Combined R2* and Diffusion Tensor Imaging Changes in the Substantia Nigra in Parkinson's Disease
Identifieur interne : 001444 ( Main/Corpus ); précédent : 001443; suivant : 001445Combined R2* and Diffusion Tensor Imaging Changes in the Substantia Nigra in Parkinson's Disease
Auteurs : Guangwei Du ; Mechelle M. Lewis ; Martin Styner ; Michele L. Shaffer ; Suman Sen ; Qing X. Yang ; Xuemei HuangSource :
- Movement Disorders [ 0885-3185 ] ; 2011-08-01.
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Abstract
Recent magnetic resonance imaging studies suggest an increased transverse relaxation rate and reduced diffusion tensor imaging fractional anisotropy values in the substantia nigra in Parkinson's disease. The transverse relaxation rate and fractional anisotropy changes may reflect different aspects of Parkinson's disease‐related pathological processes (ie, tissue iron deposition and microstructure disorganization). This study investigated the combined changes of transverse relaxation rate and fractional anisotropy in the substantia nigra in Parkinson's disease. High‐resolution magnetic resonance imaging (T2‐weighted, T2*, and diffusion tensor imaging) were obtained from 16 Parkinson's disease patients and 16 controls. Bilateral substantia nigras were delineated manually on T2‐weighted images and coregistered to transverse relaxation rate and fractional anisotropy maps. The mean transverse relaxation rate and fractional anisotropy values in each substantia nigra were then calculated and compared between Parkinson's disease subjects and controls. Logistic regression, followed by receiver operating characteristic curve analysis, was employed to investigate the sensitivity and specificity of the combined measures for differentiating Parkinson's disease subjects from controls. Compared with controls, Parkinson's disease subjects demonstrated increased transverse relaxation rate (P < .0001) and reduced fractional anisotropy (P = .0365) in the substantia nigra. There was no significant correlation between transverse relaxation rate and fractional anisotropy values. Logistic regression analyses indicated that the combined use of transverse relaxation rate and fractional anisotropy values provides excellent discrimination between Parkinson's disease subjects and controls (c‐statistic = 0.996) compared with transverse relaxation rate (c‐statistic = 0.930) or fractional anisotropy (c‐statistic = 0.742) alone. This study shows that the combined use of transverse relaxation rate and fractional anisotropy measures in the substantia nigra of Parkinson's disease enhances sensitivity and specificity in differentiating Parkinson's disease from controls. Further studies are warranted to evaluate the pathophysiological correlations of these magnetic resonance imaging measurements and their effectiveness in assisting in diagnosing Parkinson's disease and following its progression. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23643
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The transverse relaxation rate and fractional anisotropy changes may reflect different aspects of Parkinson's disease‐related pathological processes (ie, tissue iron deposition and microstructure disorganization). This study investigated the combined changes of transverse relaxation rate and fractional anisotropy in the substantia nigra in Parkinson's disease. High‐resolution magnetic resonance imaging (T2‐weighted, T2*, and diffusion tensor imaging) were obtained from 16 Parkinson's disease patients and 16 controls. Bilateral substantia nigras were delineated manually on T2‐weighted images and coregistered to transverse relaxation rate and fractional anisotropy maps. The mean transverse relaxation rate and fractional anisotropy values in each substantia nigra were then calculated and compared between Parkinson's disease subjects and controls. Logistic regression, followed by receiver operating characteristic curve analysis, was employed to investigate the sensitivity and specificity of the combined measures for differentiating Parkinson's disease subjects from controls. Compared with controls, Parkinson's disease subjects demonstrated increased transverse relaxation rate (P < .0001) and reduced fractional anisotropy (P = .0365) in the substantia nigra. There was no significant correlation between transverse relaxation rate and fractional anisotropy values. Logistic regression analyses indicated that the combined use of transverse relaxation rate and fractional anisotropy values provides excellent discrimination between Parkinson's disease subjects and controls (c‐statistic = 0.996) compared with transverse relaxation rate (c‐statistic = 0.930) or fractional anisotropy (c‐statistic = 0.742) alone. This study shows that the combined use of transverse relaxation rate and fractional anisotropy measures in the substantia nigra of Parkinson's disease enhances sensitivity and specificity in differentiating Parkinson's disease from controls. Further studies are warranted to evaluate the pathophysiological correlations of these magnetic resonance imaging measurements and their effectiveness in assisting in diagnosing Parkinson's disease and following its progression. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Guangwei Du MD, PhD</name><affiliations><json:string>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</json:string></affiliations></json:item><json:item><name>Mechelle M. Lewis PhD</name><affiliations><json:string>Department of Neurology, Pennsylvania State University—Milton S. 