Parkinson's disease patients show reduced cortical-subcortical sensorimotor connectivity.
Identifieur interne : 000B68 ( PubMed/Curation ); précédent : 000B67; suivant : 000B69Parkinson's disease patients show reduced cortical-subcortical sensorimotor connectivity.
Auteurs : Michael Sharman [France] ; Romain Valabregue ; Vincent Perlbarg ; Linda Marrakchi-Kacem ; Marie Vidailhet ; Habib Benali ; Alexis Brice ; Stephane LehéricySource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Adult, Aged, Basal Ganglia (pathology), Basal Ganglia (physiopathology), Brain Mapping (methods), Cerebral Cortex (pathology), Cerebral Cortex (physiopathology), Female, Humans, Image Processing, Computer-Assisted (methods), Magnetic Resonance Imaging (methods), Male, Middle Aged, Neural Pathways (pathology), Neural Pathways (physiopathology), Parkinson Disease (pathology), Parkinson Disease (physiopathology).
- MESH :
- methods : Brain Mapping, Image Processing, Computer-Assisted, Magnetic Resonance Imaging.
- pathology : Basal Ganglia, Cerebral Cortex, Neural Pathways, Parkinson Disease.
- physiopathology : Basal Ganglia, Cerebral Cortex, Neural Pathways, Parkinson Disease.
- Adult, Aged, Female, Humans, Male, Middle Aged.
Abstract
Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico-basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion-weighted magnetic resonance imaging (MRI) and resting-state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico-basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere.
DOI: 10.1002/mds.25255
PubMed: 23144002
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Linda" uniqKey="Marrakchi Kacem L" first="Linda" last="Marrakchi-Kacem">Linda Marrakchi-Kacem</name></author><author><name sortKey="Vidailhet, Marie" sort="Vidailhet, Marie" uniqKey="Vidailhet M" first="Marie" last="Vidailhet">Marie Vidailhet</name></author><author><name sortKey="Benali, Habib" sort="Benali, Habib" uniqKey="Benali H" first="Habib" last="Benali">Habib Benali</name></author><author><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</name></author><author><name sortKey="Lehericy, Stephane" sort="Lehericy, Stephane" uniqKey="Lehericy S" first="Stephane" last="Lehéricy">Stephane Lehéricy</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="doi">10.1002/mds.25255</idno><idno type="RBID">pubmed:23144002</idno><idno type="pmid">23144002</idno><idno type="wicri:Area/PubMed/Corpus">000B68</idno><idno type="wicri:Area/PubMed/Curation">000B68</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Parkinson's disease patients show reduced cortical-subcortical sensorimotor connectivity.</title><author><name sortKey="Sharman, Michael" sort="Sharman, Michael" uniqKey="Sharman M" first="Michael" last="Sharman">Michael Sharman</name><affiliation wicri:level="1"><nlm:affiliation>UMR-S975, CRICM-INSERM-UPMC Paris 6, Paris, Île-de-France, France. michael.sharman@etu.upmc.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>UMR-S975, CRICM-INSERM-UPMC Paris 6, Paris, Île-de-France</wicri:regionArea></affiliation></author><author><name sortKey="Valabregue, Romain" sort="Valabregue, Romain" uniqKey="Valabregue R" first="Romain" last="Valabregue">Romain Valabregue</name></author><author><name sortKey="Perlbarg, Vincent" sort="Perlbarg, Vincent" uniqKey="Perlbarg V" first="Vincent" last="Perlbarg">Vincent Perlbarg</name></author><author><name sortKey="Marrakchi Kacem, Linda" sort="Marrakchi Kacem, Linda" uniqKey="Marrakchi Kacem L" first="Linda" last="Marrakchi-Kacem">Linda Marrakchi-Kacem</name></author><author><name sortKey="Vidailhet, Marie" sort="Vidailhet, Marie" uniqKey="Vidailhet M" first="Marie" last="Vidailhet">Marie Vidailhet</name></author><author><name sortKey="Benali, Habib" sort="Benali, Habib" uniqKey="Benali H" first="Habib" last="Benali">Habib Benali</name></author><author><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</name></author><author><name sortKey="Lehericy, Stephane" sort="Lehericy, Stephane" uniqKey="Lehericy S" first="Stephane" last="Lehéricy">Stephane Lehéricy</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Basal Ganglia (pathology)</term><term>Basal Ganglia (physiopathology)</term><term>Brain Mapping (methods)</term><term>Cerebral Cortex (pathology)</term><term>Cerebral Cortex (physiopathology)</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted (methods)</term><term>Magnetic Resonance Imaging (methods)</term><term>Male</term><term>Middle Aged</term><term>Neural Pathways (pathology)</term><term>Neural Pathways (physiopathology)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Brain Mapping</term><term>Image Processing, Computer-Assisted</term><term>Magnetic