Executive processes in Parkinson's disease: FDG‐PET and network analysis
Identifieur interne : 001251 ( Main/Corpus ); précédent : 001250; suivant : 001252Executive processes in Parkinson's disease: FDG‐PET and network analysis
Auteurs : Catherine Lozza ; Jean-Claude Baron ; David Eidelberg ; Marc J. Mentis ; Maren Carbon ; Rose-Marie MariéSource :
- Human Brain Mapping [ 1065-9471 ] ; 2004-07.
English descriptors
Abstract
It is assumed widely that the clinical expression of Parkinson's Disease (PD), both motor and cognitive, is subtended by topographically distributed brain networks. However, little is known about the functional neuroanatomy of executive dysfunction in PD. Our objective was to validate further in a PD group the use of network analysis to assess the relationship between executive processes and pathological disorganization of frontostriatal networks. We studied 15 patients with idiopathic PD, and 7 age‐matched normal controls, using resting [18F]fluorodeoxyglucose (FDG) and high‐resolution positron emission tomography (PET). We carried out network analysis on regional metabolic data to identify specific covariation patterns associated with motor and executive dysfunction. We detected two independent patterns relating respectively to the two clinical abnormalities. The first pattern (principal component 1) was topographically similar to that described previously in other PD populations. Subject scores for this pattern discriminated patients from controls and correlated significantly with bradykinesia ratings (P = 0.013, r = 0.655) in PD patients. The second pattern (principal component 2) was characterized by relative ventromedial frontal, hippocampal, and striatal hypometabolism, associated with mediodorsal thalamic hypermetabolism. In the PD group, scores from this pattern correlated with scores on the conditional associative learning (CAL; P = 0.01, r = 0.690) and the Brown Peterson paradigm (BPP; P = 0.017, r = −0.651) tests, respectively assessing strategy and planning, and working memory. According to these findings, the networks subserving bradykinesia and executive dysfunction in PD seems to be topographically distinct and to involve different aspects of subcortico‐cortical processing. Hum. Brain Mapping 22:236–245, 2004. © 2004 Wiley‐Liss, Inc.
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DOI: 10.1002/hbm.20033
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ISTEX:529CFAF614C17C047BD7C7BE5C7894535011589ALe document en format XML
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Brain Mapp.</title><idno type="ISSN">1065-9471</idno><idno type="eISSN">1097-0193</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-07">2004-07</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="236">236</biblScope><biblScope unit="page" to="245">245</biblScope></imprint><idno type="ISSN">1065-9471</idno></series><idno type="istex">529CFAF614C17C047BD7C7BE5C7894535011589A</idno><idno type="DOI">10.1002/hbm.20033</idno><idno type="ArticleID">HBM20033</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1065-9471</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>FDG‐PET</term><term>Parkinson's disease</term><term>executive functions</term><term>network analysis</term><term>working memory</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It is assumed widely that the clinical expression of Parkinson's Disease (PD), both motor and cognitive, is subtended by topographically distributed brain networks. However, little is known about the functional neuroanatomy of executive dysfunction in PD. Our objective was to validate further in a PD group the use of network analysis to assess the relationship between executive processes and pathological disorganization of frontostriatal networks. We studied 15 patients with idiopathic PD, and 7 age‐matched normal controls, using resting [18F]fluorodeoxyglucose (FDG) and high‐resolution positron emission tomography (PET). We carried out network analysis on regional metabolic data to identify specific covariation patterns associated with motor and executive dysfunction. We detected two independent patterns relating respectively to the two clinical abnormalities. The first pattern (principal component 1) was topographically similar to that described previously in other PD populations. Subject scores for this pattern discriminated patients from controls and correlated significantly with bradykinesia ratings (P = 0.013, r = 0.655) in PD patients. The second pattern (principal component 2) was characterized by relative ventromedial frontal, hippocampal, and striatal hypometabolism, associated with mediodorsal thalamic hypermetabolism. In the PD group, scores from this pattern correlated with scores on the conditional associative learning (CAL; P = 0.01, r = 0.690) and the Brown Peterson paradigm (BPP; P = 0.017, r = −0.651) tests, respectively assessing strategy and planning, and working memory. According to these findings, the networks subserving bradykinesia and executive dysfunction in PD seems to be topographically distinct and to involve different aspects of subcortico‐cortical processing. Hum. Brain Mapping 22:236–245, 2004. © 2004 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Catherine Lozza</name><affiliations><json:string>INSERM U 320, Centre Cyceron, Caen, France</json:string><json:string>Equipe Universitaire‐Université de Basse Normandie, Caen, France</json:string></affiliations></json:item><json:item><name>Jean‐Claude Baron</name><affiliations><json:string>INSERM U 320, Centre Cyceron, Caen, France</json:string><json:string>Department of Neurology, University of Cambridge, Cambridge, United Kingdom</json:string></affiliations></json:item><json:item><name>David Eidelberg</name><affiliations><json:string>Center for Neurosciences, North Shore‐Long Island Jewish Research Institute, Manhasset, New York</json:string></affiliations></json:item><json:item><name>Marc J. 