Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy
Identifieur interne : 002092 ( Main/Corpus ); précédent : 002091; suivant : 002093Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy
Auteurs : C. A. Davie ; G. K. Wenning ; G. J. Barker ; P. S. Tofts ; B. E. Kendall ; N. Quinn ; W. I. Mcdonald ; C. D. Marsden ; D. H. MillerSource :
- Annals of Neurology [ 0364-5134 ] ; 1995-02.
Abstract
Proton magnetic resonance spectroscopy, localized to the lentiform nucleus, was carried out in 7 patients with the pure or predominantly striatonigral variant (SND) of multiple system atrophy (MSA), 5 patients with the olivopontocerebellar variant of MSA, 9 patients with a clinical diagnosis of idiopathic Parkinson's disease (IPD), and 9 healthy age‐matched controls. The MSA group with predominantly striatonigral involvement showed a significant reduction in the N‐acetylaspartate (NAA)/creatine ratio (median, 1.19; range, 0.96–2.0; p < 0.02) compared with the NAA/creatine ratio (median, 1.82; range, 1.19–2.31; p > 0.5). The NAA/creatine ratio was markedly reduced in 6 of the SND patients and in only 1 IPD patient. The choline/creatine ratio was also significantly lower in the SND group (median, 1.02; range, 0.91–1.23; p < 0.04) compared with the control group (median, 1.22; range, 1.05–1.65). The IPD group showed a normal lentiform choline/creatine ratio (median, 1.13; range, 0.89–1.65; p = 0.25) compared with controls. The olivopontocerebellar group also showed a significant reduction in the NAA/creatine ratio from the lentiform nucleus (median, 1.47; range, 1.22–1.68; p < 0.01) compared with the controls as well as a nonsignificant reduction in the choline/creatine ratio (median, 0.93; range, 0.85–1.27; p < 0.4). In vivo quantification of absolute metabolite concentrations was possible in 7 MSA patients and 6 controls and confirmed an absolute reduction of choline‐containing compounds and NAA in the MSA group compared with controls with no significant difference in the creatine concentrations between the MSA groups probably reflects neuronal loss, occurring predominantly in the putamen. Proton magnetic resonance spectroscopy is a useful, noninvasive technique to help differentiate MSA from IPD.
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DOI: 10.1002/ana.410370211
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Barker</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Tofts, P S" sort="Tofts, P S" uniqKey="Tofts P" first="P. S." last="Tofts">P. S. Tofts</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Kendall, B E" sort="Kendall, B E" uniqKey="Kendall B" first="B. E." last="Kendall">B. E. Kendall</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Quinn, N" sort="Quinn, N" uniqKey="Quinn N" first="N." last="Quinn">N. Quinn</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Mcdonald, W I" sort="Mcdonald, W I" uniqKey="Mcdonald W" first="W. I." last="Mcdonald">W. I. Mcdonald</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Miller, D H" sort="Miller, D H" uniqKey="Miller D" first="D. H." last="Miller">D. H. 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Davie</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G. K." last="Wenning">G. K. Wenning</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Barker, G J" sort="Barker, G J" uniqKey="Barker G" first="G. J." last="Barker">G. J. Barker</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Tofts, P S" sort="Tofts, P S" uniqKey="Tofts P" first="P. S." last="Tofts">P. S. Tofts</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Kendall, B E" sort="Kendall, B E" uniqKey="Kendall B" first="B. E." last="Kendall">B. E. Kendall</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Quinn, N" sort="Quinn, N" uniqKey="Quinn N" first="N." last="Quinn">N. Quinn</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Mcdonald, W I" sort="Mcdonald, W I" uniqKey="Mcdonald W" first="W. I." last="Mcdonald">W. I. Mcdonald</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Miller, D H" sort="Miller, D H" uniqKey="Miller D" first="D. H." last="Miller">D. H. Miller</name><affiliation><mods:affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-02">1995-02</date><biblScope unit="volume">37</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="204">204</biblScope><biblScope unit="page" to="210">210</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">0A717A31E4D3E56D589EF2037186AA64751C9431</idno><idno type="DOI">10.1002/ana.410370211</idno><idno type="ArticleID">ANA410370211</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Proton magnetic resonance spectroscopy, localized to the lentiform nucleus, was carried out in 7 patients with the pure or predominantly striatonigral variant (SND) of multiple system atrophy (MSA), 