Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease
Identifieur interne : 000977 ( Main/Corpus ); précédent : 000976; suivant : 000978Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease
Auteurs : Richard M. Camicioli ; Christopher C. Hanstock ; Thomas P. Bouchard ; Myrlene Gee ; Nancy J. Fisher ; W. R. Wayne MartinSource :
- Movement Disorders [ 0885-3185 ] ; 2007-02-15.
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Abstract
The anterior cingulate (AC) gyrus and the presupplementary motor area (pre‐SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.21288
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Hanstock</name><affiliation><mods:affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Bouchard, Thomas P" sort="Bouchard, Thomas P" uniqKey="Bouchard T" first="Thomas P." last="Bouchard">Thomas P. Bouchard</name><affiliation><mods:affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gee, Myrlene" sort="Gee, Myrlene" uniqKey="Gee M" first="Myrlene" last="Gee">Myrlene Gee</name><affiliation><mods:affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Fisher, Nancy J" sort="Fisher, Nancy J" uniqKey="Fisher N" first="Nancy J." last="Fisher">Nancy J. 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Camicioli</name><affiliation><mods:affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Hanstock, Christopher C" sort="Hanstock, Christopher C" uniqKey="Hanstock C" first="Christopher C." last="Hanstock">Christopher C. Hanstock</name><affiliation><mods:affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Bouchard, Thomas P" sort="Bouchard, Thomas P" uniqKey="Bouchard T" first="Thomas P." last="Bouchard">Thomas P. Bouchard</name><affiliation><mods:affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gee, Myrlene" sort="Gee, Myrlene" uniqKey="Gee M" first="Myrlene" last="Gee">Myrlene Gee</name><affiliation><mods:affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Fisher, Nancy J" sort="Fisher, Nancy J" uniqKey="Fisher N" first="Nancy J." last="Fisher">Nancy J. Fisher</name><affiliation><mods:affiliation>Division of Neurosciences, University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Martin, W R Wayne" sort="Martin, W R Wayne" uniqKey="Martin W" first="W. R. Wayne" last="Martin">W. R. Wayne Martin</name><affiliation><mods:affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</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. 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We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Richard M. Camicioli MD</name><affiliations><json:string>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Christopher C. Hanstock PhD</name><affiliations><json:string>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Thomas P. Bouchard BSc</name><affiliations><json:string>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Myrlene Gee PhD</name><affiliations><json:string>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Nancy J. Fisher PhD</name><affiliations><json:string>Division of Neurosciences, University of Alberta, Edmonton, Alberta, Canada</json:string></affiliations></json:item><json:item><name>W.R. 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We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. 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Wayne</forename><surname>Martin</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</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. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-02-15"></date><biblScope unit="volume">22</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="382">382</biblScope><biblScope unit="page" to="386">386</biblScope></imprint></monogr><idno type="istex">A0C2A1BAA3D06B7A30213F50E081DC25E4BEBBFA</idno><idno type="DOI">10.1002/mds.21288</idno><idno type="ArticleID">MDS21288</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The anterior cingulate (AC) gyrus and the presupplementary motor area (pre‐SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD. © 2006 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>magnetic resonance spectroscopy</term></item><item><term>motor signs</term></item><item><term>Unified Parkinson's Disease Rating Scale</term></item><item><term>Hoehn and Yahr Rating</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-06-06">Received</change><change when="2006-09-25">Registration</change><change when="2007-02-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/A0C2A1BAA3D06B7A30213F50E081DC25E4BEBBFA/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Wayne</givenNames><familyName>Martin</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>Division of Neurosciences, University of Alberta, Edmonton, Alberta, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">magnetic resonance spectroscopy</keyword><keyword xml:id="kwd3">motor signs</keyword><keyword xml:id="kwd4">Unified Parkinson's Disease Rating Scale</keyword><keyword xml:id="kwd5">Hoehn and Yahr Rating</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The anterior cingulate (AC) gyrus and the presupplementary motor area (pre‐SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; <i>P</i> = 0.045) and correlated negatively with age (r = 0.39; <i>P</i> = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (<i>P</i> > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Magnetic Resonance Spectroscopic Evidence</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Richard M.</namePart><namePart type="family">Camicioli</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</affiliation><description>Correspondence: E223, Glenrose Rehabilitation Hospital, 10230 111th Avenue, Edmonton, AB T5G 0B7, Canada</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christopher C.</namePart><namePart type="family">Hanstock</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas P.</namePart><namePart type="family">Bouchard</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Myrlene</namePart><namePart type="family">Gee</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nancy J.</namePart><namePart type="family">Fisher</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Division of Neurosciences, University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.R. Wayne</namePart><namePart type="family">Martin</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta, Canada</affiliation><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">2007-02-15</dateIssued><dateCaptured encoding="w3cdtf">2006-06-06</dateCaptured><dateValid encoding="w3cdtf">2006-09-25</dateValid><copyrightDate encoding="w3cdtf">2007</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">1</extent><extent unit="tables">2</extent><extent unit="references">36</extent><extent unit="words">3392</extent></physicalDescription><abstract lang="en">The anterior cingulate (AC) gyrus and the presupplementary motor area (pre‐SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD. © 2006 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>magnetic resonance spectroscopy</topic><topic>motor signs</topic><topic>Unified Parkinson's Disease Rating Scale</topic><topic>Hoehn and Yahr Rating</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><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research 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>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>382</start><end>386</end><total>5</total></extent></part></relatedItem><identifier type="istex">A0C2A1BAA3D06B7A30213F50E081DC25E4BEBBFA</identifier><identifier type="DOI">10.1002/mds.21288</identifier><identifier type="ArticleID">MDS21288</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Movement Disorder Society</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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