Progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease using [18F]CFT PET
Identifieur interne : 000485 ( Main/Corpus ); précédent : 000484; suivant : 000486Progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease using [18F]CFT PET
Auteurs : Elina Nurmi ; Jörgen Bergman ; Olli Eskola ; Olof Solin ; Tero Vahlberg ; Pirkko Sonninen ; Juha O. RinneSource :
- Synapse [ 0887-4476 ] ; 2003-06-01.
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Abstract
The aim of this study was to investigate the progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease (PD). We studied 12 patients with early PD and 11 healthy controls with a dopamine transporter ligand 2β‐carbomethoxy‐3β‐(4‐[18F]‐fluorophenyl)tropane ([18F]CFT) positron emission tomography (PET). The PET scan was carried out twice with an average interval of 2.2 years. The regions of interest (anterior and posterior putamen, caudate nucleus, and cerebellum) were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images, and copied onto the PET images. At the first PET scan in PD patients, the [18F]CFT uptake in the anterior putamen was 1.92 ± 0.67, which was 45% of the control mean, and in the posterior putamen 1.02 ± 0.55, being only 27% of the control mean. For the caudate nucleus the corresponding figure was 2.55 ± 0.58 (71% of the control mean). The uptake ratios had declined significantly by the time of the second PET scan and the absolute annual rate of decline of the tracer uptake was 0.23 ± 0.14 (P < 0.001) in the anterior putamen, 0.13 ± 0.13 (P = 0.005) in the posterior putamen, and 0.20 ± 0.15 (P < 0.001) in the caudate nucleus. There was a statistically significant difference of the decline in the tracer uptake between the anterior and posterior putamen (P = 0.033). When the rate of progression was calculated compared to the normal control mean, the rate of annual decline was 5.3% in the anterior putamen, 3.3% in the posterior putamen, and 5.6% in the caudate nucleus, without significant changes among striatal subregions (P = 0.10). When ipsi‐ and contralateral sides were analyzed separately, the absolute decline of [18F]CFT uptake in the putamen was higher in the side ipsilateral to the predominant symptoms than in the contralateral side (P = 0.035 for anterior putamen and P = 0.026 for posterior putamen). In the caudate nucleus the absolute decline was not different between ipsi‐ and contralateral sides (P = 0.76). In healthy controls, no significant decline of [18F]CFT uptake was detected. The results are suggestive of slower progression in the posterior putamen, where the disease is more advanced, but studies to follow up the same patient at several time points are needed to resolve this question. Synapse 48:109–115, 2003. © 2003 Wiley‐Liss, Inc.
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DOI: 10.1002/syn.10192
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Rinne</name><affiliation><mods:affiliation>Turku PET Centre, FIN‐20521, Turku, Finland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="ISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2003-06-01">2003-06-01</date><biblScope unit="volume">48</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="109">109</biblScope><biblScope unit="page" to="115">115</biblScope></imprint><idno type="ISSN">0887-4476</idno></series><idno type="istex">F2C840940035C581A4428D1F72F6B3790902B8E6</idno><idno type="DOI">10.1002/syn.10192</idno><idno type="ArticleID">SYN10192</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0887-4476</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>CFT</term><term>PET</term><term>Parkinson's disease</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 progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease (PD). We studied 12 patients with early PD and 11 healthy controls with a dopamine transporter ligand 2β‐carbomethoxy‐3β‐(4‐[18F]‐fluorophenyl)tropane ([18F]CFT) positron emission tomography (PET). The PET scan was carried out twice with an average interval of 2.2 years. The regions of interest (anterior and posterior putamen, caudate nucleus, and cerebellum) were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images, and copied onto the PET images. At the first PET scan in PD patients, the [18F]CFT uptake in the anterior putamen was 1.92 ± 0.67, which was 45% of the control mean, and in the posterior putamen 1.02 ± 0.55, being only 27% of the control mean. For the caudate nucleus the corresponding figure was 2.55 ± 0.58 (71% of the control mean). The uptake ratios had declined significantly by the time of the second PET scan and the absolute annual rate of decline of the tracer uptake was 0.23 ± 0.14 (P < 0.001) in the anterior putamen, 0.13 ± 0.13 (P = 0.005) in the posterior putamen, and 0.20 ± 0.15 (P < 0.001) in the caudate nucleus. There was a statistically significant difference of the decline in the tracer uptake between the