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Hershey Medical Center, Hershey, Pennsylvania, USA</json:string><json:string>Department of Radiology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</json:string><json:string>Department of Neurosurgery, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</json:string><json:string>Department of Kinesiology, Pennsylvania State University—Milton S. 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The transverse relaxation rate and fractional anisotropy changes may reflect different aspects of Parkinson's disease‐related pathological processes (ie, tissue iron deposition and microstructure disorganization). This study investigated the combined changes of transverse relaxation rate and fractional anisotropy in the substantia nigra in Parkinson's disease. High‐resolution magnetic resonance imaging (T2‐weighted, T2*, and diffusion tensor imaging) were obtained from 16 Parkinson's disease patients and 16 controls. Bilateral substantia nigras were delineated manually on T2‐weighted images and coregistered to transverse relaxation rate and fractional anisotropy maps. The mean transverse relaxation rate and fractional anisotropy values in each substantia nigra were then calculated and compared between Parkinson's disease subjects and controls. Logistic regression, followed by receiver operating characteristic curve analysis, was employed to investigate the sensitivity and specificity of the combined measures for differentiating Parkinson's disease subjects from controls. Compared with controls, Parkinson's disease subjects demonstrated increased transverse relaxation rate (P > .0001) and reduced fractional anisotropy (P = .0365) in the substantia nigra. There was no significant correlation between transverse relaxation rate and fractional anisotropy values. Logistic regression analyses indicated that the combined use of transverse relaxation rate and fractional anisotropy values provides excellent discrimination between Parkinson's disease subjects and controls (c‐statistic = 0.996) compared with transverse relaxation rate (c‐statistic = 0.930) or fractional anisotropy (c‐statistic = 0.742) alone. This study shows that the combined use of transverse relaxation rate and fractional anisotropy measures in the substantia nigra of Parkinson's disease enhances sensitivity and specificity in differentiating Parkinson's disease from controls. Further studies are warranted to evaluate the pathophysiological correlations of these magnetic resonance imaging measurements and their effectiveness in assisting in diagnosing Parkinson's disease and following its progression. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>6.759</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>2434</abstractCharCount><pdfWordCount>3759</pdfWordCount><pdfCharCount>23365</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>307</abstractWordCount></qualityIndicators><title>Combined R2* and Diffusion Tensor Imaging Changes in the Substantia Nigra in Parkinson's Disease</title><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>6</total><last>1632</last><first>1627</first></pages><issn><json:string>0885-3185</json:string></issn><issue>9</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23643</json:string></doi><id>FF544EB4AB4D1F55FC1914AE8BB693388B2A1850</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/FF544EB4AB4D1F55FC1914AE8BB693388B2A1850/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/FF544EB4AB4D1F55FC1914AE8BB693388B2A1850/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/FF544EB4AB4D1F55FC1914AE8BB693388B2A1850/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Combined R2* and Diffusion Tensor Imaging Changes in the Substantia Nigra in Parkinson's Disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles can be found in the online version of this article.</note><note>Unknown funding agency - No. NS060722;</note><note>HMC GCRC - No. NIH M01RR10732;</note><note>GCRC Construction Grant - No. C06RR016499;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Combined R2* and Diffusion Tensor Imaging Changes in the Substantia Nigra in Parkinson's Disease</title><author><persName><forename type="first">Guangwei</forename><surname>Du</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation></author><author><persName><forename type="first">Mechelle M.</forename><surname>Lewis</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Pharmacology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation></author><author><persName><forename type="first">Martin</forename><surname>Styner</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Computer Science, University of North Carolina, Chapel Hill, North Carolina, USA</affiliation><affiliation>Department of Psychiatry, University of North Carolina, Chapel Hill, North Carolina, USA</affiliation></author><author><persName><forename type="first">Michele L.</forename><surname>Shaffer</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Public Health Sciences, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation></author><author><persName><forename type="first">Suman</forename><surname>Sen</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation></author><author><persName><forename type="first">Qing X.