Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.
Identifieur interne : 002F26 ( Main/Corpus ); précédent : 002F25; suivant : 002F27Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.
Auteurs : D. Rougemont ; J C Baron ; P. Collard ; P. Bustany ; D. Comar ; Y. AgidSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 1984-08.
Abstract
Using the 18f-fluoro-2-deoxy-d-glucose technique and positron emission tomography (PET), the local cerebral glucose utilisation (1CMRGlc) was measured in four non-demented patients with early-onset, bilateral Parkinson's disease characterised by the predominance of akinesia. The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in 1CMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, 1CMRGlc in the basal ganglia was moderately increased in both studies. These essentially negative findings agree with most previous human or animal studies, and indicate that the functional alterations in the central dopaminergic systems of patients with Parkinson's disease have metabolic correlates that are too small to be demonstrated by current PET devices.
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DOI: 10.1136/jnnp.47.8.824
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Agid</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:FE2651B6A8FC3F9DB825797A1E648439C8C6F544</idno><date when="1984-08-01" year="1984">1984-08-01</date><idno type="doi">10.1136/jnnp.47.8.824</idno><idno type="url">https://api.istex.fr/document/FE2651B6A8FC3F9DB825797A1E648439C8C6F544/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002F26</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.</title><author><name sortKey="Rougemont, D" sort="Rougemont, D" uniqKey="Rougemont D" first="D" last="Rougemont">D. Rougemont</name></author><author><name sortKey="Baron, J C" sort="Baron, J C" uniqKey="Baron J" first="J C" last="Baron">J C Baron</name></author><author><name sortKey="Collard, P" sort="Collard, P" uniqKey="Collard P" first="P" last="Collard">P. Collard</name></author><author><name sortKey="Bustany, P" sort="Bustany, P" uniqKey="Bustany P" first="P" last="Bustany">P. Bustany</name></author><author><name sortKey="Comar, D" sort="Comar, D" uniqKey="Comar D" first="D" last="Comar">D. Comar</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="1984-08">1984-08</date><biblScope unit="volume">47</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="824">824</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">FE2651B6A8FC3F9DB825797A1E648439C8C6F544</idno><idno type="DOI">10.1136/jnnp.47.8.824</idno><idno type="href">jnnp-47-824.pdf</idno><idno type="PMID">6332176</idno><idno type="local">jnnp;47/8/824</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Using the 18f-fluoro-2-deoxy-d-glucose technique and positron emission tomography (PET), the local cerebral glucose utilisation (1CMRGlc) was measured in four non-demented patients with early-onset, bilateral Parkinson's disease characterised by the predominance of akinesia. The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in 1CMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, 1CMRGlc in the basal ganglia was moderately increased in both studies. These essentially negative findings agree with most previous human or animal studies, and indicate that the functional alterations in the central dopaminergic systems of patients with Parkinson's disease have metabolic correlates that are too small to be demonstrated by current PET devices.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>D Rougemont</name></json:item><json:item><name>J C Baron</name></json:item><json:item><name>P Collard</name></json:item><json:item><name>P Bustany</name></json:item><json:item><name>D Comar</name></json:item><json:item><name>Y Agid</name></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Research Article</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Using the 18f-fluoro-2-deoxy-d-glucose technique and positron emission tomography (PET), the local cerebral glucose utilisation (1CMRGlc) was measured in four non-demented patients with early-onset, bilateral Parkinson's disease characterised by the predominance of akinesia. The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in 1CMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, 1CMRGlc in the basal ganglia was moderately increased in both studies. These essentially negative findings agree with most previous human or animal studies, and indicate that the functional alterations in the central dopaminergic systems of patients with Parkinson's disease have metabolic correlates that are too small to be demonstrated by current PET devices.</abstract><qualityIndicators><score>5.709</score><pdfVersion>1.3</pdfVersion><pdfPageSize>525.12 x 694.56 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>918</abstractCharCount><pdfWordCount>4149</pdfWordCount><pdfCharCount>26861</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>130</abstractWordCount></qualityIndicators><title>Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.