anterior and posterior putamen (P = 0.033). When the rate of progression was calculated compared to the normal control mean, the rate of annual decline was 5.3% in the anterior putamen, 3.3% in the posterior putamen, and 5.6% in the caudate nucleus, without significant changes among striatal subregions (P = 0.10). When ipsi‐ and contralateral sides were analyzed separately, the absolute decline of [18F]CFT uptake in the putamen was higher in the side ipsilateral to the predominant symptoms than in the contralateral side (P = 0.035 for anterior putamen and P = 0.026 for posterior putamen). In the caudate nucleus the absolute decline was not different between ipsi‐ and contralateral sides (P = 0.76). In healthy controls, no significant decline of [18F]CFT uptake was detected. The results are suggestive of slower progression in the posterior putamen, where the disease is more advanced, but studies to follow up the same patient at several time points are needed to resolve this question. Synapse 48:109–115, 2003. © 2003 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Elina Nurmi</name><affiliations><json:string>Department of Neurology, University of Turku, FIN‐20521, Turku, Finland</json:string><json:string>Turku PET Centre, FIN‐20521, Turku, Finland</json:string></affiliations></json:item><json:item><name>Jörgen Bergman</name><affiliations><json:string>Turku PET Centre, FIN‐20521, Turku, Finland</json:string></affiliations></json:item><json:item><name>Olli Eskola</name><affiliations><json:string>Turku PET Centre, FIN‐20521, Turku, Finland</json:string></affiliations></json:item><json:item><name>Olof Solin</name><affiliations><json:string>Turku PET Centre, FIN‐20521, Turku, Finland</json:string></affiliations></json:item><json:item><name>Tero Vahlberg</name><affiliations><json:string>Department of Biostatistics, University of Turku, FIN‐20521, Turku, Finland</json:string></affiliations></json:item><json:item><name>Pirkko Sonninen</name><affiliations><json:string>Department of Radiology, University of Turku, FIN‐20521, Turku, Finland</json:string></affiliations></json:item><json:item><name>Juha O. Rinne</name><affiliations><json:string>Turku PET Centre, FIN‐20521, Turku, Finland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>CFT</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><articleId><json:string>SYN10192</json:string></articleId><language><json:string>eng</json:string></language><abstract>The aim of this study was to investigate the progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease (PD). We studied 12 patients with early PD and 11 healthy controls with a dopamine transporter ligand 2β‐carbomethoxy‐3β‐(4‐[18F]‐fluorophenyl)tropane ([18F]CFT) positron emission tomography (PET). The PET scan was carried out twice with an average interval of 2.2 years. The regions of interest (anterior and posterior putamen, caudate nucleus, and cerebellum) were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images, and copied onto the PET images. At the first PET scan in PD patients, the [18F]CFT uptake in the anterior putamen was 1.92 ± 0.67, which was 45% of the control mean, and in the posterior putamen 1.02 ± 0.55, being only 27% of the control mean. For the caudate nucleus the corresponding figure was 2.55 ± 0.58 (71% of the control mean). The uptake ratios had declined significantly by the time of the second PET scan and the absolute annual rate of decline of the tracer uptake was 0.23 ± 0.14 (P > 0.001) in the anterior putamen, 0.13 ± 0.13 (P = 0.005) in the posterior putamen, and 0.20 ± 0.15 (P > 0.001) in the caudate nucleus. There was a statistically significant difference of the decline in the tracer uptake between the anterior and posterior putamen (P = 0.033). When the rate of progression was calculated compared to the normal control mean, the rate of annual decline was 5.3% in the anterior putamen, 3.3% in the posterior putamen, and 5.6% in the caudate nucleus, without significant changes among striatal subregions (P = 0.10). When ipsi‐ and contralateral sides were analyzed separately, the absolute decline of [18F]CFT uptake in the putamen was higher in the side ipsilateral to the predominant symptoms than in the contralateral side (P = 0.035 for anterior putamen and P = 0.026 for posterior putamen). In the caudate nucleus the absolute decline was not different between ipsi‐ and contralateral sides (P = 0.76). In healthy controls, no significant decline of [18F]CFT uptake was detected. The results are suggestive of slower progression in the posterior putamen, where the disease is more advanced, but studies to follow up the same patient at several time points are needed to resolve this question. 