Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy
Identifieur interne : 000670 ( Main/Corpus ); précédent : 000669; suivant : 000671Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy
Auteurs : C. A. Guevara ; C. R. Blain ; D. Stahl ; D. J. Lythgoe ; P. N. Leigh ; G. J. BarkerSource :
- European Journal of Neurology [ 1351-5101 ] ; 2010-09.
English descriptors
- KwdEn :
Abstract
Background and purpose: Magnetic resonance spectroscopy (MRS) allows the measurement of a number of brain tissue metabolites in vivo, including N‐acetylaspartate (NAA), a putative marker of neuronal integrity. Unlike single voxel MRS, magnetic resonance spectroscopic imaging (MRSI) enables quantification of these metabolites simultaneously from multiple anatomically localized voxels. Both single voxel MRS and MRSI allow the absolute quantification of these metabolites and, when combined with tissue segmentation, can give accurate metabolite concentrations even in the presence of partial volume effects from nearby cerebrospinal fluid. Methods: Using MRSI with cubic voxels with a nominal volume of 1.0 cm3, we tested the hypothesis that concentrations of NAA in the basal ganglia in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) would show differences compared to Parkinson’s disease (IPD). NAA values (in mM) from MRSI voxels centred to the putamen, pallidum and thalamus were obtained from 11 patients with IPD, 11 with MSA‐P, six with MSA‐C, 13 with PSP and 18 controls. The mean concentrations of NAA and its bulk grey and white matter values were also estimated over the whole brain slab. Results: N‐acetylaspartate concentrations in the pallidum, putamen and lentiform nucleus were significantly lower in patients with MSA‐P and PSP compared to IPD and controls. The putaminal values were also significantly reduced in PSP compared to MSA‐P. There were no significant differences between groups in the thalamus and over the whole brain slab. Conclusion: Our findings support the notion that MRSI can potentially quantify basal ganglia cellular pathology in MSA and PSP.
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DOI: 10.1111/j.1468-1331.2010.03010.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy</title><author><name sortKey="Guevara, C A" sort="Guevara, C A" uniqKey="Guevara C" first="C. A." last="Guevara">C. A. Guevara</name><affiliation><mods:affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</mods:affiliation></affiliation></author><author><name sortKey="Blain, C R" sort="Blain, C R" uniqKey="Blain C" first="C. R." last="Blain">C. R. Blain</name><affiliation><mods:affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</mods:affiliation></affiliation></author><author><name sortKey="Stahl, D" sort="Stahl, D" uniqKey="Stahl D" first="D." last="Stahl">D. Stahl</name><affiliation><mods:affiliation>Department of Biostatistics and Computing, King’s College London, Institute of Psychiatry, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Lythgoe, D J" sort="Lythgoe, D J" uniqKey="Lythgoe D" first="D. J." last="Lythgoe">D. J. Lythgoe</name><affiliation><mods:affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</mods:affiliation></affiliation></author><author><name sortKey="Leigh, P N" sort="Leigh, P N" uniqKey="Leigh P" first="P. N." last="Leigh">P. N. Leigh</name><affiliation><mods:affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</mods:affiliation></affiliation></author><author><name sortKey="Barker, G J" sort="Barker, G J" uniqKey="Barker G" first="G. J." last="Barker">G. J. 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Guevara</name><affiliation><mods:affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</mods:affiliation></affiliation></author><author><name sortKey="Blain, C R" sort="Blain, C R" uniqKey="Blain C" first="C. R." last="Blain">C. R. Blain</name><affiliation><mods:affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</mods:affiliation></affiliation></author><author><name sortKey="Stahl, D" sort="Stahl, D" uniqKey="Stahl D" first="D." last="Stahl">D. Stahl</name><affiliation><mods:affiliation>Department of Biostatistics and Computing, King’s College London, Institute of Psychiatry, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Lythgoe, D J" sort="Lythgoe, D J" uniqKey="Lythgoe D" first="D. J." last="Lythgoe">D. J. Lythgoe</name><affiliation><mods:affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</mods:affiliation></affiliation></author><author><name sortKey="Leigh, P N" sort="Leigh, P N" uniqKey="Leigh P" first="P. N." last="Leigh">P. N. Leigh</name><affiliation><mods:affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</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>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neurology</title><idno