Functional brain networks in Parkinson's disease
Identifieur interne : 002472 ( Main/Corpus ); précédent : 002471; suivant : 002473Functional brain networks in Parkinson's disease
Auteurs : Masafumi Fukuda ; Christine Edwards ; David EidelbergSource :
- Parkinsonism and Related Disorders [ 1353-8020 ] ; 2001.
English descriptors
Abstract
With the advent of new methods of network analysis, we have utilized metabolic data acquired through positron emission tomography (PET) to identify disease-related patterns of functional pathology in the movement disorders. In Parkinson's disease (PD), we have used [18F]-fluorodeoxyglucose (FDG)/PET to identify a disease-related regional metabolic covariance pattern characterized by lentiform and thalamic hypermetabolism associated with regional metabolic decrements in the lateral premotor cortex, the supplementary motor area, the dorsolateral prefrontal cortex, and the parieto-occipital association regions. The expression of this network is modulated in a predictable fashion by levodopa therapy and by stereotaxic interventions for PD. We have extended this network analytical approach from studies of glucose metabolism in the resting state to dynamic studies of brain activation during motor performance. These PET studies utilized [15O]–water (H2 15O) to measure cerebral blood flow activation responses during the execution of simple and complex motor tasks. In addition to the modulation of abnormal resting metabolic networks, effective PD therapy can enhance brain activation responses during motor execution, with specific regional associations with improvements in timing and spatial accuracy. This approach is also useful in identifying specific brain networks mediating the learning of sequential information. We have found that the normal relationship between brain networks and learning performance are altered in the earliest stages of PD with a functional shift from striatal to cortical processing. Brain activation PET studies during therapeutic interventions for PD demonstrate how normal brain-behavior relationships can be restored with successful therapy. Thus, functional brain imaging with network analysis can provide insights into the mechanistic basis of basal ganglia disorders and their treatment.
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DOI: 10.1016/S1353-8020(01)00022-0
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In Parkinson's disease (PD), we have used [18F]-fluorodeoxyglucose (FDG)/PET to identify a disease-related regional metabolic covariance pattern characterized by lentiform and thalamic hypermetabolism associated with regional metabolic decrements in the lateral premotor cortex, the supplementary motor area, the dorsolateral prefrontal cortex, and the parieto-occipital association regions. The expression of this network is modulated in a predictable fashion by levodopa therapy and by stereotaxic interventions for PD. We have extended this network analytical approach from studies of glucose metabolism in the resting state to dynamic studies of brain activation during motor performance. These PET studies utilized [15O]–water (H2 15O) to measure cerebral blood flow activation responses during the execution of simple and complex motor tasks. In addition to the modulation of abnormal resting metabolic networks, effective PD therapy can enhance brain activation responses during motor execution, with specific regional associations with improvements in timing and spatial accuracy. This approach is also useful in identifying specific brain networks mediating the learning of sequential information. We have found that the normal relationship between brain networks and learning performance are altered in the earliest stages of PD with a functional shift from striatal to cortical processing. Brain activation PET studies during therapeutic interventions for PD demonstrate how normal brain-behavior relationships can be restored with successful therapy. Thus, functional brain imaging with network analysis can provide insights into the mechanistic basis of basal ganglia disorders and their treatment.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Masafumi Fukuda</name><affiliations><json:string>Department of Neurology and Neurosurgery, New York University School of Medicine, Functional Brain Imaging Laboratory, North Shore-LIJ Research Institute, Manhasset, NY, USA</json:string></affiliations></json:item><json:item><name>Christine Edwards</name><affiliations><json:string>Department of Neurology and Neurosurgery, New York University School of Medicine, Functional Brain Imaging Laboratory, North Shore-LIJ Research Institute, Manhasset, NY, USA</json:string></affiliations></json:item><json:item><name>David Eidelberg</name><affiliations><json:string>Department of Neurology and Neurosurgery, New York University School of Medicine, Functional Brain Imaging Laboratory, North Shore-LIJ Research Institute, Manhasset, NY, USA</json:string><json:string>E-mail: david1@nshs.edu</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>Brain networks</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Glucose metabolism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cerebral blood flow</value></json:item></subject><language><json:string>eng</json:string></language><abstract>With the advent of new methods of network analysis, we have utilized metabolic data acquired through positron emission tomography (PET) to identify disease-related patterns of functional pathology in the movement disorders. In Parkinson's disease (PD), we have used [18F]-fluorodeoxyglucose (FDG)/PET to identify a disease-related regional metabolic covariance pattern characterized by lentiform and thalamic hypermetabolism associated with regional metabolic decrements in the lateral premotor cortex, the supplementary motor area, the dorsolateral prefrontal cortex, and the parieto-occipital association regions. The expression of this network is modulated in a predictable fashion by levodopa therapy