Cortical hypometabolism assessed by a metabolic ratio in Parkinson's disease primarily reflects cognitive deterioration—[18F]FDG‐PET
Identifieur interne : 001565 ( Istex/Corpus ); précédent : 001564; suivant : 001566Cortical hypometabolism assessed by a metabolic ratio in Parkinson's disease primarily reflects cognitive deterioration—[18F]FDG‐PET
Auteurs : Inga Liepelt ; Matthias Reimold ; Walter Maetzler ; Jana Godau ; Gerald Reischl ; Alexandra Gaenslen ; Heinz Herbst ; Daniela BergSource :
- Movement Disorders [ 0885-3185 ] ; 2009-07-30.
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Abstract
In Parkinson's disease patients with cognitive deterioration, regional cortical hypometabolism has been observed with [18F]fluorodeoxyglucose‐positron emission tomography (FDG‐PET). Our aim was to develop a robust method to subsume the overall degree of metabolic deterioration in Parkinson's disease by means of a single index and to investigate which of the clinical features correlates best with hypometabolism. Twenty‐two Parkinson's patients (10 demented) and seven controls underwent FDG‐PET. A metabolic index (mean relative uptake in typically affected regions) was calculated for each patient and compared with scores for cognition [Minimental State Examination (MMSE)], motor performance [Unified Parkinson's Disease Rating Scale (UPDRS III)” and behavior (Neuropsychiatric Inventory). In stepwise linear regression analysis, MMSE (P < 0.001) score showed the only significant effect. Estimated sensitivity and specificity for DSM‐IV diagnosis of dementia were high for the metabolic index (MI), with 91 and 100%. Taken together, the presented data indicate that cerebral hypometabolism in Parkinson's disease is primarily associated with cognitive impairment. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22662
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Our aim was to develop a robust method to subsume the overall degree of metabolic deterioration in Parkinson's disease by means of a single index and to investigate which of the clinical features correlates best with hypometabolism. Twenty‐two Parkinson's patients (10 demented) and seven controls underwent FDG‐PET. A metabolic index (mean relative uptake in typically affected regions) was calculated for each patient and compared with scores for cognition [Minimental State Examination (MMSE)], motor performance [Unified Parkinson's Disease Rating Scale (UPDRS III)” and behavior (Neuropsychiatric Inventory). In stepwise linear regression analysis, MMSE (P < 0.001) score showed the only significant effect. Estimated sensitivity and specificity for DSM‐IV diagnosis of dementia were high for the metabolic index (MI), with 91 and 100%. Taken together, the presented data indicate that cerebral hypometabolism in Parkinson's disease is primarily associated with cognitive impairment. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Inga Liepelt PhD</name><affiliations><json:string>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</json:string></affiliations></json:item><json:item><name>Matthias Reimold MD</name><affiliations><json:string>Department of Nuclear Medicine and PET Center, University of Tuebingen, Tuebingen, Germany</json:string></affiliations></json:item><json:item><name>Walter Maetzler MD</name><affiliations><json:string>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</json:string></affiliations></json:item><json:item><name>Jana Godau MD</name><affiliations><json:string>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</json:string></affiliations></json:item><json:item><name>Gerald Reischl PhD</name><affiliations><json:string>Department of Radiopharmacy, PET Center, University of Tuebingen, Tuebingen, Germany</json:string></affiliations></json:item><json:item><name>Alexandra Gaenslen MD</name><affiliations><json:string>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</json:string></affiliations></json:item><json:item><name>Heinz Herbst MD</name><affiliations><json:string>Neurology Practice, Stuttgart, Germany</json:string></affiliations></json:item><json:item><name>Daniela Berg MD</name><affiliations><json:string>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</json:string></affiliations></json:item></author><subject><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>dementia</value></json:item></subject><language><json:string>eng</json:string></language><abstract>In Parkinson's disease patients with cognitive deterioration, regional cortical hypometabolism has been observed with [18F]fluorodeoxyglucose‐positron emission tomography (FDG‐PET). Our aim was to develop a robust method to subsume the overall degree of metabolic deterioration in Parkinson's disease by means of a single index and to investigate which of the clinical features correlates best with hypometabolism. Twenty‐two Parkinson's patients (10 demented) and seven controls underwent FDG‐PET. A metabolic index (mean relative uptake in typically affected regions) was calculated for each patient and compared with scores for cognition [Minimental State Examination (MMSE)], motor performance [Unified Parkinson's Disease Rating Scale (UPDRS III)” and behavior (Neuropsychiatric Inventory). In stepwise linear regression analysis, MMSE (P > 0.001) score showed the only significant effect. Estimated sensitivity and specificity for DSM‐IV diagnosis of dementia were high for the metabolic index (MI), with 91 and 100%. 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xml:lang="en">Cortical hypometabolism assessed by a metabolic ratio in Parkinson's disease primarily reflects cognitive deterioration—[18F]FDG‐PET</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2009</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None reported.</note><note>AKF program</note><note>University of Tuebingen</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Cortical hypometabolism assessed by a metabolic ratio in Parkinson's disease primarily reflects cognitive deterioration—[18F]FDG‐PET</title><author><persName><forename type="first">Inga</forename><surname>Liepelt</surname><roleName type="degree">PhD</roleName></persName><note type="biography">Inga Liepelt and Matthias Reimold contributed equally to this work.</note><affiliation>Inga Liepelt and Matthias Reimold contributed equally to this work.</affiliation><affiliation>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</affiliation></author><author><persName><forename type="first">Matthias</forename><surname>Reimold</surname><roleName type="degree">MD</roleName></persName><note type="biography">Inga Liepelt and Matthias Reimold contributed equally to this work.