Striatal dopa and glucose metabolism in PD patients with freezing of gait
Identifieur interne : 001A48 ( Main/Corpus ); précédent : 001A47; suivant : 001A49Striatal dopa and glucose metabolism in PD patients with freezing of gait
Auteurs : Anna L. Bartels ; Bauke M. De Jong ; Nir Giladi ; Joanna D. Schaafsma ; R. Paul Maguire ; Lammy Veenma ; Jan Pruim ; Yacov Balash ; Moussa B. H. Youdim ; Klaus L. LeendersSource :
- Movement Disorders [ 0885-3185 ] ; 2006-09.
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- KwdEn :
Abstract
In Parkinson's disease (PD), freezing suggests sudden and transient blocks of motor behavior during initiating or continuous repetitive movements. Its underlying pathophysiology remains unclear. The objective of this study is to compare striatal dopamine metabolism and cerebral glucose metabolism between PD patients with and without freezing of gait (FOG). A total of 10 PD patients with FOG at off and 7 PD patients without FOG underwent brain positron emission tomography with 18[F]‐6‐fluoro‐levodopa (FDOPA) and 18[F]‐fluordesoxyglucose (FDG). Striatum decarboxylase activity was expressed by metabolic influx constants of the striatum related to the occipital lobe (Kocc). FDG uptake in caudate and putamen was normalized to global FDG uptake. Region of interest (ROI) analysis of striatal regions was used, as well as voxel‐based analysis by statistical parametric mapping (SPM). ROI analysis did not reveal differences in striatal FDOPA and FDG uptake between the groups. SPM showed lower putaminal FDOPA uptake (P = 0.05 uncorrected) with increased FDG uptake (P = 0.01 uncorrected) in freezing PD, whereas caudate uptake of the two tracers was reduced. Freezing‐related cortical FDG decrease was found in (right) parietal regions. In conclusion, in freezing PD, caudate uptake of FDG and FDOPA was reduced, whereas putamen FDOPA decrease was associated with FDG increase. Right hemisphere circuitry seemed to be more affected in freezing patients. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.20952
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Bartels</name><affiliation><mods:affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="De Jong, Bauke M" sort="De Jong, Bauke M" uniqKey="De Jong B" first="Bauke M." last="De Jong">Bauke M. De Jong</name><affiliation><mods:affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Giladi, Nir" sort="Giladi, Nir" uniqKey="Giladi N" first="Nir" last="Giladi">Nir Giladi</name><affiliation><mods:affiliation>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</mods:affiliation></affiliation></author><author><name sortKey="Schaafsma, Joanna D" sort="Schaafsma, Joanna D" uniqKey="Schaafsma J" first="Joanna D." last="Schaafsma">Joanna D. 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Paul Maguire</name><affiliation><mods:affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Veenma, Lammy" sort="Veenma, Lammy" uniqKey="Veenma L" first="Lammy" last="Veenma">Lammy Veenma</name><affiliation><mods:affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Pruim, Jan" sort="Pruim, Jan" uniqKey="Pruim J" first="Jan" last="Pruim">Jan Pruim</name><affiliation><mods:affiliation>PET Centre of the University Medical Center Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Balash, Yacov" sort="Balash, Yacov" uniqKey="Balash Y" first="Yacov" last="Balash">Yacov Balash</name><affiliation><mods:affiliation>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</mods:affiliation></affiliation></author><author><name sortKey="Youdim, Moussa B H" sort="Youdim, Moussa B H" uniqKey="Youdim M" first="Moussa B. H." last="Youdim">Moussa B. H. Youdim</name><affiliation><mods:affiliation>Eve Topf and National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases, Technion‐Faculty of Medicine, Haifa, Israel</mods:affiliation></affiliation></author><author><name sortKey="Leenders, Klaus L" sort="Leenders, Klaus L" uniqKey="Leenders K" first="Klaus L." last="Leenders">Klaus L. Leenders</name><affiliation><mods:affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</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>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-09">2006-09</date><biblScope unit="volume">21</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1326">1326</biblScope><biblScope unit="page" to="1332">1332</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">32F8B40120EC5ECF1D85785766A13C12F5B7BD60</idno><idno type="DOI">10.1002/mds.20952</idno><idno type="ArticleID">MDS20952</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>freezing of gait</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In Parkinson's disease (PD), freezing suggests sudden and transient blocks of motor behavior during initiating or continuous repetitive movements. 