Differential diagnosis of parkinsonism with [18F]fluorodeoxyglucose and PET
Identifieur interne : 001685 ( Istex/Corpus ); précédent : 001684; suivant : 001686Differential diagnosis of parkinsonism with [18F]fluorodeoxyglucose and PET
Auteurs : Angelo Antonini ; Ken Kazumata ; Andrew Feigin ; Francine Mandel ; Vijay Dhawan ; Claude Margouleff ; EidelbergSource :
- Movement Disorders [ 0885-3185 ] ; 1998-03.
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- KwdEn :
Abstract
The clinical differentiation between typical idiopathic Parkinson's disease (IPD) and atypical parkinsonian disorders (APD) is complicated by the presence of signs and symptoms common to both forms of parkinsonism. Metabolic brain imaging with [18F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) may be a useful adjunct in differentiating APD from IPD. To explore this possibility, we studied 48 parkinsonian patients suspected as having possible APD because of a deteriorating response to dopaminergic treatment, the development of autonomic dysfunction, or both. A group of 56 patients with likely IPD served as control subjects. We used quantitative FDG/PET to measure regional rates of cerebral glucose use in IPD and APD patients. We used discriminant analysis to categorize IPD and APD patients based on their regional metabolic data. We found that a linear combination of caudate, lentiform, and thalamic values accurately discriminated APD from IPD patients (p < 0.0001). Significant metabolic abnormalities were present in the striatum and the thalamus of 36 of 48 (75%) APD patients. Our findings show that measurements of regional glucose metabolism can be used to discriminate patients with suspected APD from their counterparts with classic IPD. FDG/PET may be a useful adjunct to the clinical examination in the differential diagnosis of parkinsonism.
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DOI: 10.1002/mds.870130212
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uniqKey="Feigin A" first="Andrew" last="Feigin">Andrew Feigin</name><affiliation><mods:affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Mandel, Francine" sort="Mandel, Francine" uniqKey="Mandel F" first="Francine" last="Mandel">Francine Mandel</name><affiliation><mods:affiliation>Departments of Medicine and Research, North Shore University Hospital, Manhasset, New York, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Dhawan, Vijay" sort="Dhawan, Vijay" uniqKey="Dhawan V" first="Vijay" last="Dhawan">Vijay Dhawan</name><affiliation><mods:affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Margouleff, Claude" sort="Margouleff, Claude" uniqKey="Margouleff C" first="Claude" last="Margouleff">Claude Margouleff</name><affiliation><mods:affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Eidelberg" sort="Eidelberg" uniqKey="Eidelberg" last="Eidelberg">Eidelberg</name><affiliation><mods:affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-03">1998-03</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="268">268</biblScope><biblScope unit="page" to="274">274</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">5D101E872AAA841676D06C193DF7CDC6DD0D3CE7</idno><idno type="DOI">10.1002/mds.870130212</idno><idno type="ArticleID">MDS870130212</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atypical parkinsonism</term><term>Multiple system atrophy</term><term>Parkinson's disease</term><term>Positron emission tomography</term><term>[18F]Fluorodeoxyglucose</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The clinical differentiation between typical idiopathic Parkinson's disease (IPD) and atypical parkinsonian disorders (APD) is complicated by the presence of signs and symptoms common to both forms of parkinsonism. Metabolic brain imaging with [18F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) may be a useful adjunct in differentiating APD from IPD. To explore this possibility, we studied 48 parkinsonian patients suspected as having possible APD because of a deteriorating response to dopaminergic treatment, the development of autonomic dysfunction, or both. A group of 56 patients with likely IPD served as control subjects. We used quantitative FDG/PET to measure regional rates of cerebral glucose use in IPD and APD patients. We used discriminant analysis to categorize IPD and APD patients based on their regional metabolic data. We found that a linear combination of caudate, lentiform, and thalamic values accurately discriminated APD from IPD patients (p < 0.0001). Significant metabolic abnormalities were present in the striatum and the thalamus of 36 of 48 (75%) APD patients. Our findings show that measurements of regional glucose metabolism can be used to discriminate patients with suspected APD from their counterparts with classic IPD. FDG/PET may be a useful adjunct to the clinical examination in the differential diagnosis of parkinsonism.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Angelo Antonini MD, PhD</name><affiliations><json:string>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</json:string></affiliations></json:item><json:item><name>Ken Kazumata MD</name><affiliations><json:string>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</json:string></affiliations></json:item><json:item><name>Andrew Feigin MD</name><affiliations><json:string>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</json:string></affiliations></json:item><json:item><name>Francine Mandel PhD</name><affiliations><json:string>Departments of Medicine and Research, North Shore University Hospital, Manhasset, New York, U.S.A.