Rate of progression in Parkinson's disease: A 6‐[18F]fluoro‐L‐dopa PET study
Identifieur interne : 000248 ( Istex/Corpus ); précédent : 000247; suivant : 000249Rate of progression in Parkinson's disease: A 6‐[18F]fluoro‐L‐dopa PET study
Auteurs : Elina Nurmi ; Hanna M. Ruottinen ; Jörgen Bergman ; Merja Haaparanta ; Olof Solin ; Pirkko Sonninen ; Juha O. RinneSource :
- Movement Disorders [ 0885-3185 ] ; 2001-07.
English descriptors
Abstract
The aim of this study was to investigate the rate of progression in Parkinson's disease (PD) with 6‐[18F]fluoro‐L‐dopa (FDOPA) positron emission tomography (PET). We investigated 21 patients with PD and eight healthy controls. Ten of the patients were de novo at the time of the first PET scan and antiparkinsonian medication was started thereafter, with a favourable response. A FDOPA PET scan was carried out twice at an approximately 5‐year interval. The regions of interest were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images. At the first PET scan, in PD patients the mean kiocc (× 10−3 min−1) in the anterior putamen was 5.6 ± 2.7 (mean ± S.D.; 55% of the control mean) and in the posterior putamen 4.5 ± 2.4 (45% of the control mean). The kiocc value for the caudate nucleus was 7.5 ± 2.1 (× 10−3 min−1; 76% of the control mean). The FDOPA uptake declined by the time of the second PET scan and the annual rate of decline was 8.3 ± 6.3% (P < 0.001) of the baseline mean in the anterior putamen and 10.3 ± 4.8% (P < 0.001) in the posterior putamen. In the caudate nucleus, FDOPA uptake decreased by 5.9 ± 5.1% (P < 0.001) of the baseline mean per year. The estimated preclinical period was longest for the posterior putamen being 6.5 years. For the anterior putamen the preclinical period was 4.6 years. In the caudate nucleus, the estimated FDOPA uptake was at normal level at disease onset. In healthy controls, there was no significant decline in FDOPA uptake in any striatal subregion. Our results suggest that the disease process in PD first affects posterior putamen, followed by the anterior putamen and the caudate nucleus, but once started, the absolute rate of decline is the same. In healthy controls, no significant decline in FDOPA was detected. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1139
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Ruottinen</name><affiliation><mods:affiliation>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Bergman, Jorgen" sort="Bergman, Jorgen" uniqKey="Bergman J" first="Jörgen" last="Bergman">Jörgen Bergman</name><affiliation><mods:affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Haaparanta, Merja" sort="Haaparanta, Merja" uniqKey="Haaparanta M" first="Merja" last="Haaparanta">Merja Haaparanta</name><affiliation><mods:affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Solin, Olof" sort="Solin, Olof" uniqKey="Solin O" first="Olof" last="Solin">Olof Solin</name><affiliation><mods:affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Sonninen, Pirkko" sort="Sonninen, Pirkko" uniqKey="Sonninen P" first="Pirkko" last="Sonninen">Pirkko Sonninen</name><affiliation><mods:affiliation>Department of Radiology, University of Turku, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Rinne, Juha O" sort="Rinne, Juha O" uniqKey="Rinne J" first="Juha O." last="Rinne">Juha O. 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Ruottinen</name><affiliation><mods:affiliation>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Bergman, Jorgen" sort="Bergman, Jorgen" uniqKey="Bergman J" first="Jörgen" last="Bergman">Jörgen Bergman</name><affiliation><mods:affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Haaparanta, Merja" sort="Haaparanta, Merja" uniqKey="Haaparanta M" first="Merja" last="Haaparanta">Merja Haaparanta</name><affiliation><mods:affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Solin, Olof" sort="Solin, Olof" uniqKey="Solin O" first="Olof" last="Solin">Olof Solin</name><affiliation><mods:affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Sonninen, Pirkko" sort="Sonninen, Pirkko" uniqKey="Sonninen P" first="Pirkko" last="Sonninen">Pirkko Sonninen</name><affiliation><mods:affiliation>Department of Radiology, University of Turku, Turku, Finland</mods:affiliation></affiliation></author><author><name sortKey="Rinne, Juha O" sort="Rinne, Juha O" uniqKey="Rinne J" first="Juha O." last="Rinne">Juha O. Rinne</name><affiliation><mods:affiliation>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</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="2001-07">2001-07</date><biblScope unit="vol">16</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="608">608</biblScope><biblScope unit="page" to="615">615</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">CD92A9CF64114C39DC4DA24600A15F13E81FF7E4</idno><idno type="DOI">10.1002/mds.1139</idno><idno type="ArticleID">MDS1139</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PET</term><term>Parkinson's disease</term><term>fluorodopa</term><term>positron emission tomography</term><term>progression</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The aim of this study was to investigate the rate of progression in Parkinson's disease (PD) with 6‐[18F]fluoro‐L‐dopa (FDOPA) positron emission tomography (PET). We investigated 21 patients with PD and eight healthy controls. Ten of the patients were de novo at the time of the first PET scan and antiparkinsonian medication was started thereafter, with a favourable response. A FDOPA PET scan was