Blood oxygenation level–dependent activation in basal ganglia nuclei relates to specific symptoms in de novo Parkinson's disease
Identifieur interne : 000435 ( Istex/Corpus ); précédent : 000434; suivant : 000436Blood oxygenation level–dependent activation in basal ganglia nuclei relates to specific symptoms in de novo Parkinson's disease
Auteurs : Janey Prodoehl ; Mathew Spraker ; Daniel Corcos ; Cynthia Comella ; David VaillancourtSource :
- Movement Disorders [ 0885-3185 ] ; 2010-10-15.
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Abstract
To aid the development of symptomatic and disease modifying therapies in Parkinson's disease (PD), there is a strong need to identify noninvasive measures of basal ganglia (BG) function that are sensitive to disease severity. This study examines the relation between blood oxygenation level–dependent (BOLD) activation in every nucleus of the BG and symptom‐specific disease severity in early stage de novo PD. BOLD activation measured at 3 T was compared between 20 early stage de novo PD patients and 20 controls during an established precision grip force task. In addition to the BG nuclei, activation in specific thalamic and cortical regions was examined. There were three novel findings. First, there were significant negative correlations between total motor Unified PD Rating Scale and BOLD activation in bilateral caudate, bilateral putamen, contralateral external segment of the globus pallidus, bilateral subthalamic nucleus, contralateral substantia nigra, and thalamus. Second, bradykinesia was the symptom that most consistently predicted BOLD activation in the BG and thalamus. Also, BOLD activation in the contralateral internal globus pallidus was related to tremor. Third, the reduced cortical activity in primary motor cortex and supplementary motor area in de novo PD did not relate to motor symptoms. These findings demonstrate that BOLD activity in nuclei of the BG relates most consistently to bradykinesia and functional magnetic resonance imaging has strong potential to serve as a noninvasive marker for the state of BG function in de novo PD. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23360
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Corcos</name><affiliation><mods:affiliation>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</mods:affiliation></affiliation></author><author><name sortKey="Comella, Cynthia" sort="Comella, Cynthia" uniqKey="Comella C" first="Cynthia" last="Comella">Cynthia Comella</name><affiliation><mods:affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</mods:affiliation></affiliation></author><author><name sortKey="Vaillancourt, David" 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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-10-15">2010-10-15</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">13</biblScope><biblScope unit="page" from="2035">2035</biblScope><biblScope unit="page" to="2043">2043</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9B4C23B0A7FA67EC95349FD0105EF07BB87517D2</idno><idno type="DOI">10.1002/mds.23360</idno><idno type="ArticleID">MDS23360</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>BOLD</term><term>Parkinson's disease</term><term>basal ganglia</term><term>disease severity</term><term>fMRI</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To aid the development of symptomatic and disease modifying therapies in Parkinson's disease (PD), there is a strong need to identify noninvasive measures of basal ganglia (BG) function that are sensitive to disease severity. This study examines the relation between blood oxygenation level–dependent (BOLD) activation in every nucleus of the BG and symptom‐specific disease severity in early stage de novo PD. BOLD activation measured at 3 T was compared between 20 early stage de novo PD patients and 20 controls during an established precision grip force task. In addition to the BG nuclei, activation in specific thalamic and cortical regions was examined. There were three novel findings. First, there were significant negative correlations between total motor Unified PD Rating Scale and BOLD activation in bilateral caudate, bilateral putamen, contralateral external segment of the globus pallidus, bilateral subthalamic nucleus, contralateral substantia nigra, and thalamus. Second, bradykinesia was the symptom that most consistently predicted BOLD activation in the BG and thalamus. Also, BOLD activation in the contralateral internal globus pallidus was related to tremor. Third, the reduced cortical activity in primary motor cortex and supplementary motor area in de novo PD did not relate to motor symptoms. These findings demonstrate that BOLD activity in nuclei of the BG relates most consistently to bradykinesia and functional magnetic resonance imaging has strong potential to serve as a noninvasive marker for the state of BG function in de novo PD. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Janey Prodoehl PT, PhD</name><affiliations><json:string>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</json:string></affiliations></json:item><json:item><name>Mathew Spraker PhD</name><affiliations><json:string>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</json:string></affiliations></json:item><json:item><name>Daniel Corcos PhD</name><affiliations><json:string>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</json:string><json:string>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</json:string><json:string>Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois, USA</json:string><json:string>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</json:string></affiliations></json:item><json:item><name>Cynthia Comella MD</name><affiliations><json:string>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</json:string></affiliations></json:item><json:item><name>David Vaillancourt