type="ISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-09">2010-09</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1193">1193</biblScope><biblScope unit="page" to="1202">1202</biblScope></imprint><idno type="ISSN">1351-5101</idno></series><idno type="istex">6AB28CC0CC4AADC40AF8E7E78A31772B8CBB657E</idno><idno type="DOI">10.1111/j.1468-1331.2010.03010.x</idno><idno type="ArticleID">ENE3010</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1351-5101</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson disease</term><term>magnetic resonance spectroscopic imaging</term><term>multiple system atrophy</term><term>progressive supranuclear palsy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background and purpose: Magnetic resonance spectroscopy (MRS) allows the measurement of a number of brain tissue metabolites in vivo, including N‐acetylaspartate (NAA), a putative marker of neuronal integrity. Unlike single voxel MRS, magnetic resonance spectroscopic imaging (MRSI) enables quantification of these metabolites simultaneously from multiple anatomically localized voxels. Both single voxel MRS and MRSI allow the absolute quantification of these metabolites and, when combined with tissue segmentation, can give accurate metabolite concentrations even in the presence of partial volume effects from nearby cerebrospinal fluid. Methods: Using MRSI with cubic voxels with a nominal volume of 1.0 cm3, we tested the hypothesis that concentrations of NAA in the basal ganglia in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) would show differences compared to Parkinson’s disease (IPD). NAA values (in mM) from MRSI voxels centred to the putamen, pallidum and thalamus were obtained from 11 patients with IPD, 11 with MSA‐P, six with MSA‐C, 13 with PSP and 18 controls. The mean concentrations of NAA and its bulk grey and white matter values were also estimated over the whole brain slab. Results: N‐acetylaspartate concentrations in the pallidum, putamen and lentiform nucleus were significantly lower in patients with MSA‐P and PSP compared to IPD and controls. The putaminal values were also significantly reduced in PSP compared to MSA‐P. There were no significant differences between groups in the thalamus and over the whole brain slab. Conclusion: Our findings support the notion that MRSI can potentially quantify basal ganglia cellular pathology in MSA and PSP.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>C. A. Guevara</name><affiliations><json:string>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</json:string></affiliations></json:item><json:item><name>C. R. Blain</name><affiliations><json:string>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</json:string></affiliations></json:item><json:item><name>D. Stahl</name><affiliations><json:string>Department of Biostatistics and Computing, King’s College London, Institute of Psychiatry, London, UK</json:string></affiliations></json:item><json:item><name>D. J. Lythgoe</name><affiliations><json:string>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</json:string></affiliations></json:item><json:item><name>P. N. Leigh</name><affiliations><json:string>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</json:string></affiliations></json:item><json:item><name>G. J. Barker</name><affiliations><json:string>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>magnetic resonance spectroscopic imaging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>multiple system atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>progressive supranuclear palsy</value></json:item></subject><articleId><json:string>ENE3010</json:string></articleId><language><json:string>eng</json:string></language><abstract>Background and purpose: Magnetic resonance spectroscopy (MRS) allows the measurement of a number of brain tissue metabolites in vivo, including N‐acetylaspartate (NAA), a putative marker of neuronal integrity. Unlike single voxel MRS, magnetic resonance spectroscopic imaging (MRSI) enables quantification of these metabolites simultaneously from multiple anatomically localized voxels. Both single voxel MRS and MRSI allow the absolute quantification of these metabolites and, when combined with tissue segmentation, can give accurate metabolite concentrations even in the presence of partial volume effects from nearby cerebrospinal fluid. Methods: Using MRSI with cubic voxels with a nominal volume of 1.0 cm3, we tested the hypothesis that concentrations of NAA in the basal ganglia in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) would show differences compared to Parkinson’s disease (IPD). NAA values (in mM) from MRSI voxels centred to the putamen, pallidum and thalamus were obtained from 11 patients with IPD, 11 with MSA‐P, six with MSA‐C, 13 with PSP and 18 controls. The mean concentrations of NAA and its bulk grey and white matter values were also estimated over the whole brain slab. Results: N‐acetylaspartate concentrations in the pallidum, putamen and lentiform nucleus were significantly lower in patients with MSA‐P and PSP compared to IPD and controls. The putaminal values were also significantly reduced in PSP compared to MSA‐P. There were no significant differences between groups in the thalamus and over the whole brain slab. Conclusion: Our findings support the notion that MRSI can potentially quantify basal ganglia cellular pathology in MSA and PSP.