Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the off and on conditions with [18F]FDG‐PET
Identifieur interne : 000341 ( Istex/Corpus ); précédent : 000340; suivant : 000342Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the off and on conditions with [18F]FDG‐PET
Auteurs : Georg Berding ; Per Odin ; David J. Brooks ; Guido Nikkhah ; Cordula Matthies ; Thomas Peschel ; Mona Shing ; Hans Kolbe ; Jörg Van Den Hoff ; Harald Fricke ; Reinhard Dengler ; Madjid Samii ; Wolfram H. KnappSource :
- Movement Disorders [ 0885-3185 ] ; 2001-11.
English descriptors
- KwdEn :
Abstract
Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age‐matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [18F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [18F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1212
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ISTEX:4789B42442C1A1B00054A283DFC7B2FBACA60743Le document en format XML
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Brooks</name><affiliation><mods:affiliation>Medical Research Council Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Nikkhah, Guido" sort="Nikkhah, Guido" uniqKey="Nikkhah G" first="Guido" last="Nikkhah">Guido Nikkhah</name><affiliation><mods:affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Matthies, Cordula" sort="Matthies, Cordula" uniqKey="Matthies C" first="Cordula" last="Matthies">Cordula Matthies</name><affiliation><mods:affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Peschel, Thomas" sort="Peschel, Thomas" uniqKey="Peschel T" first="Thomas" last="Peschel">Thomas Peschel</name><affiliation><mods:affiliation>Department of Neurology, University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Shing, Mona" sort="Shing, Mona" uniqKey="Shing M" first="Mona" last="Shing">Mona Shing</name><affiliation><mods:affiliation>Department of Neurology, University of Marburg, Marburg, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kolbe, Hans" sort="Kolbe, Hans" uniqKey="Kolbe H" first="Hans" last="Kolbe">Hans Kolbe</name><affiliation><mods:affiliation>Department of Neurology, University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Van Den Hoff, Jorg" sort="Van Den Hoff, Jorg" uniqKey="Van Den Hoff J" first="Jörg" last="Van Den Hoff">Jörg Van Den Hoff</name><affiliation><mods:affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Fricke, Harald" sort="Fricke, Harald" uniqKey="Fricke H" first="Harald" last="Fricke">Harald Fricke</name><affiliation><mods:affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Dengler, Reinhard" sort="Dengler, Reinhard" uniqKey="Dengler R" first="Reinhard" last="Dengler">Reinhard Dengler</name><affiliation><mods:affiliation>Department of Neurology, University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Samii, Madjid" sort="Samii, Madjid" uniqKey="Samii M" first="Madjid" last="Samii">Madjid Samii</name><affiliation><mods:affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</mods:affiliation></affiliation></author><author><name sortKey="Knapp, Wolfram H" sort="Knapp, Wolfram H" uniqKey="Knapp W" first="Wolfram H." last="Knapp">Wolfram H. Knapp</name><affiliation><mods:affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-11">2001-11</date><biblScope unit="vol">16</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1014">1014</biblScope><biblScope unit="page" to="1022">1022</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">4789B42442C1A1B00054A283DFC7B2FBACA60743</idno><idno type="DOI">10.1002/mds.1212</idno><idno type="ArticleID">MDS1212</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>FDG</term><term>advanced Parkinson's disease</term><term>dementia</term><term>dopamine treatment</term><term>positron emission tomography</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age‐matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [18F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [18F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment. © 2001 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Georg Berding MD PhD</name><affiliations><json:string>Department of Nuclear Medicine, University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Per Odin MD, PhD</name><affiliations><json:string>Department of Neurology, University of Marburg, Marburg, Germany</json:string></affiliations></json:item><json:item><name>David J. Brooks MD, DSc</name><affiliations><json:string>Medical Research Council Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Guido Nikkhah MD, PhD</name><affiliations><json:string>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Cordula Matthies MD, PhD</name><affiliations><json:string>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Thomas Peschel</name><affiliations><json:string>Department of Neurology, University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Mona Shing MD</name><affiliations><json:string>Department of Neurology, University of Marburg, Marburg, Germany</json:string><json:string>Department of Neurology, University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Hans Kolbe MD</name><affiliations><json:string>Department of Neurology, University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Jörg van den Hoff PhD</name><affiliations><json:string>Department of Nuclear Medicine, University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Harald Fricke PhD</name><affiliations><json:string>Department of Nuclear Medicine, University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Reinhard Dengler MD, PhD</name><affiliations><json:string>Department of Neurology, University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Madjid Samii MD, PhD</name><affiliations><json:string>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</json:string></affiliations></json:item><json:item><name>Wolfram H. Knapp MD, PhD</name><affiliations><json:string>Department of Nuclear Medicine, University Medical School, Hannover, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>advanced Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dopamine treatment</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FDG</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>positron emission tomography</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age‐matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [18F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [18F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment. © 2001 Movement Disorder Society.