</forename><surname>Yang</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Radiology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Neurosurgery, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Bioengineering, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation></author><author><persName><forename type="first">Xuemei</forename><surname>Huang</surname></persName><roleName type="degree">MD, PhD</roleName><note type="correspondence"><p>Correspondence: Associate Professor of Neurology, Penn State Hershey Medical Center, 500 University Dr., H‐037, Hershey, PA 17033‐0850, USA</p></note><affiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Pharmacology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Radiology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Neurosurgery, Pennsylvania State University—Milton S. 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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="2011-08-01"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1627">1627</biblScope><biblScope unit="page" to="1632">1632</biblScope></imprint></monogr><idno type="istex">FF544EB4AB4D1F55FC1914AE8BB693388B2A1850</idno><idno type="DOI">10.1002/mds.23643</idno><idno type="ArticleID">MDS23643</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Recent magnetic resonance imaging studies suggest an increased transverse relaxation rate and reduced diffusion tensor imaging fractional anisotropy values in the substantia nigra in Parkinson's disease. The transverse relaxation rate and fractional anisotropy changes may reflect different aspects of Parkinson's disease‐related pathological processes (ie, tissue iron deposition and microstructure disorganization). This study investigated the combined changes of transverse relaxation rate and fractional anisotropy in the substantia nigra in Parkinson's disease. High‐resolution magnetic resonance imaging (T2‐weighted, T2*, and diffusion tensor imaging) were obtained from 16 Parkinson's disease patients and 16 controls. Bilateral substantia nigras were delineated manually on T2‐weighted images and coregistered to transverse relaxation rate and fractional anisotropy maps. The mean transverse relaxation rate and fractional anisotropy values in each substantia nigra were then calculated and compared between Parkinson's disease subjects and controls. Logistic regression, followed by receiver operating characteristic curve analysis, was employed to investigate the sensitivity and specificity of the combined measures for differentiating Parkinson's disease subjects from controls. Compared with controls, Parkinson's disease subjects demonstrated increased transverse relaxation rate (P < .0001) and reduced fractional anisotropy (P = .0365) in the substantia nigra. There was no significant correlation between transverse relaxation rate and fractional anisotropy values. Logistic regression analyses indicated that the combined use of transverse relaxation rate and fractional anisotropy values provides excellent discrimination between Parkinson's disease subjects and controls (c‐statistic = 0.996) compared with transverse relaxation rate (c‐statistic = 0.930) or fractional anisotropy (c‐statistic = 0.742) alone. This study shows that the combined use of transverse relaxation rate and fractional anisotropy measures in the substantia nigra of Parkinson's disease enhances sensitivity and specificity in differentiating Parkinson's disease from controls. Further studies are warranted to evaluate the pathophysiological correlations of these magnetic resonance imaging measurements and their effectiveness in assisting in diagnosing Parkinson's disease and following its progression. © 2011 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>substantia nigra</term></item><item><term>diffusion tensor imaging</term></item><item><term>transverse relaxation rate</term></item><item><term>magnetic resonance imaging</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="2010-08-20">Received</change><change when="2010-12-27">Registration</change><change when="2011-08-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/FF544EB4AB4D1F55FC1914AE8BB693388B2A1850/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="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="90"><doi origin="wiley" registered="yes">10.1002/mds.v26.9</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">9</numbering></numberingGroup><coverDate startDate="2011-08-01">1 August 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="90" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23643</doi><idGroup><id type="unit" value="MDS23643"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2011 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-08-20"></event><event type="manuscriptRevised" date="2010-12-15"></event><event type="manuscriptAccepted" date="2010-12-27"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.0.1 mode:FullText" date="2011-12-16"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-05-26"></event><event type="publishedOnlineFinalForm" date="2011-08-09"></event><event type="firstOnline" date="2011-05-26"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1627</numbering><numbering type="pageLast">1632</numbering></numberingGroup><correspondenceTo>Associate Professor of Neurology, Penn State Hershey Medical Center, 500 University Dr., H‐037, Hershey, PA 17033‐0850, USA</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23643.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="24"></count><count type="wordTotal" number="4619"></count></countGroup><titleGroup><title type="main" xml:lang="en">Combined R2* and Diffusion Tensor Imaging Changes in the Substantia Nigra in Parkinson's Disease<link href="#fn1"></link> <link href="#fn4"></link></title><title type="short" xml:lang="en">Iron AND FA Changes IN SN OF PD Patients</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Guangwei</givenNames><familyName>Du</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Mechelle M.