</note><affiliation>Inga Liepelt and Matthias Reimold contributed equally to this work.</affiliation><note type="correspondence"><p>Correspondence: Department of Nuclear Medicine and PET Center, Roentgenweg 15, 72076 Tuebingen, Germany</p></note><affiliation>Department of Nuclear Medicine and PET Center, University of Tuebingen, Tuebingen, Germany</affiliation></author><author><persName><forename 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Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Radiopharmacy, PET Center, University of Tuebingen, Tuebingen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Neurology Practice, Stuttgart, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">PET</keyword><keyword xml:id="kwd3">dementia</keyword></keywordGroup><fundingInfo><fundingAgency>AKF program</fundingAgency></fundingInfo><fundingInfo><fundingAgency>University of Tuebingen</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In Parkinson's disease patients with cognitive deterioration, regional cortical hypometabolism has been observed with [<sup>18</sup>F]fluorodeoxyglucose‐positron emission tomography (FDG‐PET). Our aim was to develop a robust method to subsume the overall degree of metabolic deterioration in Parkinson's disease by means of a single index and to investigate which of the clinical features correlates best with hypometabolism. Twenty‐two Parkinson's patients (10 demented) and seven controls underwent FDG‐PET. A metabolic index (mean relative uptake in typically affected regions) was calculated for each patient and compared with scores for cognition [Minimental State Examination (MMSE)], motor performance [Unified Parkinson's Disease Rating Scale (UPDRS III)” and behavior (Neuropsychiatric Inventory). In stepwise linear regression analysis, MMSE (<i>P</i> < 0.001) score showed the only significant effect. Estimated sensitivity and specificity for DSM‐IV diagnosis of dementia were high for the metabolic index (MI), with 91 and 100%. Taken together, the presented data indicate that cerebral hypometabolism in Parkinson's disease is primarily associated with cognitive impairment. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn6"><p>Potential conflict of interest: None reported.</p></note><note xml:id="fn7"><p>Inga Liepelt and Matthias Reimold contributed equally to this work.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Cortical hypometabolism assessed by a metabolic ratio in Parkinson's disease primarily reflects cognitive deterioration—[18F]FDG‐PET</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Cortical Hypometabolism in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cortical hypometabolism assessed by a metabolic ratio in Parkinson's disease primarily reflects cognitive deterioration—[</title></titleInfo><name type="personal"><namePart type="given">Inga</namePart><namePart type="family">Liepelt</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</affiliation><description>Inga Liepelt and Matthias Reimold contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matthias</namePart><namePart type="family">Reimold</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Nuclear Medicine and PET Center, University of Tuebingen, Tuebingen, Germany</affiliation><description>Inga Liepelt and Matthias Reimold contributed equally to this work.</description><description>Correspondence: Department of Nuclear Medicine and PET Center, Roentgenweg 15, 72076 Tuebingen, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Walter</namePart><namePart type="family">Maetzler</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jana</namePart><namePart type="family">Godau</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gerald</namePart><namePart type="family">Reischl</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Radiopharmacy, PET Center, University of Tuebingen, Tuebingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexandra</namePart><namePart type="family">Gaenslen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Heinz</namePart><namePart type="family">Herbst</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Practice, Stuttgart, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniela</namePart><namePart type="family">Berg</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Hertie Institute for Clinical Brain Research, Department of Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-07-30</dateIssued><dateCaptured encoding="w3cdtf">2008-12-20</dateCaptured><dateValid encoding="w3cdtf">2009-04-26</dateValid><copyrightDate encoding="w3cdtf">2009</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">2</extent><extent unit="references">41</extent><extent unit="words">5107</extent></physicalDescription><abstract lang="en">In Parkinson's disease patients with cognitive deterioration, regional cortical hypometabolism has been observed with [18F]fluorodeoxyglucose‐positron emission tomography (FDG‐PET). Our aim was to develop a robust method to subsume the overall degree of metabolic deterioration in Parkinson's disease by means of a single index and to investigate which of the clinical features correlates best with hypometabolism. Twenty‐two Parkinson's patients (10 demented) and seven controls underwent FDG‐PET. A metabolic index (mean relative uptake in typically affected regions) was calculated for each patient and compared with scores for cognition [Minimental State Examination (MMSE)], motor performance [Unified Parkinson's Disease Rating Scale (UPDRS III)” and behavior (Neuropsychiatric Inventory). In stepwise linear regression analysis, MMSE (P < 0.001) score showed the only significant effect. Estimated sensitivity and specificity for DSM‐IV diagnosis of dementia were high for the metabolic index (MI), with 91 and 100%. Taken together, the presented data indicate that cerebral hypometabolism in Parkinson's disease is primarily associated with cognitive impairment. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">AKF program</note><note type="funding">University of Tuebingen</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>PET</topic><topic>dementia</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>Research 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>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1504</start><end>1511</end><total>8</total></extent></part></relatedItem><identifier type="istex">A683FEF9E28DD0A4A4098C22D82C75E20B8607AB</identifier><identifier type="DOI">10.1002/mds.22662</identifier><identifier type="ArticleID">MDS22662</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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