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SPM showed lower putaminal FDOPA uptake (P = 0.05 uncorrected) with increased FDG uptake (P = 0.01 uncorrected) in freezing PD, whereas caudate uptake of the two tracers was reduced. Freezing‐related cortical FDG decrease was found in (right) parietal regions. In conclusion, in freezing PD, caudate uptake of FDG and FDOPA was reduced, whereas putamen FDOPA decrease was associated with FDG increase. Right hemisphere circuitry seemed to be more affected in freezing patients. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Anna L. Bartels MD</name><affiliations><json:string>Neurology Department of the University Medical Center Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>Bauke M. de Jong MD, PhD</name><affiliations><json:string>Neurology Department of the University Medical Center Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>Nir Giladi MD</name><affiliations><json:string>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</json:string></affiliations></json:item><json:item><name>Joanna D. Schaafsma MD</name><affiliations><json:string>Neurology Department of the University Medical Center Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>R. Paul Maguire PhD</name><affiliations><json:string>Neurology Department of the University Medical Center Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>Lammy Veenma</name><affiliations><json:string>Neurology Department of the University Medical Center Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>Jan Pruim MD</name><affiliations><json:string>PET Centre of the University Medical Center Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>Yacov Balash MD</name><affiliations><json:string>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</json:string></affiliations></json:item><json:item><name>Moussa B.H. Youdim MD</name><affiliations><json:string>Eve Topf and National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases, Technion‐Faculty of Medicine, Haifa, Israel</json:string></affiliations></json:item><json:item><name>Klaus L. Leenders MD, PhD</name><affiliations><json:string>Neurology Department of the University Medical Center Groningen, The Netherlands</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>PET</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>freezing of gait</value></json:item></subject><articleId><json:string>MDS20952</json:string></articleId><language><json:string>eng</json:string></language><abstract>In Parkinson's disease (PD), freezing suggests sudden and transient blocks of motor behavior during initiating or continuous repetitive movements. Its underlying pathophysiology remains unclear. The objective of this study is to compare striatal dopamine metabolism and cerebral glucose metabolism between PD patients with and without freezing of gait (FOG). A total of 10 PD patients with FOG at off and 7 PD patients without FOG underwent brain positron emission tomography with 18[F]‐6‐fluoro‐levodopa (FDOPA) and 18[F]‐fluordesoxyglucose (FDG). Striatum decarboxylase activity was expressed by metabolic influx constants of the striatum related to the occipital lobe (Kocc). FDG uptake in caudate and putamen was normalized to global FDG uptake. Region of interest (ROI) analysis of striatal regions was used, as well as voxel‐based analysis by statistical parametric mapping (SPM). ROI analysis did not reveal differences in striatal FDOPA and FDG uptake between the groups. SPM showed lower putaminal FDOPA uptake (P = 0.05 uncorrected) with increased FDG uptake (P = 0.01 uncorrected) in freezing PD, whereas caudate uptake of the two tracers was reduced. Freezing‐related cortical FDG decrease was found in (right) parietal regions. In conclusion, in freezing PD, caudate uptake of FDG and FDOPA was reduced, whereas putamen FDOPA decrease was associated with FDG increase. Right hemisphere circuitry seemed to be more affected in freezing patients. © 2006 Movement Disorder Society</abstract><qualityIndicators><score>6.894</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>3</keywordCount><abstractCharCount>1490</abstractCharCount><pdfWordCount>4266</pdfWordCount><pdfCharCount>27049</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>219</abstractWordCount></qualityIndicators><title>Striatal dopa and glucose metabolism in PD patients with freezing of gait</title><genre><json:string>article</json:string></genre><host><volume>21</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>7</total><last>1332</last><first>1326</first></pages><issn><json:string>0885-3185</json:string></issn><issue>9</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1002/mds.20952</json:string></doi><id>32F8B40120EC5ECF1D85785766A13C12F5B7BD60</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/32F8B40120EC5ECF1D85785766A13C12F5B7BD60/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/32F8B40120EC5ECF1D85785766A13C12F5B7BD60/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/32F8B40120EC5ECF1D85785766A13C12F5B7BD60/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Striatal dopa and glucose metabolism in PD patients with freezing of gait</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2006</date></publicationStmt><notesStmt><note>Eve Topf at Technion, (Haifa, Israel)</note><note>National Parkinson Foundation (Miami, FL) Centers</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Striatal dopa and glucose metabolism in PD patients with freezing of gait</title><author><persName><forename type="first">Anna L.