5 patients with the olivopontocerebellar variant of MSA, 9 patients with a clinical diagnosis of idiopathic Parkinson's disease (IPD), and 9 healthy age‐matched controls. The MSA group with predominantly striatonigral involvement showed a significant reduction in the N‐acetylaspartate (NAA)/creatine ratio (median, 1.19; range, 0.96–2.0; p < 0.02) compared with the NAA/creatine ratio (median, 1.82; range, 1.19–2.31; p > 0.5). The NAA/creatine ratio was markedly reduced in 6 of the SND patients and in only 1 IPD patient. The choline/creatine ratio was also significantly lower in the SND group (median, 1.02; range, 0.91–1.23; p < 0.04) compared with the control group (median, 1.22; range, 1.05–1.65). The IPD group showed a normal lentiform choline/creatine ratio (median, 1.13; range, 0.89–1.65; p = 0.25) compared with controls. The olivopontocerebellar group also showed a significant reduction in the NAA/creatine ratio from the lentiform nucleus (median, 1.47; range, 1.22–1.68; p < 0.01) compared with the controls as well as a nonsignificant reduction in the choline/creatine ratio (median, 0.93; range, 0.85–1.27; p < 0.4). In vivo quantification of absolute metabolite concentrations was possible in 7 MSA patients and 6 controls and confirmed an absolute reduction of choline‐containing compounds and NAA in the MSA group compared with controls with no significant difference in the creatine concentrations between the MSA groups probably reflects neuronal loss, occurring predominantly in the putamen. Proton magnetic resonance spectroscopy is a useful, noninvasive technique to help differentiate MSA from IPD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>C. A. Davie MRCP</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>G. K. Wenning MD</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>G. J. Barker PhD</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>P. S. Tofts D Phil</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>B. E. Kendall FRCR</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>N. Quinn MD</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>W. I. McDonald PhD</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>C. D. Marsden DSc</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>D. H. Miller MD</name><affiliations><json:string>From the Department of Clinical Neurology, Institute of Neurology, London, UK</json:string></affiliations></json:item></author><articleId><json:string>ANA410370211</json:string></articleId><language><json:string>eng</json:string></language><abstract>Proton magnetic resonance spectroscopy, localized to the lentiform nucleus, was carried out in 7 patients with the pure or predominantly striatonigral variant (SND) of multiple system atrophy (MSA), 5 patients with the olivopontocerebellar variant of MSA, 9 patients with a clinical diagnosis of idiopathic Parkinson's disease (IPD), and 9 healthy age‐matched controls. The MSA group with predominantly striatonigral involvement showed a significant reduction in the N‐acetylaspartate (NAA)/creatine ratio (median, 1.19; range, 0.96–2.0; p > 0.02) compared with the NAA/creatine ratio (median, 1.82; range, 1.19–2.31; p > 0.5). The NAA/creatine ratio was markedly reduced in 6 of the SND patients and in only 1 IPD patient. The choline/creatine ratio was also significantly lower in the SND group (median, 1.02; range, 0.91–1.23; p > 0.04) compared with the control group (median, 1.22; range, 1.05–1.65). The IPD group showed a normal lentiform choline/creatine ratio (median, 1.13; range, 0.89–1.65; p = 0.25) compared with controls. The olivopontocerebellar group also showed a significant reduction in the NAA/creatine ratio from the lentiform nucleus (median, 1.47; range, 1.22–1.68; p > 0.01) compared with the controls as well as a nonsignificant reduction in the choline/creatine ratio (median, 0.93; range, 0.85–1.27; p > 0.4). In vivo quantification of absolute metabolite concentrations was possible in 7 MSA patients and 6 controls and confirmed an absolute reduction of choline‐containing compounds and NAA in the MSA group compared with controls with no significant difference in the creatine concentrations between the MSA groups probably reflects neuronal loss, occurring predominantly in the putamen. Proton magnetic resonance spectroscopy is a useful, noninvasive technique to help differentiate MSA from IPD.