</json:string></affiliations></json:item><json:item><name>Vijay Dhawan PhD</name><affiliations><json:string>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</json:string></affiliations></json:item><json:item><name>Claude Margouleff MS</name><affiliations><json:string>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</json:string></affiliations></json:item><json:item><name>Dr. Eidelberg MD</name><affiliations><json:string>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>[18F]Fluorodeoxyglucose</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Positron emission tomography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Atypical parkinsonism</value></json:item><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>Multiple system atrophy</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The clinical differentiation between typical idiopathic Parkinson's disease (IPD) and atypical parkinsonian disorders (APD) is complicated by the presence of signs and symptoms common to both forms of parkinsonism. Metabolic brain imaging with [18F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) may be a useful adjunct in differentiating APD from IPD. To explore this possibility, we studied 48 parkinsonian patients suspected as having possible APD because of a deteriorating response to dopaminergic treatment, the development of autonomic dysfunction, or both. A group of 56 patients with likely IPD served as control subjects. We used quantitative FDG/PET to measure regional rates of cerebral glucose use in IPD and APD patients. We used discriminant analysis to categorize IPD and APD patients based on their regional metabolic data. We found that a linear combination of caudate, lentiform, and thalamic values accurately discriminated APD from IPD patients (p > 0.0001). Significant metabolic abnormalities were present in the striatum and the thalamus of 36 of 48 (75%) APD patients. Our findings show that measurements of regional glucose metabolism can be used to discriminate patients with suspected APD from their counterparts with classic IPD. FDG/PET may be a useful adjunct to the clinical examination in the differential diagnosis of parkinsonism.</abstract><qualityIndicators><score>6.084</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1382</abstractCharCount><pdfWordCount>3648</pdfWordCount><pdfCharCount>23470</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>203</abstractWordCount></qualityIndicators><title>Differential diagnosis of parkinsonism with [18F]fluorodeoxyglucose and PET</title><genre><json:string>Serial article</json:string></genre><host><volume>13</volume><pages><total>7</total><last>274</last><first>268</first></pages><issn><json:string>0885-3185</json:string></issn><issue>2</issue><subject><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1002/mds.870130212</json:string></doi><id>5D101E872AAA841676D06C193DF7CDC6DD0D3CE7</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/5D101E872AAA841676D06C193DF7CDC6DD0D3CE7/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/5D101E872AAA841676D06C193DF7CDC6DD0D3CE7/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/5D101E872AAA841676D06C193DF7CDC6DD0D3CE7/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Differential diagnosis of parkinsonism with [18F]fluorodeoxyglucose and PET</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>1998</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Differential diagnosis of parkinsonism with [18F]fluorodeoxyglucose and PET</title><author><persName><forename type="first">Angelo</forename><surname>Antonini</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation></author><author><persName><forename type="first">Ken</forename><surname>Kazumata</surname><roleName type="degree">MD</roleName></persName><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation></author><author><persName><forename type="first">Andrew</forename><surname>Feigin</surname><roleName type="degree">MD</roleName></persName><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation></author><author><persName><forename type="first">Francine</forename><surname>Mandel</surname><roleName type="degree">PhD</roleName></persName><affiliation>Departments of Medicine and Research, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation></author><author><persName><forename type="first">Vijay</forename><surname>Dhawan</surname><roleName type="degree">PhD</roleName></persName><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation></author><author><persName><forename type="first">Claude</forename><surname>Margouleff</surname><roleName type="degree">MS</roleName></persName><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation></author><author><persName><surname>Eidelberg</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: The Department of Neurology, North Shore University Hospital, 350 Community Dr., Manhasset, NY 11030, U.S.A</p></note><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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Metabolic brain imaging with [18F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) may be a useful adjunct in differentiating APD from IPD. To explore this possibility, we studied 48 parkinsonian patients suspected as having possible APD because of a deteriorating response to dopaminergic treatment, the development of autonomic dysfunction, or both. A group of 56 patients with likely IPD served as control subjects. We used quantitative FDG/PET to measure regional rates of cerebral glucose use in IPD and APD patients. We used discriminant analysis to categorize IPD and APD patients based on their regional metabolic data. We found that a linear combination of caudate, lentiform, and thalamic values accurately discriminated APD from IPD patients (p < 0.0001). Significant metabolic abnormalities were present in the striatum and the thalamus of 36 of 48 (75%) APD patients. Our findings show that measurements of regional glucose metabolism can be used to discriminate patients with suspected APD from their counterparts with classic IPD. FDG/PET may be a useful adjunct to the clinical examination in the differential diagnosis of parkinsonism.