</forename><surname>Bartels</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: University of Groningen, University Medical Center Groningen (UMCG), Department of Neurology, POB 30001, 9700 RB Groningen, The Netherlands</p></note><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation></author><author><persName><forename type="first">Bauke M.</forename><surname>de Jong</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation></author><author><persName><forename type="first">Nir</forename><surname>Giladi</surname></persName><roleName type="degree">MD</roleName><affiliation>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</affiliation></author><author><persName><forename type="first">Joanna D.</forename><surname>Schaafsma</surname></persName><roleName type="degree">MD</roleName><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation></author><author><persName><forename type="first">R. Paul</forename><surname>Maguire</surname></persName><roleName type="degree">PhD</roleName><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation></author><author><persName><forename type="first">Lammy</forename><surname>Veenma</surname></persName><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation></author><author><persName><forename type="first">Jan</forename><surname>Pruim</surname></persName><roleName type="degree">MD</roleName><affiliation>PET Centre of the University Medical Center Groningen, The Netherlands</affiliation></author><author><persName><forename type="first">Yacov</forename><surname>Balash</surname></persName><roleName type="degree">MD</roleName><affiliation>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</affiliation></author><author><persName><forename type="first">Moussa B.H.</forename><surname>Youdim</surname></persName><roleName type="degree">MD</roleName><affiliation>Eve Topf and National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases, Technion‐Faculty of Medicine, Haifa, Israel</affiliation></author><author><persName><forename type="first">Klaus L.</forename><surname>Leenders</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</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>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-09"></date><biblScope unit="volume">21</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1326">1326</biblScope><biblScope unit="page" to="1332">1332</biblScope></imprint></monogr><idno type="istex">32F8B40120EC5ECF1D85785766A13C12F5B7BD60</idno><idno type="DOI">10.1002/mds.20952</idno><idno type="ArticleID">MDS20952</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In Parkinson's disease (PD), freezing suggests sudden and transient blocks of motor behavior during initiating or continuous repetitive movements. Its underlying pathophysiology remains unclear. The objective of this study is to compare striatal dopamine metabolism and cerebral glucose metabolism between PD patients with and without freezing of gait (FOG). A total of 10 PD patients with FOG at off and 7 PD patients without FOG underwent brain positron emission tomography with 18[F]‐6‐fluoro‐levodopa (FDOPA) and 18[F]‐fluordesoxyglucose (FDG). Striatum decarboxylase activity was expressed by metabolic influx constants of the striatum related to the occipital lobe (Kocc). FDG uptake in caudate and putamen was normalized to global FDG uptake. Region of interest (ROI) analysis of striatal regions was used, as well as voxel‐based analysis by statistical parametric mapping (SPM). ROI analysis did not reveal differences in striatal FDOPA and FDG uptake between the groups. SPM showed lower putaminal FDOPA uptake (P = 0.05 uncorrected) with increased FDG uptake (P = 0.01 uncorrected) in freezing PD, whereas caudate uptake of the two tracers was reduced. Freezing‐related cortical FDG decrease was found in (right) parietal regions. In conclusion, in freezing PD, caudate uptake of FDG and FDOPA was reduced, whereas putamen FDOPA decrease was associated with FDG increase. Right hemisphere circuitry seemed to be more affected in freezing patients. © 2006 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>PET</term></item><item><term>Parkinson's disease</term></item><item><term>freezing of gait</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-04-01">Received</change><change when="2006-01-15">Registration</change><change