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However, little is known about the functional neuroanatomy of executive dysfunction in PD. Our objective was to validate further in a PD group the use of network analysis to assess the relationship between executive processes and pathological disorganization of frontostriatal networks. We studied 15 patients with idiopathic PD, and 7 age‐matched normal controls, using resting [18F]fluorodeoxyglucose (FDG) and high‐resolution positron emission tomography (PET). We carried out network analysis on regional metabolic data to identify specific covariation patterns associated with motor and executive dysfunction. We detected two independent patterns relating respectively to the two clinical abnormalities. The first pattern (principal component 1) was topographically similar to that described previously in other PD populations. Subject scores for this pattern discriminated patients from controls and correlated significantly with bradykinesia ratings (P = 0.013, r = 0.655) in PD patients. The second pattern (principal component 2) was characterized by relative ventromedial frontal, hippocampal, and striatal hypometabolism, associated with mediodorsal thalamic hypermetabolism. In the PD group, scores from this pattern correlated with scores on the conditional associative learning (CAL; P = 0.01, r = 0.690) and the Brown Peterson paradigm (BPP; P = 0.017, r = −0.651) tests, respectively assessing strategy and planning, and working memory. According to these findings, the networks subserving bradykinesia and executive dysfunction in PD seems to be topographically distinct and to involve different aspects of subcortico‐cortical processing. Hum. 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However, little is known about the functional neuroanatomy of executive dysfunction in PD. Our objective was to validate further in a PD group the use of network analysis to assess the relationship between executive processes and pathological disorganization of frontostriatal networks. We studied 15 patients with idiopathic PD, and 7 age‐matched normal controls, using resting [18F]fluorodeoxyglucose (FDG) and high‐resolution positron emission tomography (PET). We carried out network analysis on regional metabolic data to identify specific covariation patterns associated with motor and executive dysfunction. We detected two independent patterns relating respectively to the two clinical abnormalities. The first pattern (principal component 1) was topographically similar to that described previously in other PD populations. Subject scores for this pattern discriminated patients from controls and correlated significantly with bradykinesia ratings (P = 0.013, r = 0.655) in PD patients. The second pattern (principal component 2) was characterized by relative ventromedial frontal, hippocampal, and striatal hypometabolism, associated with mediodorsal thalamic hypermetabolism. In the PD group, scores from this pattern correlated with scores on the conditional associative learning (CAL; P = 0.01, r = 0.690) and the Brown Peterson paradigm (BPP; P = 0.017, r = −0.651) tests, respectively assessing strategy and planning, and working memory. According to these findings, the networks subserving bradykinesia and executive dysfunction in PD seems to be topographically distinct and to involve different aspects of subcortico‐cortical processing. Hum. 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However, little is known about the functional neuroanatomy of executive dysfunction in PD. Our objective was to validate further in a PD group the use of network analysis to assess the relationship between executive processes and pathological disorganization of frontostriatal networks. We studied 15 patients with idiopathic PD, and 7 age‐matched normal controls, using resting [<sup>18</sup>F]fluorodeoxyglucose (FDG) and high‐resolution positron emission tomography (PET). We carried out network analysis on regional metabolic data to identify specific covariation patterns associated with motor and executive dysfunction. We detected two independent patterns relating respectively to the two clinical abnormalities. The first pattern (principal component 1) was topographically similar to that described previously in other PD populations. Subject scores for this pattern discriminated patients from controls and correlated significantly with bradykinesia ratings (<i>P</i> = 0.013, <i>r</i> = 0.655) in PD patients. The second pattern (principal component 2) was characterized by relative ventromedial frontal, hippocampal, and striatal hypometabolism, associated with mediodorsal thalamic hypermetabolism. In the PD group, scores from this pattern correlated with scores on the conditional associative learning (CAL; <i>P</i> = 0.01, <i>r</i> = 0.690) and the Brown Peterson paradigm (BPP; <i>P</i> = 0.017, <i>r</i> = −0.651) tests, respectively assessing strategy and planning, and working memory. According to these findings, the networks subserving