</givenNames><familyName>Lewis</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3 #af4"><personName><givenNames>Martin</givenNames><familyName>Styner</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Michele L.</givenNames><familyName>Shaffer</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Suman</givenNames><familyName>Sen</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af6 #af7 #af8"><personName><givenNames>Qing X.</givenNames><familyName>Yang</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af2 #af6 #af7 #af9" corresponding="yes"><personName><givenNames>Xuemei</givenNames><familyName>Huang</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>xuemei@psu.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Pharmacology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Computer Science, University of North Carolina, Chapel Hill, North Carolina, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Psychiatry, University of North Carolina, Chapel Hill, North Carolina, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Public Health Sciences, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="US" type="organization"><unparsedAffiliation>Department of Radiology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurosurgery, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="US" type="organization"><unparsedAffiliation>Department of Bioengineering, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</unparsedAffiliation></affiliation><affiliation xml:id="af9" countryCode="US" type="organization"><unparsedAffiliation>Department of Kinesiology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">substantia nigra</keyword><keyword xml:id="kwd3">diffusion tensor imaging</keyword><keyword xml:id="kwd4">transverse relaxation rate</keyword><keyword xml:id="kwd5">magnetic resonance imaging</keyword></keywordGroup><fundingInfo><fundingAgency>Unknown funding agency</fundingAgency><fundingNumber>NS060722</fundingNumber></fundingInfo><fundingInfo><fundingAgency>HMC GCRC</fundingAgency><fundingNumber>NIH M01RR10732</fundingNumber></fundingInfo><fundingInfo><fundingAgency>GCRC Construction Grant</fundingAgency><fundingNumber>C06RR016499</fundingNumber></fundingInfo><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Recent magnetic resonance imaging studies suggest an increased transverse relaxation rate and reduced diffusion tensor imaging fractional anisotropy values in the substantia nigra in Parkinson's disease. The transverse relaxation rate and fractional anisotropy changes may reflect different aspects of Parkinson's disease‐related pathological processes (ie, tissue iron deposition and microstructure disorganization). This study investigated the combined changes of transverse relaxation rate and fractional anisotropy in the substantia nigra in Parkinson's disease. High‐resolution magnetic resonance imaging (T2‐weighted, T2*, and diffusion tensor imaging) were obtained from 16 Parkinson's disease patients and 16 controls. Bilateral substantia nigras were delineated manually on T2‐weighted images and coregistered to transverse relaxation rate and fractional anisotropy maps. The mean transverse relaxation rate and fractional anisotropy values in each substantia nigra were then calculated and compared between Parkinson's disease subjects and controls. Logistic regression, followed by receiver operating characteristic curve analysis, was employed to investigate the sensitivity and specificity of the combined measures for differentiating Parkinson's disease subjects from controls. Compared with controls, Parkinson's disease subjects demonstrated increased transverse relaxation rate (<i>P</i> < .0001) and reduced fractional anisotropy (<i>P</i> = .0365) in the substantia nigra. There was no significant correlation between transverse relaxation rate and fractional anisotropy values. Logistic regression analyses indicated that the combined use of transverse relaxation rate and fractional anisotropy values provides excellent discrimination between Parkinson's disease subjects and controls (c‐statistic = 0.996) compared with transverse relaxation rate (c‐statistic = 0.930) or fractional anisotropy (c‐statistic = 0.742) alone. This study shows that the combined use of transverse relaxation rate and fractional anisotropy measures in the substantia nigra of Parkinson's disease enhances sensitivity and specificity in differentiating Parkinson's disease from controls. Further studies are warranted to evaluate the pathophysiological correlations of these magnetic resonance imaging measurements and their effectiveness in assisting in diagnosing Parkinson's disease and following its progression. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="fn4"><p>Full financial disclosures and author roles can be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Combined R2* and Diffusion Tensor Imaging Changes in the Substantia Nigra in Parkinson's Disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Iron AND FA Changes IN SN OF PD Patients</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Combined R2* and Diffusion Tensor Imaging Changes in the Substantia Nigra in Parkinson's Disease</title></titleInfo><name type="personal"><namePart type="given">Guangwei</namePart><namePart type="family">Du</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mechelle M.