and by stereotaxic interventions for PD. We have extended this network analytical approach from studies of glucose metabolism in the resting state to dynamic studies of brain activation during motor performance. These PET studies utilized [15O]–water (H2 15O) to measure cerebral blood flow activation responses during the execution of simple and complex motor tasks. In addition to the modulation of abnormal resting metabolic networks, effective PD therapy can enhance brain activation responses during motor execution, with specific regional associations with improvements in timing and spatial accuracy. This approach is also useful in identifying specific brain networks mediating the learning of sequential information. We have found that the normal relationship between brain networks and learning performance are altered in the earliest stages of PD with a functional shift from striatal to cortical processing. Brain activation PET studies during therapeutic interventions for PD demonstrate how normal brain-behavior relationships can be restored with successful therapy. 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Tel.: +1-516-562-2498; fax: +1-516-562-1008</p></note><affiliation>Department of Neurology and Neurosurgery, New York University School of Medicine, Functional Brain Imaging Laboratory, North Shore-LIJ Research Institute, Manhasset, NY, USA</affiliation></author></analytic><monogr><title level="j">Parkinsonism and Related Disorders</title><title level="j" type="abbrev">PRD</title><idno type="pISSN">1353-8020</idno><idno type="PII">S1353-8020(00)X0029-6</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">8</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="91">91</biblScope><biblScope unit="page" to="94">94</biblScope></imprint></monogr><idno type="istex">403A90DF26C101E40056E7AA7B9E6DBF405AAF96</idno><idno type="DOI">10.1016/S1353-8020(01)00022-0</idno><idno type="PII">S1353-8020(01)00022-0</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>With the advent of new methods of network analysis, we have utilized metabolic data acquired through positron emission tomography (PET) to identify disease-related patterns of functional pathology in the movement disorders. In Parkinson's disease (PD), we have used [18F]-fluorodeoxyglucose (FDG)/PET to identify a disease-related regional metabolic covariance pattern characterized by lentiform and thalamic hypermetabolism associated with regional metabolic decrements in the lateral premotor cortex, the supplementary motor area, the dorsolateral prefrontal cortex, and the parieto-occipital association regions. The expression of this network is modulated in a predictable fashion by levodopa therapy and by stereotaxic interventions for PD. We have extended this network analytical approach from studies of glucose metabolism in the resting state to dynamic studies of brain activation during motor performance. These PET studies utilized [15O]–water (H2 15O) to measure cerebral blood flow activation responses during the execution of simple and complex motor tasks. In addition to the modulation of abnormal resting metabolic networks, effective PD therapy can enhance brain activation responses during motor execution, with specific regional associations with improvements in timing and spatial accuracy. This approach is also useful in identifying specific brain networks mediating the learning of sequential information. We have found that the normal relationship between brain networks and learning performance are altered in the earliest stages of PD with a functional shift from striatal to cortical processing. Brain activation PET studies during therapeutic interventions for PD demonstrate how normal brain-behavior relationships can be restored with successful therapy. Thus, functional brain imaging with network analysis can provide insights into the mechanistic basis of basal ganglia disorders and their treatment.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>PET</term></item><item><term>Brain networks</term></item><item><term>Glucose metabolism</term></item><item><term>Cerebral blood flow</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>PRD</jid><aid>291</aid><ce:pii>S1353-8020(01)00022-0</ce:pii><ce:doi>10.1016/S1353-8020(01)00022-0</ce:doi><ce:copyright type="full-transfer" year="2001">Elsevier Science Ltd</ce:copyright></item-info><head><ce:title>Functional brain networks in Parkinson's disease</ce:title><ce:author-group><ce:author><ce:given-name>Masafumi</ce:given-name><ce:surname>Fukuda</ce:surname></ce:author><ce:author><ce:given-name>Christine</ce:given-name><ce:surname>Edwards</ce:surname></ce:author><ce:author><ce:given-name>David</ce:given-name><ce:surname>Eidelberg</ce:surname><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>david1@nshs.edu</ce:e-address></ce:author><ce:affiliation><ce:textfn>Department of Neurology and Neurosurgery, New York University School of Medicine, Functional Brain Imaging Laboratory, North Shore-LIJ Research Institute, Manhasset, NY, USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1-516-562-2498; fax: +1-516-562-1008</ce:text></ce:correspondence></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>With the advent of new methods of network analysis, we have utilized metabolic data acquired through positron emission tomography (PET) to identify disease-related patterns of functional pathology in the movement disorders. In Parkinson's disease (PD), we have used [<ce:sup loc="pre">18</ce:sup>F]-fluorodeoxyglucose (FDG)/PET to identify a disease-related regional metabolic covariance pattern characterized by lentiform and thalamic hypermetabolism associated with regional metabolic decrements in the lateral premotor cortex, the supplementary motor area, the dorsolateral prefrontal cortex, and the parieto-occipital association regions. The expression of this network is modulated in a predictable fashion by levodopa therapy and by stereotaxic interventions for PD.