the asymptomatic hemisphere. This finding of a spatially enlarged area of dopamine release, following cortical stimulation, may represent a possible in vivo expression of a loss of functional segregation of cortical information to the striatum and an indirect evidence of abnormal corticostriatal transmission in early PD. This has potential implications for models of basal ganglia function in PD.</abstract><subject lang="en"><genre>keywords</genre><topic>Parkinson's disease</topic><topic>positron emission tomography</topic><topic>raclopride</topic><topic>motor cortex stimulation</topic><topic>transcranial magnetic stimulation</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>2946</start><end>2952</end><total>7</total></extent></part></relatedItem><identifier type="istex">0F33C5B6FA15A84C75CAF06847B3E0B63CAEAEE6</identifier><identifier type="DOI">10.1111/j.1460-9568.2005.04476.x</identifier><identifier type="ArticleID">EJN4476</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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