</abstract><qualityIndicators><score>7.546</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1827</abstractCharCount><pdfWordCount>4546</pdfWordCount><pdfCharCount>27214</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>264</abstractWordCount></qualityIndicators><title>Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy</title><genre><json:string>article</json:string></genre><host><volume>37</volume><publisherId><json:string>ANA</json:string></publisherId><pages><total>7</total><last>210</last><first>204</first></pages><issn><json:string>0364-5134</json:string></issn><issue>2</issue><subject><json:item><value>Original Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8249</json:string></eissn><title>Annals of Neurology</title><doi><json:string>10.1002/(ISSN)1531-8249</json:string></doi></host><publicationDate>1995</publicationDate><copyrightDate>1995</copyrightDate><doi><json:string>10.1002/ana.410370211</json:string></doi><id>0A717A31E4D3E56D589EF2037186AA64751C9431</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/0A717A31E4D3E56D589EF2037186AA64751C9431/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/0A717A31E4D3E56D589EF2037186AA64751C9431/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/0A717A31E4D3E56D589EF2037186AA64751C9431/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>1995</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy</title><author><persName><forename type="first">C. A.</forename><surname>Davie</surname></persName><roleName type="degree">MRCP</roleName><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author><author><persName><forename type="first">G. K.</forename><surname>Wenning</surname></persName><roleName type="degree">MD</roleName><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author><author><persName><forename type="first">G. J.</forename><surname>Barker</surname></persName><roleName type="degree">PhD</roleName><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author><author><persName><forename type="first">P. S.</forename><surname>Tofts</surname></persName><roleName type="degree">D Phil</roleName><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author><author><persName><forename type="first">B. E.</forename><surname>Kendall</surname></persName><roleName type="degree">FRCR</roleName><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author><author><persName><forename type="first">N.</forename><surname>Quinn</surname></persName><roleName type="degree">MD</roleName><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author><author><persName><forename type="first">W. I.</forename><surname>McDonald</surname></persName><roleName type="degree">PhD</roleName><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author><author><persName><forename type="first">C. D.</forename><surname>Marsden</surname></persName><roleName type="degree">DSc</roleName><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author><author><persName><forename type="first">D. H.</forename><surname>Miller</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: NMR Research Group, Institute of Neurology, Queen Square House, London WCIN 3BG, UK</p></note><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-02"></date><biblScope unit="volume">37</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="204">204</biblScope><biblScope unit="page" to="210">210</biblScope></imprint></monogr><idno type="istex">0A717A31E4D3E56D589EF2037186AA64751C9431</idno><idno type="DOI">10.1002/ana.410370211</idno><idno type="ArticleID">ANA410370211</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Proton magnetic resonance spectroscopy, localized to the lentiform nucleus, was carried out in 7 patients with the pure or predominantly striatonigral variant (SND) of multiple system atrophy (MSA), 5 patients with the olivopontocerebellar variant of MSA, 9 patients with a clinical diagnosis of idiopathic Parkinson's disease (IPD), and 9 healthy age‐matched controls. The MSA group with predominantly striatonigral involvement showed a significant reduction in the N‐acetylaspartate (NAA)/creatine ratio (median, 1.19; range, 0.96–2.0; p < 0.02) compared with the NAA/creatine ratio (median, 1.82; range, 1.19–2.31; p > 0.5). The NAA/creatine ratio was markedly reduced in 6 of the SND patients and in only 1 IPD patient. The choline/creatine ratio was also significantly lower in the SND group (median, 1.02; range, 0.91–1.23; p < 0.04) compared with the control group (median, 1.22; range, 1.05–1.65). The IPD group showed a normal lentiform choline/creatine ratio (median, 1.13; range, 0.89–1.65; p = 0.25) compared with controls. The olivopontocerebellar group also showed a significant reduction in the NAA/creatine ratio from the lentiform nucleus (median, 1.47; range, 1.22–1.68; p < 0.01) compared with the controls as well as a nonsignificant reduction in the choline/creatine ratio (median, 0.93; range, 0.85–1.27; p < 0.4). In vivo quantification of absolute metabolite concentrations was possible in 7 MSA patients and 6 controls and confirmed an absolute reduction of choline‐containing compounds and NAA in the MSA group compared with controls with no significant difference in the creatine concentrations between the MSA groups probably reflects neuronal loss, occurring predominantly in the putamen. Proton magnetic resonance spectroscopy is a useful, noninvasive technique to help differentiate MSA from IPD.