PhD</name><affiliations><json:string>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</json:string><json:string>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</json:string><json:string>Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, Illinois, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>fMRI</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>basal ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>BOLD</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>disease severity</value></json:item></subject><language><json:string>eng</json:string></language><abstract>To aid the development of symptomatic and disease modifying therapies in Parkinson's disease (PD), there is a strong need to identify noninvasive measures of basal ganglia (BG) function that are sensitive to disease severity. This study examines the relation between blood oxygenation level–dependent (BOLD) activation in every nucleus of the BG and symptom‐specific disease severity in early stage de novo PD. BOLD activation measured at 3 T was compared between 20 early stage de novo PD patients and 20 controls during an established precision grip force task. In addition to the BG nuclei, activation in specific thalamic and cortical regions was examined. There were three novel findings. First, there were significant negative correlations between total motor Unified PD Rating Scale and BOLD activation in bilateral caudate, bilateral putamen, contralateral external segment of the globus pallidus, bilateral subthalamic nucleus, contralateral substantia nigra, and thalamus. Second, bradykinesia was the symptom that most consistently predicted BOLD activation in the BG and thalamus. Also, BOLD activation in the contralateral internal globus pallidus was related to tremor. Third, the reduced cortical activity in primary motor cortex and supplementary motor area in de novo PD did not relate to motor symptoms. These findings demonstrate that BOLD activity in nuclei of the BG relates most consistently to bradykinesia and functional magnetic resonance imaging has strong potential to serve as a noninvasive marker for the state of BG function in de novo PD. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>7.644</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1602</abstractCharCount><pdfWordCount>4764</pdfWordCount><pdfCharCount>30573</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>240</abstractWordCount></qualityIndicators><title>Blood oxygenation level–dependent activation in basal ganglia nuclei relates to specific symptoms in de novo Parkinson's disease</title><genre><json:string>Serial article</json:string></genre><host><volume>25</volume><pages><total>9</total><last>2043</last><first>2035</first></pages><issn><json:string>0885-3185</json:string></issn><issue>13</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.23360</json:string></doi><id>9B4C23B0A7FA67EC95349FD0105EF07BB87517D2</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/9B4C23B0A7FA67EC95349FD0105EF07BB87517D2/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/9B4C23B0A7FA67EC95349FD0105EF07BB87517D2/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/9B4C23B0A7FA67EC95349FD0105EF07BB87517D2/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Blood oxygenation level–dependent activation in basal ganglia nuclei relates to specific symptoms in de novo Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None.</note><note>National Institutes of Health - No. R01‐NS‐52318; No. R01‐NS‐58487; No. R01‐NS‐40902; No. R01‐NS‐28127;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Blood oxygenation level–dependent activation in basal ganglia nuclei relates to specific symptoms in de novo Parkinson's disease</title><author><persName><forename type="first">Janey</forename><surname>Prodoehl</surname><roleName type="degree">PT, PhD</roleName></persName><affiliation>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation></author><author><persName><forename type="first">Mathew</forename><surname>Spraker</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation></author><author><persName><forename type="first">Daniel</forename><surname>Corcos</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</affiliation></author><author><persName><forename type="first">Cynthia</forename><surname>Comella</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</affiliation></author><author><persName><forename type="first">David</forename><surname>Vaillancourt</surname><roleName type="degree">PhD</roleName></persName><note type="correspondence"><p>Correspondence: University of Illinois at Chicago, 1919 West Taylor Street, 650 AHSB, M/C 994 Chicago, IL 60612</p></note><affiliation>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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This study examines the relation between blood oxygenation level–dependent (BOLD) activation in every nucleus of the BG and symptom‐specific disease severity in early stage de novo PD. BOLD activation measured at 3 T was compared between 20 early stage de novo PD patients and 20 controls during an established precision grip force task. In addition to the BG nuclei, activation in specific thalamic and cortical regions was examined. There were three novel findings. First, there were significant negative correlations between total motor Unified PD Rating Scale and BOLD activation in bilateral caudate, bilateral putamen, contralateral external segment of the globus pallidus, bilateral subthalamic nucleus, contralateral substantia nigra, and thalamus. Second, bradykinesia was the symptom that most consistently predicted BOLD activation in the BG and thalamus. Also, BOLD activation in the contralateral internal globus pallidus was related to tremor. Third, the reduced cortical activity in primary motor cortex and supplementary motor area in de novo PD did not relate to motor symptoms. 