carried out twice at an approximately 5‐year interval. The regions of interest were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images. At the first PET scan, in PD patients the mean kiocc (× 10−3 min−1) in the anterior putamen was 5.6 ± 2.7 (mean ± S.D.; 55% of the control mean) and in the posterior putamen 4.5 ± 2.4 (45% of the control mean). The kiocc value for the caudate nucleus was 7.5 ± 2.1 (× 10−3 min−1; 76% of the control mean). The FDOPA uptake declined by the time of the second PET scan and the annual rate of decline was 8.3 ± 6.3% (P < 0.001) of the baseline mean in the anterior putamen and 10.3 ± 4.8% (P < 0.001) in the posterior putamen. In the caudate nucleus, FDOPA uptake decreased by 5.9 ± 5.1% (P < 0.001) of the baseline mean per year. The estimated preclinical period was longest for the posterior putamen being 6.5 years. For the anterior putamen the preclinical period was 4.6 years. In the caudate nucleus, the estimated FDOPA uptake was at normal level at disease onset. In healthy controls, there was no significant decline in FDOPA uptake in any striatal subregion. Our results suggest that the disease process in PD first affects posterior putamen, followed by the anterior putamen and the caudate nucleus, but once started, the absolute rate of decline is the same. In healthy controls, no significant decline in FDOPA was detected. © 2001 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Elina Nurmi MD</name><affiliations><json:string>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</json:string></affiliations></json:item><json:item><name>Hanna M. Ruottinen MD, PhD</name><affiliations><json:string>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</json:string></affiliations></json:item><json:item><name>Jörgen Bergman MSc</name><affiliations><json:string>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</json:string></affiliations></json:item><json:item><name>Merja Haaparanta MSc</name><affiliations><json:string>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</json:string></affiliations></json:item><json:item><name>Olof Solin PhD</name><affiliations><json:string>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</json:string></affiliations></json:item><json:item><name>Pirkko Sonninen MD</name><affiliations><json:string>Department of Radiology, University of Turku, Turku, Finland</json:string></affiliations></json:item><json:item><name>Juha O. Rinne MD, PhD</name><affiliations><json:string>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>fluorodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>positron emission tomography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>progression</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The aim of this study was to investigate the rate of progression in Parkinson's disease (PD) with 6‐[18F]fluoro‐L‐dopa (FDOPA) positron emission tomography (PET). We investigated 21 patients with PD and eight healthy controls. Ten of the patients were de novo at the time of the first PET scan and antiparkinsonian medication was started thereafter, with a favourable response. A FDOPA PET scan was carried out twice at an approximately 5‐year interval. The regions of interest were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images.At the first PET scan, in PD patients the mean kiocc (× 10−3 min−1) in the anterior putamen was 5.6 ± 2.7 (mean ± S.D.; 55% of the control mean) and in the posterior putamen 4.5 ± 2.4 (45% of the control mean). The kiocc value for the caudate nucleus was 7.5 ± 2.1 (× 10−3 min−1; 76% of the control mean). The FDOPA uptake declined by the time of the second PET scan and the annual rate of decline was 8.3 ± 6.3% (P > 0.001) of the baseline mean in the anterior putamen and 10.3 ± 4.8% (P > 0.001) in the posterior putamen. In the caudate nucleus, FDOPA uptake decreased by 5.9 ± 5.1% (P > 0.001) of the baseline mean per year. The estimated preclinical period was longest for the posterior putamen being 6.5 years. For the anterior putamen the preclinical period was 4.6 years. In the caudate nucleus, the estimated FDOPA uptake was at normal level at disease onset. In healthy controls, there was no significant decline in FDOPA uptake in any striatal subregion.Our results suggest that the disease process in PD first affects posterior putamen, followed by the anterior putamen and the caudate nucleus, but once started, the absolute rate of decline is the same. 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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="2001-07"></date><biblScope unit="vol">16</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="608">608</biblScope><biblScope unit="page" to="615">615</biblScope></imprint></monogr><idno type="istex">CD92A9CF64114C39DC4DA24600A15F13E81FF7E4</idno><idno type="DOI">10.1002/mds.1139</idno><idno type="ArticleID">MDS1139</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The aim of this study was to investigate the rate of progression in Parkinson's disease (PD) with 6‐[18F]fluoro‐L‐dopa (FDOPA) positron emission tomography (PET). We investigated 21 patients with PD and eight healthy controls. Ten of the patients were de novo at the time of the first PET scan and antiparkinsonian medication was started thereafter, with a favourable response. A FDOPA PET scan was carried out twice at an approximately 5‐year interval. The regions of interest were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images.At the first PET scan, in PD