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-03-31">Received</change><change when="1994-08-11">Registration</change><change when="1995-02">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0A717A31E4D3E56D589EF2037186AA64751C9431/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)1531-8249</doi><issn type="print">0364-5134</issn><issn type="electronic">1531-8249</issn><idGroup><id type="product" value="ANA"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="ANNALS OF NEUROLOGY">Annals of Neurology</title><title type="subtitle">Official Journal of the American Neurological Association and the Child Neurology Society</title><title type="short">Ann Neurol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="20"><doi origin="wiley" registered="yes">10.1002/ana.v37:2</doi><numberingGroup><numbering type="journalVolume" number="37">37</numbering><numbering type="journalIssue">2</numbering></numberingGroup><coverDate startDate="1995-02">February 1995</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="11" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ana.410370211</doi><idGroup><id type="unit" value="ANA410370211"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1995 American Neurological Association</copyright><eventGroup><event type="manuscriptReceived" date="1994-03-31"></event><event type="manuscriptRevised" date="1994-08-05"></event><event type="manuscriptAccepted" date="1994-08-11"></event><event type="firstOnline" date="2004-10-08"></event><event type="publishedOnlineFinalForm" date="2004-10-08"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.1 mode:FullText source:HeaderRef result:HeaderRef" date="2010-02-23"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst">204</numbering><numbering type="pageLast">210</numbering></numberingGroup><correspondenceTo>NMR Research Group, Institute of Neurology, Queen Square House, London WCIN 3BG, UK</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA410370211.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="40"></count></countGroup><titleGroup><title type="main" xml:lang="en">Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy</title><title type="short" xml:lang="en">Differentiation by Proton MRS</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>C. A.</givenNames><familyName>Davie</familyName><degrees>MRCP</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>G. K.</givenNames><familyName>Wenning</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>G. J.</givenNames><familyName>Barker</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>P. S.</givenNames><familyName>Tofts</familyName><degrees>D Phil</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>B. E.</givenNames><familyName>Kendall</familyName><degrees>FRCR</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>N.</givenNames><familyName>Quinn</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>W. I.</givenNames><familyName>McDonald</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>C. D.</givenNames><familyName>Marsden</familyName><degrees>DSc</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>D. H.</givenNames><familyName>Miller</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Proton magnetic resonance spectroscopy, localized to the lentiform nucleus, was carried out in 7 patients with the pure or predominantly striatonigral variant (SND) of multiple system atrophy (MSA), 5 patients with the olivopontocerebellar variant of MSA, 9 patients with a clinical diagnosis of idiopathic Parkinson's disease (IPD), and 9 healthy age‐matched controls. The MSA group with predominantly striatonigral involvement showed a significant reduction in the <i>N</i>‐acetylaspartate (NAA)/creatine ratio (median, 1.19; range, 0.96–2.0; <i>p</i> < 0.02) compared with the NAA/creatine ratio (median, 1.82; range, 1.19–2.31; <i>p</i> > 0.5). The NAA/creatine ratio was markedly reduced in 6 of the SND patients and in only 1 IPD patient. The choline/creatine ratio was also significantly lower in the SND group (median, 1.02; range, 0.91–1.23; <i>p</i> < 0.04) compared with the control group (median, 1.22; range, 1.05–1.65). The IPD group showed a normal lentiform choline/creatine ratio (median, 1.13; range, 0.89–1.65; <i>p</i> = 0.25) compared with controls. The olivopontocerebellar group also showed a significant reduction in the NAA/creatine ratio from the lentiform nucleus (median, 1.47; range, 1.22–1.68; <i>p</i> < 0.01) compared with the controls as well as a nonsignificant reduction in the