</abstract><qualityIndicators><score>7.893</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1711</abstractCharCount><pdfWordCount>4893</pdfWordCount><pdfCharCount>31637</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>251</abstractWordCount></qualityIndicators><title>Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy</title><genre><json:string>article</json:string></genre><host><volume>17</volume><publisherId><json:string>ENE</json:string></publisherId><pages><total>10</total><last>1202</last><first>1193</first></pages><issn><json:string>1351-5101</json:string></issn><issue>9</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-1331</json:string></eissn><title>European Journal of Neurology</title><doi><json:string>10.1111/(ISSN)1468-1331</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1111/j.1468-1331.2010.03010.x</json:string></doi><id>6AB28CC0CC4AADC40AF8E7E78A31772B8CBB657E</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6AB28CC0CC4AADC40AF8E7E78A31772B8CBB657E/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6AB28CC0CC4AADC40AF8E7E78A31772B8CBB657E/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6AB28CC0CC4AADC40AF8E7E78A31772B8CBB657E/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy</title><author><persName><forename type="first">C. A.</forename><surname>Guevara</surname></persName><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation></author><author><persName><forename type="first">C. R.</forename><surname>Blain</surname></persName><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation></author><author><persName><forename type="first">D.</forename><surname>Stahl</surname></persName><affiliation>Department of Biostatistics and Computing, King’s College London, Institute of Psychiatry, London, UK</affiliation></author><author><persName><forename type="first">D. J.</forename><surname>Lythgoe</surname></persName><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation></author><author><persName><forename type="first">P. N.</forename><surname>Leigh</surname></persName><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation></author><author><persName><forename type="first">G. J.</forename><surname>Barker</surname></persName><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation></author></analytic><monogr><title level="j">European Journal of Neurology</title><idno type="pISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><idno type="DOI">10.1111/(ISSN)1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-09"></date><biblScope unit="volume">17</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1193">1193</biblScope><biblScope unit="page" to="1202">1202</biblScope></imprint></monogr><idno type="istex">6AB28CC0CC4AADC40AF8E7E78A31772B8CBB657E</idno><idno type="DOI">10.1111/j.1468-1331.2010.03010.x</idno><idno type="ArticleID">ENE3010</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background and purpose: Magnetic resonance spectroscopy (MRS) allows the measurement of a number of brain tissue metabolites in vivo, including N‐acetylaspartate (NAA), a putative marker of neuronal integrity. Unlike single voxel MRS, magnetic resonance spectroscopic imaging (MRSI) enables quantification of these metabolites simultaneously from multiple anatomically localized voxels. Both single voxel MRS and MRSI allow the absolute quantification of these metabolites and, when combined with tissue segmentation, can give accurate metabolite concentrations even in the presence of partial volume effects from nearby cerebrospinal fluid. Methods: Using MRSI with cubic voxels with a nominal volume of 1.0 cm3, we tested the hypothesis that concentrations of NAA in the basal ganglia in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) would show differences compared to Parkinson’s disease (IPD). NAA values (in mM) from MRSI voxels centred to the putamen, pallidum and thalamus were obtained from 11 patients with IPD, 11 with MSA‐P, six with MSA‐C, 13 with PSP and 18 controls. The mean concentrations of NAA and its bulk grey and white matter values were also estimated over the whole brain slab. Results: N‐acetylaspartate concentrations in the pallidum, putamen and lentiform nucleus were significantly lower in patients with MSA‐P and PSP compared to IPD and controls. The putaminal values were also significantly reduced in PSP compared to MSA‐P. There were no significant differences between groups in the thalamus and over the whole brain slab. Conclusion: Our findings support the notion that MRSI can potentially quantify basal ganglia cellular pathology in MSA and PSP.