when="2006-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/32F8B40120EC5ECF1D85785766A13C12F5B7BD60/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>Hoboken</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="90"><doi origin="wiley" registered="yes">10.1002/mds.v21:9</doi><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue">9</numbering></numberingGroup><coverDate startDate="2006-09">September 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="40" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.20952</doi><idGroup><id type="unit" value="MDS20952"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2006 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2005-04-01"></event><event type="manuscriptRevised" date="2006-01-03"></event><event type="manuscriptAccepted" date="2006-01-15"></event><event type="publishedOnlineEarlyUnpaginated" date="2006-05-23"></event><event type="firstOnline" date="2006-05-23"></event><event type="publishedOnlineFinalForm" date="2006-09-20"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-04-21"></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">1326</numbering><numbering type="pageLast">1332</numbering></numberingGroup><correspondenceTo>University of Groningen, University Medical Center Groningen (UMCG), Department of Neurology, POB 30001, 9700 RB Groningen, The Netherlands</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS20952.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="5"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="39"></count><count type="wordTotal" number="4719"></count></countGroup><titleGroup><title type="main" xml:lang="en">Striatal dopa and glucose metabolism in PD patients with freezing of gait</title><title type="short" xml:lang="en">Dopa and Glucose Metabolism in Patients with Fog</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Anna L.</givenNames><familyName>Bartels</familyName><degrees>MD</degrees></personName><contactDetails><email>a.l.bartels@neuro.umcg.nl</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Bauke M.</givenNames><familyName>de Jong</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Nir</givenNames><familyName>Giladi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Joanna D.</givenNames><familyName>Schaafsma</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>R. Paul</givenNames><familyName>Maguire</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Lammy</givenNames><familyName>Veenma</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Jan</givenNames><familyName>Pruim</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Yacov</givenNames><familyName>Balash</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Moussa B.H.</givenNames><familyName>Youdim</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Klaus L.</givenNames><familyName>Leenders</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="NL" type="organization"><unparsedAffiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IL" type="organization"><unparsedAffiliation>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="NL" type="organization"><unparsedAffiliation>PET Centre of the University Medical Center Groningen, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="IL" type="organization"><unparsedAffiliation>Eve Topf and National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases, Technion‐Faculty of Medicine, Haifa, Israel</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">PET</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">freezing of gait</keyword></keywordGroup><fundingInfo><fundingAgency>Eve Topf at Technion, (Haifa, Israel)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Parkinson Foundation (Miami, FL) Centers</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In Parkinson's disease (PD), freezing suggests sudden and transient blocks of motor behavior during initiating or continuous repetitive movements. Its underlying pathophysiology remains unclear. The objective of this study is to compare striatal dopamine metabolism and cerebral glucose metabolism between PD patients with and without freezing of gait (FOG). A total of 10 PD patients with FOG at <i>off</i> and 7 PD patients without FOG underwent brain positron emission tomography with <sup>18</sup>[F]‐6‐fluoro‐levodopa (FDOPA) and <sup>18</sup>[F]‐fluordesoxyglucose (FDG). Striatum decarboxylase activity was expressed by metabolic influx constants of the striatum related to the occipital lobe (Kocc). FDG uptake in caudate and putamen was normalized to global FDG uptake. Region of interest (ROI) analysis of striatal regions was used, as well as voxel‐based analysis by statistical parametric mapping (SPM). ROI analysis did not reveal differences in striatal FDOPA and FDG uptake between the groups. SPM showed lower putaminal FDOPA uptake (<i>P</i> = 0.05 uncorrected) with increased FDG uptake (<i>P</i> = 0.01 uncorrected) in freezing PD, whereas caudate uptake of the two tracers was reduced. Freezing‐related cortical FDG decrease was found in (right) parietal regions. In conclusion, in freezing PD, caudate uptake of FDG and FDOPA was reduced, whereas putamen FDOPA decrease was associated with FDG increase. Right hemisphere circuitry seemed to be more affected in freezing patients. