Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the off and on conditions with [(18)F]FDG-PET.
Identifieur interne : 003C43 ( PubMed/Curation ); précédent : 003C42; suivant : 003C44Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the off and on conditions with [(18)F]FDG-PET.
Auteurs : G. Berding [Allemagne] ; P. Odin ; D J Brooks ; G. Nikkhah ; C. Matthies ; T. Peschel ; M. Shing ; H. Kolbe ; J. Van Den Hoff ; H. Fricke ; R. Dengler ; M. Samii ; W H KnappSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2001.
English descriptors
- KwdEn :
- Adult, Antiparkinson Agents (adverse effects), Case-Control Studies, Cerebral Cortex (drug effects), Cerebral Cortex (metabolism), Cerebral Cortex (radionuclide imaging), Diagnosis, Differential, Female, Fluorodeoxyglucose F18 (diagnostic use), Glucose (metabolism), Humans, Levodopa (adverse effects), Male, Middle Aged, Parkinson Disease (metabolism), Parkinson Disease (radionuclide imaging), Predictive Value of Tests, Radiopharmaceuticals (diagnostic use), Severity of Illness Index, Tomography, Emission-Computed (methods).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , diagnostic use : Fluorodeoxyglucose F18, Radiopharmaceuticals.
- drug effects : Cerebral Cortex.
- metabolism : Cerebral Cortex, Glucose, Parkinson Disease.
- methods : Tomography, Emission-Computed.
- radionuclide imaging : Cerebral Cortex, Parkinson Disease.
- Adult, Case-Control Studies, Diagnosis, Differential, Female, Humans, Male, Middle Aged, Predictive Value of Tests, Severity of Illness Index.
Abstract
Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [(18)F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [(18)F] activity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [(18)F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment.
PubMed: 11748732
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Nikkhah</name></author><author><name sortKey="Matthies, C" sort="Matthies, C" uniqKey="Matthies C" first="C" last="Matthies">C. Matthies</name></author><author><name sortKey="Peschel, T" sort="Peschel, T" uniqKey="Peschel T" first="T" last="Peschel">T. Peschel</name></author><author><name sortKey="Shing, M" sort="Shing, M" uniqKey="Shing M" first="M" last="Shing">M. Shing</name></author><author><name sortKey="Kolbe, H" sort="Kolbe, H" uniqKey="Kolbe H" first="H" last="Kolbe">H. Kolbe</name></author><author><name sortKey="Van Den Hoff, J" sort="Van Den Hoff, J" uniqKey="Van Den Hoff J" first="J" last="Van Den Hoff">J. Van Den Hoff</name></author><author><name sortKey="Fricke, H" sort="Fricke, H" uniqKey="Fricke H" first="H" last="Fricke">H. Fricke</name></author><author><name sortKey="Dengler, R" sort="Dengler, R" uniqKey="Dengler R" first="R" last="Dengler">R. Dengler</name></author><author><name sortKey="Samii, M" sort="Samii, M" uniqKey="Samii M" first="M" last="Samii">M. 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Berding</name><affiliation wicri:level="1"><nlm:affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany. berding.georg@mh-hannover.de</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Nuclear Medicine, University Medical School, Hannover</wicri:regionArea></affiliation></author><author><name sortKey="Odin, P" sort="Odin, P" uniqKey="Odin P" first="P" last="Odin">P. Odin</name></author><author><name sortKey="Brooks, D J" sort="Brooks, D J" uniqKey="Brooks D" first="D J" last="Brooks">D J Brooks</name></author><author><name sortKey="Nikkhah, G" sort="Nikkhah, G" uniqKey="Nikkhah G" first="G" last="Nikkhah">G. Nikkhah</name></author><author><name sortKey="Matthies, C" sort="Matthies, C" uniqKey="Matthies C" first="C" last="Matthies">C. Matthies</name></author><author><name sortKey="Peschel, T" sort="Peschel, T" uniqKey="Peschel T" first="T" last="Peschel">T. Peschel</name></author><author><name sortKey="Shing, M" sort="Shing, M" uniqKey="Shing M" first="M" last="Shing">M. Shing</name></author><author><name sortKey="Kolbe, H" sort="Kolbe, H" uniqKey="Kolbe H" first="H" last="Kolbe">H. Kolbe</name></author><author><name sortKey="Van Den Hoff, J" sort="Van Den Hoff, J" uniqKey="Van Den Hoff J" first="J" last="Van Den Hoff">J. Van Den Hoff</name></author><author><name sortKey="Fricke, H" sort="Fricke, H" uniqKey="Fricke H" first="H" last="Fricke">H. Fricke</name></author><author><name sortKey="Dengler, R" sort="Dengler, R" uniqKey="Dengler R" first="R" last="Dengler">R. Dengler</name></author><author><name sortKey="Samii, M" sort="Samii, M" uniqKey="Samii M" first="M" last="Samii">M. Samii</name></author><author><name sortKey="Knapp, W H" sort="Knapp, W H" uniqKey="Knapp W" first="W H" last="Knapp">W H Knapp</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Antiparkinson Agents (adverse effects)</term><term>Case-Control Studies</term><term>Cerebral Cortex (drug effects)</term><term>Cerebral Cortex (metabolism)</term><term>Cerebral Cortex (radionuclide imaging)</term><term>Diagnosis, Differential</term><term>Female</term><term>Fluorodeoxyglucose F18 (diagnostic use)</term><term>Glucose (metabolism)</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Predictive Value of Tests</term><term>Radiopharmaceuticals (diagnostic use)</term><term>Severity of Illness Index</term><term>Tomography, Emission-Computed (methods)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Fluorodeoxyglucose F18</term><term>Radiopharmaceuticals</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cerebral Cortex</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cerebral Cortex</term><term>Glucose</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Tomography, Emission-Computed</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Cerebral