Cerebral white matter alterations in idiopathic restless legs syndrome, as measured by diffusion tensor imaging.
Identifieur interne : 002136 ( Ncbi/Merge ); précédent : 002135; suivant : 002137Cerebral white matter alterations in idiopathic restless legs syndrome, as measured by diffusion tensor imaging.
Auteurs : Alexander Unrath [Allemagne] ; Hans-Peter Müller ; Albert C. Ludolph ; Axel Riecker ; Jan KassubekSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- MESH :
- metabolism : Cerebral Cortex.
- methods : Diffusion Magnetic Resonance Imaging.
- pathology : Cerebral Cortex, Restless Legs Syndrome.
- Aged, Anisotropy, Brain Mapping, Chi-Square Distribution, Female, Humans, Image Processing, Computer-Assisted, Male, Middle Aged.
Abstract
In search for the pathoanatomical correlate of the restless legs syndrome (RLS), various neuroimaging and electrophysiological techniques have demonstrated partly conflicting results of cortical, subcortical, brainstem, and spinal alterations. In a novel approach, the delineation of potential cerebral white matter tract disruption was investigated by application of quantitative whole brain-based diffusion tensor imaging (DTI) to a well characterized group of 45 patients with idiopathic RLS. The data of patients and 30 healthy controls were statistically compared including computation of regional fractional anisotropy (FA) as a quantitative marker of white matter integrity by use of the tensor imaging and fiber tracking software. In the patient group, multiple subcortical areas of significantly reduced FA were observed bihemispherically in close proximity to the primary and associate motor and somatosensory cortices, in the right-hemispheric thalamus (posterior ventral lateral nucleus), in motor projectional fibers and adjacent to the left anterior cingulum. Together with the results of a recent study by use of an MRI-based gray matter analysis, which localized RLS-associated changes in the sensorimotor cortices, these findings gave support to an altered subcortical network, with the major component of altered cerebral sensorimotor pathways, within a hodological concept of the RLS pathoanatomy.
DOI: 10.1002/mds.22074
PubMed: 18464282
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In a novel approach, the delineation of potential cerebral white matter tract disruption was investigated by application of quantitative whole brain-based diffusion tensor imaging (DTI) to a well characterized group of 45 patients with idiopathic RLS. The data of patients and 30 healthy controls were statistically compared including computation of regional fractional anisotropy (FA) as a quantitative marker of white matter integrity by use of the tensor imaging and fiber tracking software. In the patient group, multiple subcortical areas of significantly reduced FA were observed bihemispherically in close proximity to the primary and associate motor and somatosensory cortices, in the right-hemispheric thalamus (posterior ventral lateral nucleus), in motor projectional fibers and adjacent to the left anterior cingulum. Together with the results of a recent study by use of an MRI-based gray matter analysis, which localized RLS-associated changes in the sensorimotor cortices, these findings gave support to an altered subcortical network, with the major component of altered cerebral sensorimotor pathways, within a hodological concept of the RLS pathoanatomy.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18464282</PMID><DateCreated><Year>2008</Year><Month>08</Month><Day>05</Day></DateCreated><DateCompleted><Year>2009</Year><Month>01</Month><Day>12</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>9</Issue><PubDate><Year>2008</Year><Month>Jul</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Cerebral white matter alterations in idiopathic restless legs syndrome, as measured by diffusion tensor imaging.</ArticleTitle><Pagination><MedlinePgn>1250-5</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22074</ELocationID><Abstract><AbstractText>In search for the pathoanatomical correlate of the restless legs syndrome (RLS), various neuroimaging and electrophysiological techniques have demonstrated partly conflicting results of cortical, subcortical, brainstem, and spinal alterations. In a novel approach, the delineation of potential cerebral white matter tract disruption was investigated by application of quantitative whole brain-based diffusion tensor imaging (DTI) to a well characterized group of 45 patients with idiopathic RLS. The data of patients and 30 healthy controls were statistically compared including computation of regional fractional anisotropy (FA) as a quantitative marker of white matter integrity by use of the tensor imaging and fiber tracking software. In the patient group, multiple subcortical areas of significantly reduced FA were observed bihemispherically in close proximity to the primary and associate motor and somatosensory cortices, in the right-hemispheric thalamus (posterior ventral lateral nucleus), in motor projectional fibers and adjacent to the left anterior cingulum. Together with the results of a recent study by use of an MRI-based gray matter analysis, which localized RLS-associated changes in the sensorimotor cortices, these findings gave support to an altered subcortical network, with the major component of altered cerebral sensorimotor pathways, within a hodological concept of the RLS pathoanatomy.</AbstractText><CopyrightInformation>(c) 2008 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Unrath</LastName><ForeName>Alexander</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Neurology, University of Ulm, Ulm, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Müller</LastName><ForeName>Hans-Peter</ForeName><Initials>HP</Initials></Author><Author ValidYN="Y"><LastName>Ludolph</LastName><ForeName>Albert C</ForeName><Initials>AC</Initials></Author><Author ValidYN="Y"><LastName>Riecker</LastName><ForeName>Axel</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Kassubek</LastName><ForeName>Jan</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016880">Anisotropy</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D001931">Brain Mapping</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002540">Cerebral Cortex</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016009">Chi-Square Distribution</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D038524">Diffusion Magnetic Resonance Imaging</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000379">methods</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></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="D012148">Restless Legs Syndrome</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>5</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>1</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>5</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.22074</ArticleId><ArticleId IdType="pubmed">18464282</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>Bade-Wurtemberg</li><li>District de Tübingen</li></region><settlement><li>Ulm</li></settlement><orgName><li>Université d'Ulm</li></orgName></list><tree><noCountry><name sortKey="Kassubek, Jan" sort="Kassubek, Jan" uniqKey="Kassubek J" first="Jan" last="Kassubek">Jan Kassubek</name><name sortKey="Ludolph, Albert C" sort="Ludolph, Albert C" uniqKey="Ludolph A" first="Albert C" last="Ludolph">Albert C. Ludolph</name><name sortKey="Muller, Hans Peter" sort="Muller, Hans Peter" uniqKey="Muller H" first="Hans-Peter" last="Müller">Hans-Peter Müller</name><name sortKey="Riecker, Axel" sort="Riecker, Axel" uniqKey="Riecker A" first="Axel" last="Riecker">Axel Riecker</name></noCountry><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Unrath, Alexander" sort="Unrath, Alexander" uniqKey="Unrath A" first="Alexander" last="Unrath">Alexander Unrath</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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