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>[18F]Fluorodeoxyglucose</term></item><item><term>Positron emission tomography</term></item><item><term>Atypical parkinsonism</term></item><item><term>Parkinson's disease</term></item><item><term>Multiple system atrophy</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-01-17">Received</change><change when="1997-06-27">Registration</change><change when="1998-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/5D101E872AAA841676D06C193DF7CDC6DD0D3CE7/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="tocForm">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Metabolic brain imaging with [<sup>18</sup>F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) may be a useful adjunct in differentiating APD from IPD. To explore this possibility, we studied 48 parkinsonian patients suspected as having possible APD because of a deteriorating response to dopaminergic treatment, the development of autonomic dysfunction, or both. A group of 56 patients with likely IPD served as control subjects. We used quantitative FDG/PET to measure regional rates of cerebral glucose use in IPD and APD patients. We used discriminant analysis to categorize IPD and APD patients based on their regional metabolic data. We found that a linear combination of caudate, lentiform, and thalamic values accurately discriminated APD from IPD patients (p < 0.0001). Significant metabolic abnormalities were present in the striatum and the thalamus of 36 of 48 (75%) APD patients. Our findings show that measurements of regional glucose metabolism can be used to discriminate patients with suspected APD from their counterparts with classic IPD. FDG/PET may be a useful adjunct to the clinical examination in the differential diagnosis of parkinsonism.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Differential diagnosis of parkinsonism with [18F]fluorodeoxyglucose and PET</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>FDG/PET IN DIFFERENTIAL DIAGNOSIS OF PARKINSONISM</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Differential diagnosis of parkinsonism with [</title></titleInfo><name type="personal"><namePart type="given">Angelo</namePart><namePart type="family">Antonini</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ken</namePart><namePart type="family">Kazumata</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew</namePart><namePart type="family">Feigin</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Francine</namePart><namePart type="family">Mandel</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Departments of Medicine and Research, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vijay</namePart><namePart type="family">Dhawan</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Claude</namePart><namePart type="family">Margouleff</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Eidelberg</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Movement Disorders Center and Functional Brain Imaging Laboratory, Department of Neurology, North Shore University Hospital, Manhasset, New York, U.S.A.</affiliation><description>Correspondence: The Department of Neurology, North Shore University Hospital, 350 Community Dr., Manhasset, NY 11030, U.S.A</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-03</dateIssued><dateCaptured encoding="w3cdtf">1997-01-17</dateCaptured><dateValid encoding="w3cdtf">1997-06-27</dateValid><copyrightDate encoding="w3cdtf">1998</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">2</extent><extent unit="tables">4</extent><extent unit="references">29</extent></physicalDescription><abstract lang="en">The clinical differentiation between typical idiopathic Parkinson's disease (IPD) and atypical parkinsonian disorders (APD) is complicated by the presence of signs and symptoms common to both forms of parkinsonism. Metabolic brain imaging with [18F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) may be a useful adjunct in differentiating APD from IPD. To explore this possibility, we studied 48 parkinsonian patients suspected as having possible APD because of a deteriorating response to dopaminergic treatment, the development of autonomic dysfunction, or both. A group of 56 patients with likely IPD served as control subjects. We used quantitative FDG/PET to measure regional rates of cerebral glucose use in IPD and APD patients. We used discriminant analysis to categorize IPD and APD patients based on their regional metabolic data. We found that a linear combination of caudate, lentiform, and thalamic values accurately discriminated APD from IPD patients (p < 0.0001). Significant metabolic abnormalities were present in the striatum and the thalamus of 36 of 48 (75%) APD patients. Our findings show that measurements of regional glucose metabolism can be used to discriminate patients with suspected APD from their counterparts with classic IPD. FDG/PET may be a useful adjunct to the clinical examination in the differential diagnosis of parkinsonism.</abstract><subject lang="en"><genre>Keywords</genre><topic>[18F]Fluorodeoxyglucose</topic><topic>Positron emission tomography</topic><topic>Atypical parkinsonism</topic><topic>Parkinson's disease</topic><topic>Multiple system atrophy</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</topic></subject><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>1998</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>268</start><end>274</end><total>7</total></extent></part></relatedItem><identifier type="istex">5D101E872AAA841676D06C193DF7CDC6DD0D3CE7</identifier><identifier type="DOI">10.1002/mds.870130212</identifier><identifier type="ArticleID">MDS870130212</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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