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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<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>
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<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.</abstract>
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<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>
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<creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Elina</givenNames>
<familyName>Nurmi</familyName>
<degrees>MD</degrees>
</personName>
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<creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Hanna M.</givenNames>
<familyName>Ruottinen</familyName>
<degrees>MD, PhD</degrees>
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<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>
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<creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Pirkko</givenNames>
<familyName>Sonninen</familyName>
<degrees>MD</degrees>
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<creator xml:id="au7" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Juha O.</givenNames>
<familyName>Rinne</familyName>
<degrees>MD, PhD</degrees>
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<contactDetails><email>juha.rinne@pet.tyks.fi</email>
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<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>
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<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>
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<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>
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<subject><genre>article category</genre>
<topic>Article</topic>
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<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>
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<identifier type="DOI">10.1002/mds.1139</identifier>
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<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2001 Movement Disorder Society</accessCondition>
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