bradykinesia and executive dysfunction in PD seems to be topographically distinct and to involve different aspects of subcortico‐cortical processing. Hum. Brain Mapping 22:236–245, 2004. © 2004 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Executive processes in Parkinson's disease: FDG‐PET and network analysis</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Executive Processes in PD: Network Analysis</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Executive processes in Parkinson's disease: FDG‐PET and network analysis</title></titleInfo><name type="personal"><namePart type="given">Catherine</namePart><namePart type="family">Lozza</namePart><affiliation>INSERM U 320, Centre Cyceron, Caen, France</affiliation><affiliation>Equipe Universitaire‐Université de Basse Normandie, Caen, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Claude</namePart><namePart type="family">Baron</namePart><affiliation>INSERM U 320, Centre Cyceron, Caen, France</affiliation><affiliation>Department of Neurology, University of Cambridge, Cambridge, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Eidelberg</namePart><affiliation>Center for Neurosciences, North Shore‐Long Island Jewish Research Institute, Manhasset, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marc J.</namePart><namePart type="family">Mentis</namePart><affiliation>Center for Neurosciences, North Shore‐Long Island Jewish Research Institute, Manhasset, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maren</namePart><namePart type="family">Carbon</namePart><affiliation>Center for Neurosciences, North Shore‐Long Island Jewish Research Institute, Manhasset, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rose‐Marie</namePart><namePart type="family">Marié</namePart><affiliation>INSERM U 320, Centre Cyceron, Caen, France</affiliation><affiliation>Equipe Universitaire‐Université de Basse Normandie, Caen, France</affiliation><description>Correspondence: Service de Neurologie Déjérine, CHU Côte de Nacre, 14000 Caen, France</description><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">2004-07</dateIssued><dateCaptured encoding="w3cdtf">2003-06-30</dateCaptured><dateValid encoding="w3cdtf">2003-12-11</dateValid><copyrightDate encoding="w3cdtf">2004</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">4</extent><extent unit="tables">3</extent><extent unit="references">51</extent><extent unit="words">6665</extent></physicalDescription><abstract lang="en">It is assumed widely that the clinical expression of Parkinson's Disease (PD), both motor and cognitive, is subtended by topographically distributed brain networks. However, little is known about the functional neuroanatomy of executive dysfunction in PD. Our objective was to validate further in a PD group the use of network analysis to assess the relationship between executive processes and pathological disorganization of frontostriatal networks. We studied 15 patients with idiopathic PD, and 7 age‐matched normal controls, using resting [18F]fluorodeoxyglucose (FDG) and high‐resolution positron emission tomography (PET). We carried out network analysis on regional metabolic data to identify specific covariation patterns associated with motor and executive dysfunction. We detected two independent patterns relating respectively to the two clinical abnormalities. The first pattern (principal component 1) was topographically similar to that described previously in other PD populations. Subject scores for this pattern discriminated patients from controls and correlated significantly with bradykinesia ratings (P = 0.013, r = 0.655) in PD patients. The second pattern (principal component 2) was characterized by relative ventromedial frontal, hippocampal, and striatal hypometabolism, associated with mediodorsal thalamic hypermetabolism. In the PD group, scores from this pattern correlated with scores on the conditional associative learning (CAL; P = 0.01, r = 0.690) and the Brown Peterson paradigm (BPP; P = 0.017, r = −0.651) tests, respectively assessing strategy and planning, and working memory. According to these findings, the networks subserving bradykinesia and executive dysfunction in PD seems to be topographically distinct and to involve different aspects of subcortico‐cortical processing. Hum. Brain Mapping 22:236–245, 2004. © 2004 Wiley‐Liss, Inc.</abstract><note type="funding">Association France‐Parkinson</note><note type="funding">Association Neuro‐Psycho‐Pharmacologie</note><subject lang="en"><genre>Keywords</genre><topic>executive functions</topic><topic>Parkinson's disease</topic><topic>FDG‐PET</topic><topic>network analysis</topic><topic>working memory</topic></subject><relatedItem type="host"><titleInfo><title>Human Brain Mapping</title></titleInfo><titleInfo type="abbreviated"><title>Hum. Brain Mapp.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1065-9471</identifier><identifier type="eISSN">1097-0193</identifier><identifier type="DOI">10.1002/(ISSN)1097-0193</identifier><identifier type="PublisherID">HBM</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>236</start><end>245</end><total>10</total></extent></part></relatedItem><identifier type="istex">529CFAF614C17C047BD7C7BE5C7894535011589A</identifier><identifier type="DOI">10.1002/hbm.20033</identifier><identifier type="ArticleID">HBM20033</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2004 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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