patients the mean kiocc (× 10−3 min−1) in the anterior putamen was 5.6 ± 2.7 (mean ± S.D.; 55% of the control mean) and in the posterior putamen 4.5 ± 2.4 (45% of the control mean). The kiocc value for the caudate nucleus was 7.5 ± 2.1 (× 10−3 min−1; 76% of the control mean). The FDOPA uptake declined by the time of the second PET scan and the annual rate of decline was 8.3 ± 6.3% (P < 0.001) of the baseline mean in the anterior putamen and 10.3 ± 4.8% (P < 0.001) in the posterior putamen. In the caudate nucleus, FDOPA uptake decreased by 5.9 ± 5.1% (P < 0.001) of the baseline mean per year. The estimated preclinical period was longest for the posterior putamen being 6.5 years. For the anterior putamen the preclinical period was 4.6 years. In the caudate nucleus, the estimated FDOPA uptake was at normal level at disease onset. In healthy controls, there was no significant decline in FDOPA uptake in any striatal subregion.Our results suggest that the disease process in PD first affects posterior putamen, followed by the anterior putamen and the caudate nucleus, but once started, the absolute rate of decline is the same. In healthy controls, no significant decline in FDOPA was detected. © 2001 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>fluorodopa</term></item><item><term>Parkinson's disease</term></item><item><term>PET</term></item><item><term>positron emission tomography</term></item><item><term>progression</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="2000-07-05">Received</change><change when="2001-02-16">Registration</change><change when="2001-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CD92A9CF64114C39DC4DA24600A15F13E81FF7E4/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="40"><doi origin="wiley" registered="yes">10.1002/mds.v16:4</doi><numberingGroup><numbering type="journalVolume" number="16">16</numbering><numbering type="journalIssue">4</numbering></numberingGroup><coverDate startDate="2001-07">July 2001</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="4" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.1139</doi><idGroup><id type="unit" value="MDS1139"></id></idGroup><countGroup><count type="pageTotal" number="8"></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="2000-07-05"></event><event type="manuscriptRevised" date="2001-02-09"></event><event type="manuscriptAccepted" date="2001-02-16"></event><event type="firstOnline" date="2001-07-16"></event><event type="publishedOnlineFinalForm" date="2001-07-26"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></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">608</numbering><numbering type="pageLast">615</numbering></numberingGroup><correspondenceTo>Turku PET Centre, University of Turku, FIN‐20520 Turku, Finland.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS1139.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="44"></count><count type="wordTotal" number="4676"></count></countGroup><titleGroup><title type="main" xml:lang="en">Rate of progression in Parkinson's disease: A 6‐[<sup>18</sup>F]fluoro‐L‐dopa PET study</title><title type="short" xml:lang="en">6‐[<sup>18</sup>F]fluoro‐L‐dopa in Progression of PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Elina</givenNames><familyName>Nurmi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Hanna M.</givenNames><familyName>Ruottinen</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Jörgen</givenNames><familyName>Bergman</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Merja</givenNames><familyName>Haaparanta</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Olof</givenNames><familyName>Solin</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Pirkko</givenNames><familyName>Sonninen</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Juha O.</givenNames><familyName>Rinne</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>juha.rinne@pet.tyks.fi</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FI" type="organization"><unparsedAffiliation>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FI" type="organization"><unparsedAffiliation>Department of Radiology, University of Turku, Turku, Finland</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FI" type="organization"><unparsedAffiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">fluorodopa</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">PET</keyword><keyword xml:id="kwd4">positron emission tomography</keyword><keyword xml:id="kwd5">progression</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The aim of this study was to investigate the rate of progression in Parkinson's disease (PD) with 6‐[<sup>18</sup>F]fluoro‐L‐dopa (FDOPA) positron emission tomography (PET). We investigated 21 patients with PD and eight healthy controls. Ten of the patients were de novo at the time of the first PET scan and antiparkinsonian medication was started thereafter, with a favourable response. A FDOPA PET scan was carried out twice at an approximately 5‐year interval. The regions of interest were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images.