</abstract><qualityIndicators><score>7.702</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1936</abstractCharCount><pdfWordCount>4702</pdfWordCount><pdfCharCount>32382</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>274</abstractWordCount></qualityIndicators><title>Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the off and on conditions with [18F]FDG‐PET</title><genre><json:string>Serial 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PhD</roleName></persName><affiliation>Department of Neurology, University of Marburg, Marburg, Germany</affiliation></author><author><persName><forename type="first">David J.</forename><surname>Brooks</surname><roleName type="degree">MD, DSc</roleName></persName><affiliation>Medical Research Council Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom</affiliation></author><author><persName><forename type="first">Guido</forename><surname>Nikkhah</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Cordula</forename><surname>Matthies</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Thomas</forename><surname>Peschel</surname></persName><affiliation>Department of Neurology, University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Mona</forename><surname>Shing</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University of Marburg, Marburg, Germany</affiliation><affiliation>Department of Neurology, University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Hans</forename><surname>Kolbe</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Jörg</forename><surname>van den Hoff</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Harald</forename><surname>Fricke</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Reinhard</forename><surname>Dengler</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurology, University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Madjid</forename><surname>Samii</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</affiliation></author><author><persName><forename type="first">Wolfram H.</forename><surname>Knapp</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-11"></date><biblScope unit="vol">16</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1014">1014</biblScope><biblScope unit="page" to="1022">1022</biblScope></imprint></monogr><idno type="istex">4789B42442C1A1B00054A283DFC7B2FBACA60743</idno><idno type="DOI">10.1002/mds.1212</idno><idno type="ArticleID">MDS1212</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age‐matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [18F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [18F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment. © 2001 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>advanced Parkinson's disease</term></item><item><term>dementia</term></item><item><term>dopamine treatment</term></item><item><term>FDG</term></item><item><term>positron emission tomography</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000-10-31">Received</change><change when="2001-03-29">Registration</change><change when="2001-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/4789B42442C1A1B00054A283DFC7B2FBACA60743/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>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="60"><doi origin="wiley" registered="yes">10.1002/mds.v16:6</doi><numberingGroup><numbering type="journalVolume" number="16">16</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="2001-11">November 2001</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="30" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.1212</doi><idGroup><id type="unit" value="MDS1212"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2001 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2000-10-31"></event><event type="manuscriptRevised" date="2001-03-19"></event><event type="manuscriptAccepted" date="2001-03-29"></event><event type="publishedOnlineEarlyUnpaginated" date="2001-11-07"></event><event type="firstOnline" date="2001-11-07"></event><event type="publishedOnlineFinalForm" date="2001-11-29"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-09"></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">1014</numbering><numbering type="pageLast">1022</numbering></numberingGroup><correspondenceTo>Department of Nuclear Medicine, University Medical School, Carl Neuberg Strasse 1, D‐30625 Hannover, Germany</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS1212.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="6"></count><count type="referenceTotal" number="53"></count><count type="wordTotal" number="4551"></count></countGroup><titleGroup><title type="main" xml:lang="en">Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the <i>off</i> and <i>on</i> conditions with [<sup>18</sup>F]FDG‐PET</title><title type="short" xml:lang="en">Glucose Metabolism in Advanced Parkinson's Disease</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Georg</givenNames><familyName>Berding</familyName><degrees>MD PhD</degrees></personName><contactDetails><email normalForm="berding.georg@mh-hannover.de">berding.georg@mh‐hannover.de</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Per</givenNames><familyName>Odin</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>David J.