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Box 52, FIN‐20521 Turku, Finland</p></note><affiliation>Turku PET Centre, FIN‐20521, Turku, Finland</affiliation></author></analytic><monogr><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="pISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><idno type="DOI">10.1002/(ISSN)1098-2396</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2003-06-01"></date><biblScope unit="volume">48</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="109">109</biblScope><biblScope unit="page" to="115">115</biblScope></imprint></monogr><idno type="istex">F2C840940035C581A4428D1F72F6B3790902B8E6</idno><idno type="DOI">10.1002/syn.10192</idno><idno type="ArticleID">SYN10192</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The aim of this study was to investigate the progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease (PD). We studied 12 patients with early PD and 11 healthy controls with a dopamine transporter ligand 2β‐carbomethoxy‐3β‐(4‐[18F]‐fluorophenyl)tropane ([18F]CFT) positron emission tomography (PET). The PET scan was carried out twice with an average interval of 2.2 years. The regions of interest (anterior and posterior putamen, caudate nucleus, and cerebellum) were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images, and copied onto the PET images. At the first PET scan in PD patients, the [18F]CFT uptake in the anterior putamen was 1.92 ± 0.67, which was 45% of the control mean, and in the posterior putamen 1.02 ± 0.55, being only 27% of the control mean. For the caudate nucleus the corresponding figure was 2.55 ± 0.58 (71% of the control mean). The uptake ratios had declined significantly by the time of the second PET scan and the absolute annual rate of decline of the tracer uptake was 0.23 ± 0.14 (P < 0.001) in the anterior putamen, 0.13 ± 0.13 (P = 0.005) in the posterior putamen, and 0.20 ± 0.15 (P < 0.001) in the caudate nucleus. There was a statistically significant difference of the decline in the tracer uptake between the anterior and posterior putamen (P = 0.033). When the rate of progression was calculated compared to the normal control mean, the rate of annual decline was 5.3% in the anterior putamen, 3.3% in the posterior putamen, and 5.6% in the caudate nucleus, without significant changes among striatal subregions (P = 0.10). When ipsi‐ and contralateral sides were analyzed separately, the absolute decline of [18F]CFT uptake in the putamen was higher in the side ipsilateral to the predominant symptoms than in the contralateral side (P = 0.035 for anterior putamen and P = 0.026 for posterior putamen). In the caudate nucleus the absolute decline was not different between ipsi‐ and contralateral sides (P = 0.76). In healthy controls, no significant decline of [18F]CFT uptake was detected. The results are suggestive of slower progression in the posterior putamen, where the disease is more advanced, but studies to follow up the same patient at several time points are needed to resolve this question. Synapse 48:109–115, 2003. © 2003 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>CFT</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></profileDesc><revisionDesc><change when="2002-07-10">Received</change><change when="2003-01-14">Registration</change><change when="2003-06-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F2C840940035C581A4428D1F72F6B3790902B8E6/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1098-2396</doi><issn type="print">0887-4476</issn><issn type="electronic">1098-2396</issn><idGroup><id type="product" value="SYN"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="SYNAPSE">Synapse</title><title type="short">Synapse</title></titleGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/syn.v48:3</doi><numberingGroup><numbering type="journalVolume" number="48">48</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="2003-06-01">1 June 2003</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="10" status="forIssue"><doi origin="wiley" registered="yes">10.1002/syn.10192</doi><idGroup><id type="unit" value="SYN10192"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><copyright ownership="publisher">Copyright © 2003 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2002-07-10"></event><event type="manuscriptAccepted" date="2003-01-14"></event><event type="firstOnline" date="2003-03-04"></event><event type="publishedOnlineFinalForm" date="2003-03-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-04"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-10"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst">109</numbering><numbering type="pageLast">115</numbering></numberingGroup><correspondenceTo>Turku PET Centre, University of Turku, P.O. Box 52, FIN‐20521 Turku, Finland</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:SYN.SYN10192.