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Striatal dopa and glucose metabolism in PD patients with freezing of gait</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dopa and Glucose Metabolism in Patients with Fog</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Striatal dopa and glucose metabolism in PD patients with freezing of gait</title></titleInfo><name type="personal"><namePart type="given">Anna L.</namePart><namePart type="family">Bartels</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation><description>Correspondence: University of Groningen, University Medical Center Groningen (UMCG), Department of Neurology, POB 30001, 9700 RB Groningen, The Netherlands</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bauke M.</namePart><namePart type="family">de Jong</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nir</namePart><namePart type="family">Giladi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joanna D.</namePart><namePart type="family">Schaafsma</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. Paul</namePart><namePart type="family">Maguire</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lammy</namePart><namePart type="family">Veenma</namePart><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan</namePart><namePart type="family">Pruim</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>PET Centre of the University Medical Center Groningen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yacov</namePart><namePart type="family">Balash</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Department of the Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Moussa B.H.</namePart><namePart type="family">Youdim</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Eve Topf and National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases, Technion‐Faculty of Medicine, Haifa, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Klaus L.</namePart><namePart type="family">Leenders</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Neurology Department of the University Medical Center Groningen, The Netherlands</affiliation><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">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2006-09</dateIssued><dateCaptured encoding="w3cdtf">2005-04-01</dateCaptured><dateValid encoding="w3cdtf">2006-01-15</dateValid><copyrightDate encoding="w3cdtf">2006</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">5</extent><extent unit="tables">1</extent><extent unit="references">39</extent><extent unit="words">4719</extent></physicalDescription><abstract lang="en">In Parkinson's disease (PD), freezing suggests sudden and transient blocks of motor behavior during initiating or continuous repetitive movements. Its underlying pathophysiology remains unclear. The objective of this study is to compare striatal dopamine metabolism and cerebral glucose metabolism between PD patients with and without freezing of gait (FOG). A total of 10 PD patients with FOG at off and 7 PD patients without FOG underwent brain positron emission tomography with 18[F]‐6‐fluoro‐levodopa (FDOPA) and 18[F]‐fluordesoxyglucose (FDG). Striatum decarboxylase activity was expressed by metabolic influx constants of the striatum related to the occipital lobe (Kocc). FDG uptake in caudate and putamen was normalized to global FDG uptake. Region of interest (ROI) analysis of striatal regions was used, as well as voxel‐based analysis by statistical parametric mapping (SPM). ROI analysis did not reveal differences in striatal FDOPA and FDG uptake between the groups. SPM showed lower putaminal FDOPA uptake (P = 0.05 uncorrected) with increased FDG uptake (P = 0.01 uncorrected) in freezing PD, whereas caudate uptake of the two tracers was reduced. Freezing‐related cortical FDG decrease was found in (right) parietal regions. In conclusion, in freezing PD, caudate uptake of FDG and FDOPA was reduced, whereas putamen FDOPA decrease was associated with FDG increase. Right hemisphere circuitry seemed to be more affected in freezing patients. © 2006 Movement Disorder Society</abstract><note type="funding">Eve Topf at Technion, (Haifa, Israel)</note><note type="funding">National Parkinson Foundation (Miami, FL) Centers</note><subject lang="en"><genre>Keywords</genre><topic>PET</topic><topic>Parkinson's disease</topic><topic>freezing of gait</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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