choline/creatine ratio (median, 0.93; range, 0.85–1.27; <i>p</i> < 0.4). In vivo quantification of absolute metabolite concentrations was possible in 7 MSA patients and 6 controls and confirmed an absolute reduction of choline‐containing compounds and NAA in the MSA group compared with controls with no significant difference in the creatine concentrations between the MSA groups probably reflects neuronal loss, occurring predominantly in the putamen. Proton magnetic resonance spectroscopy is a useful, noninvasive technique to help differentiate MSA from IPD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Differentiation by Proton MRS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy</title></titleInfo><name type="personal"><namePart type="given">C. A.</namePart><namePart type="family">Davie</namePart><namePart type="termsOfAddress">MRCP</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G. K.</namePart><namePart type="family">Wenning</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G. J.</namePart><namePart type="family">Barker</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P. S.</namePart><namePart type="family">Tofts</namePart><namePart type="termsOfAddress">D Phil</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B. E.</namePart><namePart type="family">Kendall</namePart><namePart type="termsOfAddress">FRCR</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Quinn</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W. I.</namePart><namePart type="family">McDonald</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. D.</namePart><namePart type="family">Marsden</namePart><namePart type="termsOfAddress">DSc</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. H.</namePart><namePart type="family">Miller</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>From the Department of Clinical Neurology, Institute of Neurology, London, UK</affiliation><description>Correspondence: NMR Research Group, Institute of Neurology, Queen Square House, London WCIN 3BG, UK</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">1995-02</dateIssued><dateCaptured encoding="w3cdtf">1994-03-31</dateCaptured><dateValid encoding="w3cdtf">1994-08-11</dateValid><copyrightDate encoding="w3cdtf">1995</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">3</extent><extent unit="references">40</extent></physicalDescription><abstract lang="en">Proton magnetic resonance spectroscopy, localized to the lentiform nucleus, was carried out in 7 patients with the pure or predominantly striatonigral variant (SND) of multiple system atrophy (MSA), 5 patients with the olivopontocerebellar variant of MSA, 9 patients with a clinical diagnosis of idiopathic Parkinson's disease (IPD), and 9 healthy age‐matched controls. The MSA group with predominantly striatonigral involvement showed a significant reduction in the N‐acetylaspartate (NAA)/creatine ratio (median, 1.19; range, 0.96–2.0; p < 0.02) compared with the NAA/creatine ratio (median, 1.82; range, 1.19–2.31; p > 0.5). The NAA/creatine ratio was markedly reduced in 6 of the SND patients and in only 1 IPD patient. The choline/creatine ratio was also significantly lower in the SND group (median, 1.02; range, 0.91–1.23; p < 0.04) compared with the control group (median, 1.22; range, 1.05–1.65). The IPD group showed a normal lentiform choline/creatine ratio (median, 1.13; range, 0.89–1.65; p = 0.25) compared with controls. The olivopontocerebellar group also showed a significant reduction in the NAA/creatine ratio from the lentiform nucleus (median, 1.47; range, 1.22–1.68; p < 0.01) compared with the controls as well as a nonsignificant reduction in the choline/creatine ratio (median, 0.93; range, 0.85–1.27; p < 0.4). In vivo quantification of absolute metabolite concentrations was possible in 7 MSA patients and 6 controls and confirmed an absolute reduction of choline‐containing compounds and NAA in the MSA group compared with controls with no significant difference in the creatine concentrations between the MSA groups probably reflects neuronal loss, occurring predominantly in the putamen. Proton magnetic resonance spectroscopy is a useful, noninvasive technique to help differentiate MSA from IPD.</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>37</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>204</start><end>210</end><total>7</total></extent></part></relatedItem><identifier type="istex">0A717A31E4D3E56D589EF2037186AA64751C9431</identifier><identifier type="DOI">10.1002/ana.410370211</identifier><identifier type="ArticleID">ANA410370211</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1995 American Neurological Association</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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