</title><pmid><json:string>6332176</json:string></pmid><genre><json:string>research-article</json:string></genre><host><volume>47</volume><pages><first>824</first></pages><issn><json:string>0022-3050</json:string></issn><issue>8</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-330X</json:string></eissn><title>Journal of Neurology, Neurosurgery & Psychiatry</title></host><publicationDate>1984</publicationDate><doi><json:string>10.1136/jnnp.47.8.824</json:string></doi><id>FE2651B6A8FC3F9DB825797A1E648439C8C6F544</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/FE2651B6A8FC3F9DB825797A1E648439C8C6F544/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/FE2651B6A8FC3F9DB825797A1E648439C8C6F544/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/FE2651B6A8FC3F9DB825797A1E648439C8C6F544/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>BMJ Publishing Group Ltd</publisher><availability><p>BMJ</p></availability><date>1984-08-01</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.</title><author><persName><forename type="first">D</forename><surname>Rougemont</surname></persName></author><author><persName><forename type="first">J C</forename><surname>Baron</surname></persName></author><author><persName><forename type="first">P</forename><surname>Collard</surname></persName></author><author><persName><forename type="first">P</forename><surname>Bustany</surname></persName></author><author><persName><forename type="first">D</forename><surname>Comar</surname></persName></author><author><persName><forename type="first">Y</forename><surname>Agid</surname></persName></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="1984-08"></date><biblScope unit="volume">47</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="824">824</biblScope></imprint></monogr><idno type="istex">FE2651B6A8FC3F9DB825797A1E648439C8C6F544</idno><idno type="DOI">10.1136/jnnp.47.8.824</idno><idno type="href">jnnp-47-824.pdf</idno><idno type="PMID">6332176</idno><idno type="local">jnnp;47/8/824</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1984-08-01</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Using the 18f-fluoro-2-deoxy-d-glucose technique and positron emission tomography (PET), the local cerebral glucose utilisation (1CMRGlc) was measured in four non-demented patients with early-onset, bilateral Parkinson's disease characterised by the predominance of akinesia. The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in 1CMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, 1CMRGlc in the basal ganglia was moderately increased in both studies. 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The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in 1CMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, 1CMRGlc in the basal ganglia was moderately increased in both studies. These essentially negative findings agree with most previous human or animal studies, and indicate that the functional alterations in the central dopaminergic systems of patients with Parkinson's disease have metabolic correlates that are too small to be demonstrated by current PET devices.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Rougemont</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J C</namePart><namePart type="family">Baron</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Collard</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Bustany</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Comar</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Agid</namePart><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">1984-08</dateIssued><dateCreated encoding="w3cdtf">1984-08-01</dateCreated></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">Using the 18f-fluoro-2-deoxy-d-glucose technique and positron emission tomography (PET), the local cerebral glucose utilisation (1CMRGlc) was measured in four non-demented patients with early-onset, bilateral Parkinson's disease characterised by the predominance of akinesia. The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in 1CMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, 1CMRGlc in the basal ganglia was moderately increased in both studies. These essentially negative findings agree with most previous human or animal studies, and indicate that the functional alterations in the central dopaminergic systems of patients with Parkinson's disease have metabolic correlates that are too small to be demonstrated by current PET devices.</abstract><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>1984</date><detail type="volume"><caption>vol.</caption><number>47</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>824</start></extent></part></relatedItem><identifier type="istex">FE2651B6A8FC3F9DB825797A1E648439C8C6F544</identifier><identifier type="DOI">10.1136/jnnp.47.8.824</identifier><identifier type="href">jnnp-47-824.pdf</identifier><identifier type="PMID">6332176</identifier><identifier type="local">jnnp;47/8/824</identifier><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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