</namePart><namePart type="family">Lewis</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Pharmacology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martin</namePart><namePart type="family">Styner</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Computer Science, University of North Carolina, Chapel Hill, North Carolina, USA</affiliation><affiliation>Department of Psychiatry, University of North Carolina, Chapel Hill, North Carolina, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michele L.</namePart><namePart type="family">Shaffer</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Public Health Sciences, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Suman</namePart><namePart type="family">Sen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Qing X.</namePart><namePart type="family">Yang</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Radiology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Neurosurgery, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Bioengineering, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Xuemei</namePart><namePart type="family">Huang</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Pharmacology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Radiology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Neurosurgery, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><affiliation>Department of Kinesiology, Pennsylvania State University—Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA</affiliation><description>Correspondence: Associate Professor of Neurology, Penn State Hershey Medical Center, 500 University Dr., H‐037, Hershey, PA 17033‐0850, USA</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">2011-08-01</dateIssued><dateCaptured encoding="w3cdtf">2010-08-20</dateCaptured><dateValid encoding="w3cdtf">2010-12-27</dateValid><copyrightDate encoding="w3cdtf">2011</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">2</extent><extent unit="references">24</extent><extent unit="words">4619</extent></physicalDescription><abstract lang="en">Recent magnetic resonance imaging studies suggest an increased transverse relaxation rate and reduced diffusion tensor imaging fractional anisotropy values in the substantia nigra in Parkinson's disease. The transverse relaxation rate and fractional anisotropy changes may reflect different aspects of Parkinson's disease‐related pathological processes (ie, tissue iron deposition and microstructure disorganization). This study investigated the combined changes of transverse relaxation rate and fractional anisotropy in the substantia nigra in Parkinson's disease. High‐resolution magnetic resonance imaging (T2‐weighted, T2*, and diffusion tensor imaging) were obtained from 16 Parkinson's disease patients and 16 controls. Bilateral substantia nigras were delineated manually on T2‐weighted images and coregistered to transverse relaxation rate and fractional anisotropy maps. The mean transverse relaxation rate and fractional anisotropy values in each substantia nigra were then calculated and compared between Parkinson's disease subjects and controls. Logistic regression, followed by receiver operating characteristic curve analysis, was employed to investigate the sensitivity and specificity of the combined measures for differentiating Parkinson's disease subjects from controls. Compared with controls, Parkinson's disease subjects demonstrated increased transverse relaxation rate (P < .0001) and reduced fractional anisotropy (P = .0365) in the substantia nigra. There was no significant correlation between transverse relaxation rate and fractional anisotropy values. Logistic regression analyses indicated that the combined use of transverse relaxation rate and fractional anisotropy values provides excellent discrimination between Parkinson's disease subjects and controls (c‐statistic = 0.996) compared with transverse relaxation rate (c‐statistic = 0.930) or fractional anisotropy (c‐statistic = 0.742) alone. This study shows that the combined use of transverse relaxation rate and fractional anisotropy measures in the substantia nigra of Parkinson's disease enhances sensitivity and specificity in differentiating Parkinson's disease from controls. Further studies are warranted to evaluate the pathophysiological correlations of these magnetic resonance imaging measurements and their effectiveness in assisting in diagnosing Parkinson's disease and following its progression. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles can be found in the online version of this article.</note><note type="funding">Unknown funding agency - No. NS060722; </note><note type="funding">HMC GCRC - No. NIH M01RR10732; </note><note type="funding">GCRC Construction Grant - No. C06RR016499; </note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>substantia nigra</topic><topic>diffusion tensor imaging</topic><topic>transverse relaxation rate</topic><topic>magnetic resonance imaging</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.</note><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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1627</start><end>1632</end><total>6</total></extent></part></relatedItem><identifier type="istex">FF544EB4AB4D1F55FC1914AE8BB693388B2A1850</identifier><identifier type="DOI">10.1002/mds.23643</identifier><identifier type="ArticleID">MDS23643</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 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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