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>magnetic resonance spectroscopic imaging</term></item><item><term>multiple system atrophy</term></item><item><term>Parkinson disease</term></item><item><term>progressive supranuclear palsy</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6AB28CC0CC4AADC40AF8E7E78A31772B8CBB657E/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1468-1331</doi><issn type="print">1351-5101</issn><issn type="electronic">1468-1331</issn><idGroup><id type="product" value="ENE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROLOGY">European Journal of Neurology</title></titleGroup></publicationMeta><publicationMeta level="part" position="09109"><doi origin="wiley">10.1111/ene.2010.17.issue-9</doi><numberingGroup><numbering type="journalVolume" number="17">17</numbering><numbering type="journalIssue" number="9">9</numbering></numberingGroup><coverDate startDate="2010-09">September 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="12" status="forIssue"><doi origin="wiley">10.1111/j.1468-1331.2010.03010.x</doi><idGroup><id type="unit" value="ENE3010"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><copyright>© 2010 The Author(s). European Journal of Neurology © 2010 EFNS</copyright><eventGroup><event type="firstOnline" date="2010-04-14"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2010-04-14"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.25 mode:FullText source:FullText result:FullText" date="2010-11-05"></event><event type="publishedOnlineFinalForm" date="2010-08-16"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-17"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1193">1193</numbering><numbering type="pageLast" number="1202">1202</numbering></numberingGroup><correspondenceTo>Prof. P. Nigel Leigh, King’s College London, Institute of Psychiatry, PO 41, London SE5 8AF, UK (tel.: +44(0)20 7848 5187; fax: +44(0)20 7848 5186; e‐mail: <email>n.leigh@kcl.ac.uk</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE3010.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 23 July 2009 Accepted 26 January 2010</unparsedEditorialHistory><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="3"></count></countGroup><titleGroup><title type="main">Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy</title><title type="shortAuthors">C. A. Guevara <i>et al.</i></title><title type="short">Quantitative magnetic resonance spectroscopic imaging in Parkinson plus syndromes</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>C. A.</givenNames><familyName>Guevara</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>C. R.</givenNames><familyName>Blain</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>D.</givenNames><familyName>Stahl</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>D. J.</givenNames><familyName>Lythgoe</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>P. N.</givenNames><familyName>Leigh</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>G. J.</givenNames><familyName>Barker</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="GB"><unparsedAffiliation>Department of Biostatistics and Computing, King’s College London, Institute of Psychiatry, London, UK</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">magnetic resonance spectroscopic imaging</keyword><keyword xml:id="k2">multiple system atrophy</keyword><keyword xml:id="k3">Parkinson disease</keyword><keyword xml:id="k4">progressive supranuclear palsy</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Background and purpose: </b> Magnetic resonance spectroscopy (MRS) allows the measurement of a number of brain tissue metabolites <i>in vivo</i>, including N‐acetylaspartate (NAA), a putative marker of neuronal integrity. Unlike single voxel MRS, magnetic resonance spectroscopic imaging (MRSI) enables quantification of these metabolites simultaneously from multiple anatomically localized voxels. Both single voxel MRS and MRSI allow the absolute quantification of these metabolites and, when combined with tissue segmentation, can give accurate metabolite concentrations even in the presence of partial volume effects from nearby cerebrospinal fluid.