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="41"></count><count type="wordTotal" number="6232"></count></countGroup><titleGroup><title type="main" xml:lang="en">Progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease using [<sup>18</sup>F]CFT PET</title><title type="short" xml:lang="en">[<sup>18</sup>F]CFT PET in Progression of PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Elina</givenNames><familyName>Nurmi</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Jörgen</givenNames><familyName>Bergman</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Olli</givenNames><familyName>Eskola</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Olof</givenNames><familyName>Solin</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Tero</givenNames><familyName>Vahlberg</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Pirkko</givenNames><familyName>Sonninen</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2" corresponding="yes"><personName><givenNames>Juha O.</givenNames><familyName>Rinne</familyName></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, University of Turku, FIN‐20521, Turku, Finland</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FI" type="organization"><unparsedAffiliation>Turku PET Centre, FIN‐20521, Turku, Finland</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FI" type="organization"><unparsedAffiliation>Department of Biostatistics, University of Turku, FIN‐20521, Turku, Finland</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FI" type="organization"><unparsedAffiliation>Department of Radiology, University of Turku, FIN‐20521, Turku, Finland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">CFT</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><fundingInfo><fundingAgency>Päivikki and Sakari Sohlberg Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Turku University Central Hospital (EVO)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Finnish Parkinson Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Medical Society Duodecim in Turku</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The aim of this study was to investigate the progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease (PD). We studied 12 patients with early PD and 11 healthy controls with a dopamine transporter ligand 2β‐carbomethoxy‐3β‐(4‐[<sup>18</sup>F]‐fluorophenyl)tropane ([<sup>18</sup>F]CFT) positron emission tomography (PET). The PET scan was carried out twice with an average interval of 2.2 years. The regions of interest (anterior and posterior putamen, caudate nucleus, and cerebellum) were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images, and copied onto the PET images. At the first PET scan in PD patients, the [<sup>18</sup>F]CFT uptake in the anterior putamen was 1.92 ± 0.67, which was 45% of the control mean, and in the posterior putamen 1.02 ± 0.55, being only 27% of the control mean. For the caudate nucleus the corresponding figure was 2.55 ± 0.58 (71% of the control mean). The uptake ratios had declined significantly by the time of the second PET scan and the absolute annual rate of decline of the tracer uptake was 0.23 ± 0.14 (<i>P</i> < 0.001) in the anterior putamen, 0.13 ± 0.13 (<i>P</i> = 0.005) in the posterior putamen, and 0.20 ± 0.15 (<i>P</i> < 0.001) in the caudate nucleus. There was a statistically significant difference of the decline in the tracer uptake between the anterior and posterior putamen (<i>P</i> = 0.033). When the rate of progression was calculated compared to the normal control mean, the rate of annual decline was 5.3% in the anterior putamen, 3.3% in the posterior putamen, and 5.6% in the caudate nucleus, without significant changes among striatal subregions (<i>P</i> = 0.10). When ipsi‐ and contralateral sides were analyzed separately, the absolute decline of [<sup>18</sup>F]CFT uptake in the putamen was higher in the side ipsilateral to the predominant symptoms than in the contralateral side (<i>P</i> = 0.035 for anterior putamen and <i>P</i> = 0.026 for posterior putamen). In the caudate nucleus the absolute decline was not different between ipsi‐ and contralateral sides (<i>P</i> = 0.76). In healthy controls, no significant decline of [<sup>18</sup>F]CFT uptake was detected. The results are suggestive of slower progression in the posterior putamen, where the disease is more advanced, but studies to follow up the same patient at several time points are needed to resolve this question. Synapse 48:109–115, 2003. © 2003 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease using [18F]CFT PET</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>[18F]CFT PET in Progression of PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease using [</title></titleInfo><name type="personal"><namePart type="given">Elina</namePart><namePart type="family">Nurmi</namePart><affiliation>Department of Neurology, University of Turku, FIN‐20521, Turku, Finland</affiliation><affiliation>Turku PET Centre, FIN‐20521, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jörgen</namePart><namePart type="family">Bergman</namePart><affiliation>Turku PET