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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<front><div type="abstract" xml: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</div>
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F]FDG‐PET<link href="#fn6"></link>
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<title type="short" xml:lang="en">Cortical Hypometabolism in Parkinson's Disease</title>
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<creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" noteRef="#fn7"><personName><givenNames>Inga</givenNames>
<familyName>Liepelt</familyName>
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<creator xml:id="au2" creatorRole="author" affiliationRef="#af2" corresponding="yes" noteRef="#fn7"><personName><givenNames>Matthias</givenNames>
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<contactDetails><email normalForm="matthias.reimold@uni-tuebingen.de">matthias.reimold@uni‐tuebingen.de</email>
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<creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Walter</givenNames>
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<creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jana</givenNames>
<familyName>Godau</familyName>
<degrees>MD</degrees>
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<creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Gerald</givenNames>
<familyName>Reischl</familyName>
<degrees>PhD</degrees>
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<creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Alexandra</givenNames>
<familyName>Gaenslen</familyName>
<degrees>MD</degrees>
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<creator xml:id="au7" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Heinz</givenNames>
<familyName>Herbst</familyName>
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<creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Daniela</givenNames>
<familyName>Berg</familyName>
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<affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Nuclear Medicine and PET Center, University of Tuebingen, Tuebingen, Germany</unparsedAffiliation>
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<affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Department of Radiopharmacy, PET Center, University of Tuebingen, Tuebingen, Germany</unparsedAffiliation>
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<affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Neurology Practice, Stuttgart, Germany</unparsedAffiliation>
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<keyword xml:id="kwd3">dementia</keyword>
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<fundingInfo><fundingAgency>University of Tuebingen</fundingAgency>
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<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>
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<noteGroup><note xml:id="fn6"><p>Potential conflict of interest: None reported.</p>
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<note xml:id="fn7"><p>Inga Liepelt and Matthias Reimold contributed equally to this work.</p>
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<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>
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<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
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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>2009</date>
<detail type="volume"><caption>vol.</caption>
<number>24</number>
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<detail type="issue"><caption>no.</caption>
<number>10</number>
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