</p><p><b>Methods: </b> Using MRSI with cubic voxels with a nominal volume of 1.0 cm<sup>3</sup>, we tested the hypothesis that concentrations of NAA in the basal ganglia in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) would show differences compared to Parkinson’s disease (IPD). NAA values (in <i>mM</i>) from MRSI voxels centred to the putamen, pallidum and thalamus were obtained from 11 patients with IPD, 11 with MSA‐P, six with MSA‐C, 13 with PSP and 18 controls. The mean concentrations of NAA and its bulk grey and white matter values were also estimated over the whole brain slab.</p><p><b>Results: </b> N‐acetylaspartate concentrations in the pallidum, putamen and lentiform nucleus were significantly lower in patients with MSA‐P and PSP compared to IPD and controls. The putaminal values were also significantly reduced in PSP compared to MSA‐P. There were no significant differences between groups in the thalamus and over the whole brain slab.</p><p><b>Conclusion: </b> Our findings support the notion that MRSI can potentially quantify basal ganglia cellular pathology in MSA and PSP.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy</title></titleInfo><titleInfo type="abbreviated"><title>Quantitative magnetic resonance spectroscopic imaging in Parkinson plus syndromes</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Quantitative magnetic resonance spectroscopic imaging in Parkinson’s disease, progressive supranuclear palsy and multiple system atrophy</title></titleInfo><name type="personal"><namePart type="given">C. A.</namePart><namePart type="family">Guevara</namePart><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. R.</namePart><namePart type="family">Blain</namePart><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Stahl</namePart><affiliation>Department of Biostatistics and Computing, King’s College London, Institute of Psychiatry, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. J.</namePart><namePart type="family">Lythgoe</namePart><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P. N.</namePart><namePart type="family">Leigh</namePart><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G. J.</namePart><namePart type="family">Barker</namePart><affiliation>Department of Clinical Neuroscience, King’s College London, Institute of Psychiatry, London</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-09</dateIssued><edition>Received 23 July 2009 Accepted 26 January 2010</edition><copyrightDate encoding="w3cdtf">2010</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="tables">3</extent></physicalDescription><abstract lang="en">Background and purpose: Magnetic resonance spectroscopy (MRS) allows the measurement of a number of brain tissue metabolites in vivo, including N‐acetylaspartate (NAA), a putative marker of neuronal integrity. Unlike single voxel MRS, magnetic resonance spectroscopic imaging (MRSI) enables quantification of these metabolites simultaneously from multiple anatomically localized voxels. Both single voxel MRS and MRSI allow the absolute quantification of these metabolites and, when combined with tissue segmentation, can give accurate metabolite concentrations even in the presence of partial volume effects from nearby cerebrospinal fluid. Methods: Using MRSI with cubic voxels with a nominal volume of 1.0 cm3, we tested the hypothesis that concentrations of NAA in the basal ganglia in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) would show differences compared to Parkinson’s disease (IPD). NAA values (in mM) from MRSI voxels centred to the putamen, pallidum and thalamus were obtained from 11 patients with IPD, 11 with MSA‐P, six with MSA‐C, 13 with PSP and 18 controls. The mean concentrations of NAA and its bulk grey and white matter values were also estimated over the whole brain slab. Results: N‐acetylaspartate concentrations in the pallidum, putamen and lentiform nucleus were significantly lower in patients with MSA‐P and PSP compared to IPD and controls. The putaminal values were also significantly reduced in PSP compared to MSA‐P. There were no significant differences between groups in the thalamus and over the whole brain slab. Conclusion: Our findings support the notion that MRSI can potentially quantify basal ganglia cellular pathology in MSA and PSP.</abstract><subject lang="en"><genre>Keywords</genre><topic>magnetic resonance spectroscopic imaging</topic><topic>multiple system atrophy</topic><topic>Parkinson disease</topic><topic>progressive supranuclear palsy</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1193</start><end>1202</end><total>10</total></extent></part></relatedItem><identifier type="istex">6AB28CC0CC4AADC40AF8E7E78A31772B8CBB657E</identifier><identifier type="DOI">10.1111/j.1468-1331.2010.03010.x</identifier><identifier type="ArticleID">ENE3010</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 The Author(s). 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