</ce:simple-para><ce:simple-para>We have extended this network analytical approach from studies of glucose metabolism in the resting state to dynamic studies of brain activation during motor performance. These PET studies utilized [<ce:sup loc="pre">15</ce:sup>O]–water (H<ce:inf>2</ce:inf> <ce:sup loc="pre">15</ce:sup>O) to measure cerebral blood flow activation responses during the execution of simple and complex motor tasks. In addition to the modulation of abnormal resting metabolic networks, effective PD therapy can enhance brain activation responses during motor execution, with specific regional associations with improvements in timing and spatial accuracy.</ce:simple-para><ce:simple-para>This approach is also useful in identifying specific brain networks mediating the learning of sequential information. We have found that the normal relationship between brain networks and learning performance are altered in the earliest stages of PD with a functional shift from striatal to cortical processing. Brain activation PET studies during therapeutic interventions for PD demonstrate how normal brain-behavior relationships can be restored with successful therapy. Thus, functional brain imaging with network analysis can provide insights into the mechanistic basis of basal ganglia disorders and their treatment.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword" xml:lang="en"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>PET</ce:text></ce:keyword><ce:keyword><ce:text>Brain networks</ce:text></ce:keyword><ce:keyword><ce:text>Glucose metabolism</ce:text></ce:keyword><ce:keyword><ce:text>Cerebral blood flow</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Functional brain networks in Parkinson's disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Functional brain networks in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Masafumi</namePart><namePart type="family">Fukuda</namePart><affiliation>Department of Neurology and Neurosurgery, New York University School of Medicine, Functional Brain Imaging Laboratory, North Shore-LIJ Research Institute, Manhasset, NY, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Edwards</namePart><affiliation>Department of Neurology and Neurosurgery, New York University School of Medicine, Functional Brain Imaging Laboratory, North Shore-LIJ Research Institute, Manhasset, NY, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Eidelberg</namePart><affiliation>Department of Neurology and Neurosurgery, New York University School of Medicine, Functional Brain Imaging Laboratory, North Shore-LIJ Research Institute, Manhasset, NY, USA</affiliation><affiliation>E-mail: david1@nshs.edu</affiliation><description>Corresponding author. Tel.: +1-516-562-2498; fax: +1-516-562-1008</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">With the advent of new methods of network analysis, we have utilized metabolic data acquired through positron emission tomography (PET) to identify disease-related patterns of functional pathology in the movement disorders. In Parkinson's disease (PD), we have used [18F]-fluorodeoxyglucose (FDG)/PET to identify a disease-related regional metabolic covariance pattern characterized by lentiform and thalamic hypermetabolism associated with regional metabolic decrements in the lateral premotor cortex, the supplementary motor area, the dorsolateral prefrontal cortex, and the parieto-occipital association regions. The expression of this network is modulated in a predictable fashion by levodopa therapy and by stereotaxic interventions for PD. We have extended this network analytical approach from studies of glucose metabolism in the resting state to dynamic studies of brain activation during motor performance. These PET studies utilized [15O]–water (H2 15O) to measure cerebral blood flow activation responses during the execution of simple and complex motor tasks. In addition to the modulation of abnormal resting metabolic networks, effective PD therapy can enhance brain activation responses during motor execution, with specific regional associations with improvements in timing and spatial accuracy. This approach is also useful in identifying specific brain networks mediating the learning of sequential information. We have found that the normal relationship between brain networks and learning performance are altered in the earliest stages of PD with a functional shift from striatal to cortical processing. Brain activation PET studies during therapeutic interventions for PD demonstrate how normal brain-behavior relationships can be restored with successful therapy. Thus, functional brain imaging with network analysis can provide insights into the mechanistic basis of basal ganglia disorders and their treatment.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>PET</topic><topic>Brain networks</topic><topic>Glucose metabolism</topic><topic>Cerebral blood flow</topic></subject><relatedItem type="host"><titleInfo><title>Parkinsonism and Related Disorders</title></titleInfo><titleInfo type="abbreviated"><title>PRD</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">200110</dateIssued></originInfo><identifier type="ISSN">1353-8020</identifier><identifier type="PII">S1353-8020(00)X0029-6</identifier><part><date>200110</date><detail type="volume"><number>8</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>77</start><end>156</end></extent><extent unit="pages"><start>91</start><end>94</end></extent></part></relatedItem><identifier type="istex">403A90DF26C101E40056E7AA7B9E6DBF405AAF96</identifier><identifier type="DOI">10.1016/S1353-8020(01)00022-0</identifier><identifier type="PII">S1353-8020(01)00022-0</identifier><accessCondition type="use and reproduction" contentType="">© 2001Elsevier Science Ltd</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science Ltd, ©2001</recordOrigin></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/403A90DF26C101E40056E7AA7B9E6DBF405AAF96/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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