</givenNames><familyName>Brooks</familyName><degrees>MD, DSc</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Guido</givenNames><familyName>Nikkhah</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Cordula</givenNames><familyName>Matthies</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Thomas</givenNames><familyName>Peschel</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2 #af5"><personName><givenNames>Mona</givenNames><familyName>Shing</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Hans</givenNames><familyName>Kolbe</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jörg</givenNames><familyName>van den Hoff</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Harald</givenNames><familyName>Fricke</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Reinhard</givenNames><familyName>Dengler</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Madjid</givenNames><familyName>Samii</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au13" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Wolfram H.</givenNames><familyName>Knapp</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University of Marburg, Marburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>Medical Research Council Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University Medical School, Hannover, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">advanced Parkinson's disease</keyword><keyword xml:id="kwd2">dementia</keyword><keyword xml:id="kwd3">dopamine treatment</keyword><keyword xml:id="kwd4">FDG</keyword><keyword xml:id="kwd5">positron emission tomography</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [<sup>18</sup>F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age‐matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined <i>off</i> condition, and a second time 1 hour after levodopa, resulting in a clinical <i>on</i> state. Dynamic PET scans and simultaneous arterialised venous blood samples of [<sup>18</sup>F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the <i>on</i> but not in the <i>off</i> condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between <i>on</i> and <i>off</i> conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during <i>on</i>. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [<sup>18</sup>F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment. © 2001 Movement Disorder Society.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the off and on conditions with [18F]FDG‐PET</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Glucose Metabolism in Advanced Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the</title></titleInfo><name type="personal"><namePart type="given">Georg</namePart><namePart type="family">Berding</namePart><namePart type="termsOfAddress">MD PhD</namePart><affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</affiliation><description>Correspondence: Department of Nuclear Medicine, University Medical School, Carl Neuberg Strasse 1, D‐30625 Hannover, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Per</namePart><namePart type="family">Odin</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University of Marburg, Marburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Brooks</namePart><namePart type="termsOfAddress">MD, DSc</namePart><affiliation>Medical Research Council Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Guido</namePart><namePart type="family">Nikkhah</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cordula</namePart><namePart type="family">Matthies</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Peschel</namePart><affiliation>Department of Neurology, University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mona</namePart><namePart type="family">Shing</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Marburg, Marburg, Germany</affiliation><affiliation>Department of Neurology, University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hans</namePart><namePart type="family">Kolbe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jörg</namePart><namePart type="family">van den Hoff</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Harald</namePart><namePart type="family">Fricke</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Reinhard</namePart><namePart type="family">Dengler</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Madjid</namePart><namePart type="family">Samii</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurosurgery, Nordstadt Hospital and University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wolfram H.</namePart><namePart type="family">Knapp</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2001-11</dateIssued><dateCaptured encoding="w3cdtf">2000-10-31</dateCaptured><dateValid encoding="w3cdtf">2001-03-29</dateValid><copyrightDate encoding="w3cdtf">2001</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">3</extent><extent unit="tables">6</extent><extent unit="references">53</extent><extent unit="words">4551</extent></physicalDescription><abstract lang="en">Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age‐matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [18F] acticvity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [18F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment. © 2001 Movement Disorder Society.</abstract><subject lang="en"><genre>Keywords</genre><topic>advanced Parkinson's disease</topic><topic>dementia</topic><topic>dopamine treatment</topic><topic>FDG</topic><topic>positron emission tomography</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. 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