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xml:id="kwd5">disease severity</keyword></keywordGroup><fundingInfo><fundingAgency>National Institutes of Health</fundingAgency><fundingNumber>R01‐NS‐52318</fundingNumber><fundingNumber>R01‐NS‐58487</fundingNumber><fundingNumber>R01‐NS‐40902</fundingNumber><fundingNumber>R01‐NS‐28127</fundingNumber></fundingInfo><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23360:MDS_23360_sm_suppinfo"></mediaResource><caption>Supporting Information</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To aid the development of symptomatic and disease modifying therapies in Parkinson's disease (PD), there is a strong need to identify noninvasive measures of basal ganglia (BG) function that are sensitive to disease severity. This study examines the relation between blood oxygenation level–dependent (BOLD) activation in every nucleus of the BG and symptom‐specific disease severity in early stage de novo PD. BOLD activation measured at 3 T was compared between 20 early stage de novo PD patients and 20 controls during an established precision grip force task. In addition to the BG nuclei, activation in specific thalamic and cortical regions was examined. There were three novel findings. First, there were significant negative correlations between total motor Unified PD Rating Scale and BOLD activation in bilateral caudate, bilateral putamen, contralateral external segment of the globus pallidus, bilateral subthalamic nucleus, contralateral substantia nigra, and thalamus. Second, bradykinesia was the symptom that most consistently predicted BOLD activation in the BG and thalamus. Also, BOLD activation in the contralateral internal globus pallidus was related to tremor. Third, the reduced cortical activity in primary motor cortex and supplementary motor area in de novo PD did not relate to motor symptoms. These findings demonstrate that BOLD activity in nuclei of the BG relates most consistently to bradykinesia and functional magnetic resonance imaging has strong potential to serve as a noninvasive marker for the state of BG function in de novo PD. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Blood oxygenation level–dependent activation in basal ganglia nuclei relates to specific symptoms in de novo Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Bold Activity and Disease Severity in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Blood oxygenation level–dependent activation in basal ganglia nuclei relates to specific symptoms in de novo Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Janey</namePart><namePart type="family">Prodoehl</namePart><namePart type="termsOfAddress">PT, PhD</namePart><affiliation>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mathew</namePart><namePart type="family">Spraker</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniel</namePart><namePart type="family">Corcos</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cynthia</namePart><namePart type="family">Comella</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Vaillancourt</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Bioengineering, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><description>Correspondence: University of Illinois at Chicago, 1919 West Taylor Street, 650 AHSB, M/C 994 Chicago, IL 60612</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-10-15</dateIssued><dateCaptured encoding="w3cdtf">2010-02-12</dateCaptured><dateValid encoding="w3cdtf">2010-06-28</dateValid><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><extent unit="references">26</extent><extent unit="words">7092</extent></physicalDescription><abstract lang="en">To aid the development of symptomatic and disease modifying therapies in Parkinson's disease (PD), there is a strong need to identify noninvasive measures of basal ganglia (BG) function that are sensitive to disease severity. This study examines the relation between blood oxygenation level–dependent (BOLD) activation in every nucleus of the BG and symptom‐specific disease severity in early stage de novo PD. BOLD activation measured at 3 T was compared between 20 early stage de novo PD patients and 20 controls during an established precision grip force task. In addition to the BG nuclei, activation in specific thalamic and cortical regions was examined. There were three novel findings. First, there were significant negative correlations between total motor Unified PD Rating Scale and BOLD activation in bilateral caudate, bilateral putamen, contralateral external segment of the globus pallidus, bilateral subthalamic nucleus, contralateral substantia nigra, and thalamus. Second, bradykinesia was the symptom that most consistently predicted BOLD activation in the BG and thalamus. Also, BOLD activation in the contralateral internal globus pallidus was related to tremor. Third, the reduced cortical activity in primary motor cortex and supplementary motor area in de novo PD did not relate to motor symptoms. These findings demonstrate that BOLD activity in nuclei of the BG relates most consistently to bradykinesia and functional magnetic resonance imaging has strong potential to serve as a noninvasive marker for the state of BG function in de novo PD. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None.</note><note type="funding">National Institutes of Health - No. R01‐NS‐52318; No. R01‐NS‐58487; No. R01‐NS‐40902; No. R01‐NS‐28127; </note><subject lang="en"><genre>Keywords</genre><topic>fMRI</topic><topic>Parkinson's disease</topic><topic>basal ganglia</topic><topic>BOLD</topic><topic>disease severity</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information - </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>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>13</number></detail><extent unit="pages"><start>2035</start><end>2043</end><total>9</total></extent></part></relatedItem><identifier type="istex">9B4C23B0A7FA67EC95349FD0105EF07BB87517D2</identifier><identifier type="DOI">10.1002/mds.23360</identifier><identifier type="ArticleID">MDS23360</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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