</p><p>At the first PET scan, in PD patients the mean k<sub>i</sub><sup>occ</sup> (× 10<sup>−3</sup> min<sup>−1</sup>) in the anterior putamen was 5.6 ± 2.7 (mean ± S.D.; 55% of the control mean) and in the posterior putamen 4.5 ± 2.4 (45% of the control mean). The k<sub>i</sub><sup>occ</sup> value for the caudate nucleus was 7.5 ± 2.1 (× 10<sup>−3</sup> min<sup>−1</sup>; 76% of the control mean). The FDOPA uptake declined by the time of the second PET scan and the annual rate of decline was 8.3 ± 6.3% (<i>P</i> < 0.001) of the baseline mean in the anterior putamen and 10.3 ± 4.8% (<i>P</i> < 0.001) in the posterior putamen. In the caudate nucleus, FDOPA uptake decreased by 5.9 ± 5.1% (<i>P</i> < 0.001) of the baseline mean per year. The estimated preclinical period was longest for the posterior putamen being 6.5 years. For the anterior putamen the preclinical period was 4.6 years. In the caudate nucleus, the estimated FDOPA uptake was at normal level at disease onset. In healthy controls, there was no significant decline in FDOPA uptake in any striatal subregion.</p><p>Our results suggest that the disease process in PD first affects posterior putamen, followed by the anterior putamen and the caudate nucleus, but once started, the absolute rate of decline is the same. In healthy controls, no significant decline in FDOPA was detected. © 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>Rate of progression in Parkinson's disease: A 6‐[18F]fluoro‐L‐dopa PET study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>6‐[18F]fluoro‐L‐dopa in Progression of PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Rate of progression in Parkinson's disease: A 6‐[</title></titleInfo><name type="personal"><namePart type="given">Elina</namePart><namePart type="family">Nurmi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hanna M.</namePart><namePart type="family">Ruottinen</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jörgen</namePart><namePart type="family">Bergman</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Merja</namePart><namePart type="family">Haaparanta</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olof</namePart><namePart type="family">Solin</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Radiochemistry Laboratory, Turku PET Centre, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pirkko</namePart><namePart type="family">Sonninen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Radiology, University of Turku, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Juha O.</namePart><namePart type="family">Rinne</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, and Turku PET Centre, University of Turku, Turku, Finland</affiliation><description>Correspondence: Turku PET Centre, University of Turku, FIN‐20520 Turku, Finland.</description><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">2001-07</dateIssued><dateCaptured encoding="w3cdtf">2000-07-05</dateCaptured><dateValid encoding="w3cdtf">2001-02-16</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">2</extent><extent unit="tables">1</extent><extent unit="references">44</extent><extent unit="words">4676</extent></physicalDescription><abstract lang="en">The aim of this study was to investigate the rate of progression in Parkinson's disease (PD) with 6‐[18F]fluoro‐L‐dopa (FDOPA) positron emission tomography (PET). We investigated 21 patients with PD and eight healthy controls. Ten of the patients were de novo at the time of the first PET scan and antiparkinsonian medication was started thereafter, with a favourable response. A FDOPA PET scan was carried out twice at an approximately 5‐year interval. The regions of interest were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images. At the first PET scan, in PD patients the mean kiocc (× 10−3 min−1) in the anterior putamen was 5.6 ± 2.7 (mean ± S.D.; 55% of the control mean) and in the posterior putamen 4.5 ± 2.4 (45% of the control mean). The kiocc value for the caudate nucleus was 7.5 ± 2.1 (× 10−3 min−1; 76% of the control mean). The FDOPA uptake declined by the time of the second PET scan and the annual rate of decline was 8.3 ± 6.3% (P < 0.001) of the baseline mean in the anterior putamen and 10.3 ± 4.8% (P < 0.001) in the posterior putamen. In the caudate nucleus, FDOPA uptake decreased by 5.9 ± 5.1% (P < 0.001) of the baseline mean per year. The estimated preclinical period was longest for the posterior putamen being 6.5 years. For the anterior putamen the preclinical period was 4.6 years. In the caudate nucleus, the estimated FDOPA uptake was at normal level at disease onset. In healthy controls, there was no significant decline in FDOPA uptake in any striatal subregion. Our results suggest that the disease process in PD first affects posterior putamen, followed by the anterior putamen and the caudate nucleus, but once started, the absolute rate of decline is the same. In healthy controls, no significant decline in FDOPA was detected. © 2001 Movement Disorder Society.</abstract><subject lang="en"><genre>Keywords</genre><topic>fluorodopa</topic><topic>Parkinson's disease</topic><topic>PET</topic><topic>positron emission tomography</topic><topic>progression</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. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</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>2001</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>608</start><end>615</end><total>8</total></extent></part></relatedItem><identifier type="istex">CD92A9CF64114C39DC4DA24600A15F13E81FF7E4</identifier><identifier type="DOI">10.1002/mds.1139</identifier><identifier type="ArticleID">MDS1139</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2001 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>John Wiley & Sons, Inc.</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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