Resonance Imaging</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Cerebral Cortex</term><term>Neural Pathways</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Cerebral Cortex</term><term>Neural Pathways</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico-basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion-weighted magnetic resonance imaging (MRI) and resting-state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico-basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23144002</PMID><DateCreated><Year>2013</Year><Month>04</Month><Day>09</Day></DateCreated><DateCompleted><Year>2013</Year><Month>11</Month><Day>27</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>4</Issue><PubDate><Year>2013</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Parkinson's disease patients show reduced cortical-subcortical sensorimotor connectivity.</ArticleTitle><Pagination><MedlinePgn>447-54</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25255</ELocationID><Abstract><AbstractText>Reduced dopamine input to cortical and subcortical brain structures, particularly those in the sensorimotor network, is a hallmark of Parkinson's disease (PD). The extent to which dopamine dysfunction affects connectivity within this and other brain networks remains to be investigated. The purpose of this study was to measure anatomical and functional connectivity in groups of PD patients and controls to determine whether connectivity deficits within the cortico-basal ganglia thalamocortical system could be attributed to PD, particularly in sensorimotor connections. A neuroimaging paradigm involving diffusion-weighted magnetic resonance imaging (MRI) and resting-state functional MRI was implemented in a large cohort of PD patients and control subjects. Probabilistic tractography and functional correlation analyses were performed to map connections between brain structures and to derive indices of connectivity that were then used to compare groups. Anatomical connectivity deficits were demonstrated in PD patients, specifically for sensorimotor connections. Functional deficits were also found in some of the same connections. In addition, functional connectivity was found to increase in associative and limbic connections in PD patients compared with controls. This study lends support to findings regarding the dysfunction of the sensorimotor circuit in PD. As deficits in anatomical and functional connectivity within this circuit were in some cases concordant in PD patients, a possible link between brain structure and function is suggested. Increases in functional connectivity in other cortico-basal ganglia thalamocortical circuits may be indicative of compensatory effects in response to system deficits elsewhere.</AbstractText><CopyrightInformation>Copyright © 2012 Movement Disorders Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sharman</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>UMR-S975, CRICM-INSERM-UPMC Paris 6, Paris, Île-de-France, France. michael.sharman@etu.upmc.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Valabregue</LastName><ForeName>Romain</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Perlbarg</LastName><ForeName>Vincent</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Marrakchi-Kacem</LastName><ForeName>Linda</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Vidailhet</LastName><ForeName>Marie</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Benali</LastName><ForeName>Habib</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Brice</LastName><ForeName>Alexis</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Lehéricy</LastName><ForeName>Stephane</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>11</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Mov Disord. 2013 Apr;28(4):411-2</RefSource><PMID Version="1">23450512</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001479">Basal Ganglia</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D001931">Brain Mapping</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002540">Cerebral Cortex</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007091">Image Processing, Computer-Assisted</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008279">Magnetic Resonance Imaging</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009434">Neural Pathways</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>4</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2012</Year><Month>7</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>9</Month><Day>25</Day></PubMedPubDate><PubMedPubDate 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