Cortex</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Case-Control Studies</term><term>Diagnosis, Differential</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Predictive Value of Tests</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [(18)F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [(18)F] activity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [(18)F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">11748732</PMID><DateCreated><Year>2001</Year><Month>12</Month><Day>18</Day></DateCreated><DateCompleted><Year>2002</Year><Month>01</Month><Day>25</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>16</Volume><Issue>6</Issue><PubDate><Year>2001</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Resting regional cerebral glucose metabolism in advanced Parkinson's disease studied in the off and on conditions with [(18)F]FDG-PET.</ArticleTitle><Pagination><MedlinePgn>1014-22</MedlinePgn></Pagination><Abstract><AbstractText>Studies of resting regional cerebral glucose consumption (rCMRGlc) in nondemented patients with Parkinson's disease (PD) have produced conflicting results, reporting both reduced and normal metabolism in advanced disease and reduced or normal metabolism after dopaminergic therapy. To investigate these issues, [(18)F]fluorodeoxyglucose (FDG) positron emission tomography (PET) was performed in 11 nondemented PD patients with advanced disease and 10 age-matched controls. PD patients were studied after withdrawal of all dopaminergic medication to produce a practically defined off condition, and a second time 1 hour after levodopa, resulting in a clinical on state. Dynamic PET scans and simultaneous arterialised venous blood samples of [(18)F] activity were obtained. A graphical approach was used to generate parametric images of rCMRGlc and statistical parametric mapping to localise significant metabolic changes in PD. Compared with controls, global rCMRGlc was reduced in the on but not in the off condition in PD. In both states, significant regional reductions of glucose uptake were found in the parietal, frontal, temporal cortex, and caudate nucleus. Reductions correlated with the severity of disability in frontal and temporal cortex. Direct comparison between on and off conditions revealed relatively greater reductions of uptake in the ventral/orbital frontal cortex and the thalamus during on. Results suggest that cortical and caudate hypometabolism are common in advanced PD and that caution is mandatory if [(18)F]FDG PET is being used to differentiate advanced PD from dementia and progressive supranuclear palsy where similar reductions are seen. Furthermore, in PD, administration of levodopa is associated with further hypometabolism in orbitofrontal cortex; an area known to be relevant for reversal learning where performance is typically impaired after dopaminergic treatment.</AbstractText><CopyrightInformation>Copyright 2001 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Berding</LastName><ForeName>G</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Nuclear Medicine, University Medical School, Hannover, Germany. berding.georg@mh-hannover.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Odin</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Brooks</LastName><ForeName>D J</ForeName><Initials>DJ</Initials></Author><Author ValidYN="Y"><LastName>Nikkhah</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Matthies</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Peschel</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Shing</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Kolbe</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>van Den Hoff</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Fricke</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Dengler</LastName><ForeName>R</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Samii</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Knapp</LastName><ForeName>W H</ForeName><Initials>WH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019275">Radiopharmaceuticals</NameOfSubstance></Chemical><Chemical><RegistryNumber>0Z5B2CJX4D</RegistryNumber><NameOfSubstance UI="D019788">Fluorodeoxyglucose F18</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016022">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002540">Cerebral Cortex</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003937">Diagnosis, Differential</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019788">Fluorodeoxyglucose F18</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000176">diagnostic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005947">Glucose</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000531">radionuclide imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011237">Predictive Value of Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019275">Radiopharmaceuticals</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000176">diagnostic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012720">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D014055">Tomography, Emission-Computed</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2001</Year><Month>12</Month><Day>19</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>1</Month><Day>26</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2001</Year><Month>12</Month><Day>19</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11748732</ArticleId><ArticleId IdType="pii">10.1002/mds.1212</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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