Centre, FIN‐20521, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olli</namePart><namePart type="family">Eskola</namePart><affiliation>Turku PET Centre, FIN‐20521, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olof</namePart><namePart type="family">Solin</namePart><affiliation>Turku PET Centre, FIN‐20521, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tero</namePart><namePart type="family">Vahlberg</namePart><affiliation>Department of Biostatistics, University of Turku, FIN‐20521, Turku, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pirkko</namePart><namePart type="family">Sonninen</namePart><affiliation>Department of Radiology, University of Turku, FIN‐20521, 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><affiliation>Turku PET Centre, FIN‐20521, Turku, Finland</affiliation><description>Correspondence: Turku PET Centre, University of Turku, P.O. Box 52, FIN‐20521 Turku, Finland</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2003-06-01</dateIssued><dateCaptured encoding="w3cdtf">2002-07-10</dateCaptured><dateValid encoding="w3cdtf">2003-01-14</dateValid><copyrightDate encoding="w3cdtf">2003</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">1</extent><extent unit="tables">2</extent><extent unit="references">41</extent><extent unit="words">6232</extent></physicalDescription><abstract lang="en">The aim of this study was to investigate the progression of dopaminergic hypofunction in striatal subregions in Parkinson's disease (PD). We studied 12 patients with early PD and 11 healthy controls with a dopamine transporter ligand 2β‐carbomethoxy‐3β‐(4‐[18F]‐fluorophenyl)tropane ([18F]CFT) positron emission tomography (PET). The PET scan was carried out twice with an average interval of 2.2 years. The regions of interest (anterior and posterior putamen, caudate nucleus, and cerebellum) were drawn on individual magnetic resonance imaging (MRI) images, matched with the PET images, and copied onto the PET images. At the first PET scan in PD patients, the [18F]CFT uptake in the anterior putamen was 1.92 ± 0.67, which was 45% of the control mean, and in the posterior putamen 1.02 ± 0.55, being only 27% of the control mean. For the caudate nucleus the corresponding figure was 2.55 ± 0.58 (71% of the control mean). The uptake ratios had declined significantly by the time of the second PET scan and the absolute annual rate of decline of the tracer uptake was 0.23 ± 0.14 (P < 0.001) in the anterior putamen, 0.13 ± 0.13 (P = 0.005) in the posterior putamen, and 0.20 ± 0.15 (P < 0.001) in the caudate nucleus. There was a statistically significant difference of the decline in the tracer uptake between the anterior and posterior putamen (P = 0.033). When the rate of progression was calculated compared to the normal control mean, the rate of annual decline was 5.3% in the anterior putamen, 3.3% in the posterior putamen, and 5.6% in the caudate nucleus, without significant changes among striatal subregions (P = 0.10). When ipsi‐ and contralateral sides were analyzed separately, the absolute decline of [18F]CFT uptake in the putamen was higher in the side ipsilateral to the predominant symptoms than in the contralateral side (P = 0.035 for anterior putamen and P = 0.026 for posterior putamen). In the caudate nucleus the absolute decline was not different between ipsi‐ and contralateral sides (P = 0.76). In healthy controls, no significant decline of [18F]CFT uptake was detected. The results are suggestive of slower progression in the posterior putamen, where the disease is more advanced, but studies to follow up the same patient at several time points are needed to resolve this question. Synapse 48:109–115, 2003. © 2003 Wiley‐Liss, Inc.</abstract><note type="funding">Päivikki and Sakari Sohlberg Foundation</note><note type="funding">Turku University Central Hospital (EVO)</note><note type="funding">Finnish Parkinson Foundation</note><note type="funding">Medical Society Duodecim in Turku</note><subject lang="en"><genre>Keywords</genre><topic>CFT</topic><topic>Parkinson's disease</topic><topic>PET</topic><topic>positron emission tomography</topic><topic>progression</topic></subject><relatedItem type="host"><titleInfo><title>Synapse</title></titleInfo><titleInfo type="abbreviated"><title>Synapse</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0887-4476</identifier><identifier type="eISSN">1098-2396</identifier><identifier type="DOI">10.1002/(ISSN)1098-2396</identifier><identifier type="PublisherID">SYN</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>48</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>109</start><end>115</end><total>7</total></extent></part></relatedItem><identifier type="istex">F2C840940035C581A4428D1F72F6B3790902B8E6</identifier><identifier type="DOI">10.1002/syn.10192</identifier><identifier type="ArticleID">SYN10192</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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