Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis
Background: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. MS lesions show a typical distribution pattern and primarily affect the white matter (WM) in the periventricular zone and in the centrum semiovale. Objective: To track lesion development during disea...
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| Veröffentlicht in: | Multiple sclerosis 2012-11, Vol.18 (11), p.1577-1584 |
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| container_title | Multiple sclerosis |
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| creator | Filli, Lukas Hofstetter, Louis Kuster, Pascal Traud, Stefan Mueller-Lenke, Nicole Naegelin, Yvonne Kappos, Ludwig Gass, Achim Sprenger, Till Nichols, Thomas E Vrenken, Hugo Barkhof, Frederik Polman, Chris Radue, Ernst-Wilhelm Borgwardt, Stefan J Bendfeldt, Kerstin |
| description | Background:
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. MS lesions show a typical distribution pattern and primarily affect the white matter (WM) in the periventricular zone and in the centrum semiovale.
Objective:
To track lesion development during disease progression, we compared the spatiotemporal distribution patterns of lesions in relapsing–remitting MS (RRMS) and secondary progressive MS (SPMS).
Methods:
We used T1 and T2 weighted MR images of 209 RRMS and 62 SPMS patients acquired on two different 1.5 Tesla MR scanners in two clinical centers followed up for 25 (± 1.7) months. Both cross-sectional and longitudinal differences in lesion distribution between RRMS and SPMS patients were analyzed with lesion probability maps (LPMs) and permutation-based inference.
Results:
MS lesions clustered around the lateral ventricles and in the centrum semiovale. Cross-sectionally, compared to RRMS patients, the SPMS patients showed a significantly higher regional probability of T1 hypointense lesions (p≤0.03) in the callosal body, the corticospinal tract, and other tracts adjacent to the lateral ventricles, but not of T2 lesions (peak probabilities were RRMS: T1 9%, T2 18%; SPMS: T1 21%, T2 27%). No longitudinal changes of regional T1 and T2 lesion volumes between baseline and follow-up scan were found.
Conclusion:
The results suggest a particular vulnerability to neurodegeneration during disease progression in a number of WM tracts. |
| doi_str_mv | 10.1177/1352458512442756 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1115530720</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_1352458512442756</sage_id><sourcerecordid>2818918681</sourcerecordid><originalsourceid>FETCH-LOGICAL-c461t-7ab8d8038d6e05cfbaad928dfe71cac8a525b5cc433eccdabd89abc808b7ce143</originalsourceid><addsrcrecordid>eNp1kU1rFjEQxxdRbK3ePUlABC9bk2yyyR6l-AaFHtTzMpvMPqZkX8xkK735HfyGfpKmPI9aCp5mmPnNf_7DVNVzwU-FMOaNaLRU2mohlZJGtw-qY6GMqXln-MOSl3Z92z-qnhBdcs6NafTj6khK1elO6ePq-vMKOSwZp3VJEJkPlFMYtlKb2TKyH99CRjZBzphYRCplYmFmCSOsFObd75-_Ek4h55IzmD0jdMvsIV2zNS27hEThqihsMYc1IiMXMS0U6Gn1aIRI-OwQT6qv7999OftYn198-HT29rx2qhW5NjBYb3ljfYtcu3EA8J20fkQjHDgLWupBO6eaBp3zMHjbweAst4NxKFRzUr3e6xY73zek3E-BHMYIMy4b9UIIrRtuJC_oy3vo5bKlubgrlOGtaDWXheJ7ypU7KOHYrylM5eBe8FvO9PffUkZeHIS3YUL_d-DPHwrw6gAAOYhjgtkF-se12rSd7ApX7zmCHd5x97_FN476prw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1170616502</pqid></control><display><type>article</type><title>Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis</title><source>MEDLINE</source><source>SAGE Complete</source><creator>Filli, Lukas ; Hofstetter, Louis ; Kuster, Pascal ; Traud, Stefan ; Mueller-Lenke, Nicole ; Naegelin, Yvonne ; Kappos, Ludwig ; Gass, Achim ; Sprenger, Till ; Nichols, Thomas E ; Vrenken, Hugo ; Barkhof, Frederik ; Polman, Chris ; Radue, Ernst-Wilhelm ; Borgwardt, Stefan J ; Bendfeldt, Kerstin</creator><creatorcontrib>Filli, Lukas ; Hofstetter, Louis ; Kuster, Pascal ; Traud, Stefan ; Mueller-Lenke, Nicole ; Naegelin, Yvonne ; Kappos, Ludwig ; Gass, Achim ; Sprenger, Till ; Nichols, Thomas E ; Vrenken, Hugo ; Barkhof, Frederik ; Polman, Chris ; Radue, Ernst-Wilhelm ; Borgwardt, Stefan J ; Bendfeldt, Kerstin</creatorcontrib><description>Background:
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. MS lesions show a typical distribution pattern and primarily affect the white matter (WM) in the periventricular zone and in the centrum semiovale.
Objective:
To track lesion development during disease progression, we compared the spatiotemporal distribution patterns of lesions in relapsing–remitting MS (RRMS) and secondary progressive MS (SPMS).
Methods:
We used T1 and T2 weighted MR images of 209 RRMS and 62 SPMS patients acquired on two different 1.5 Tesla MR scanners in two clinical centers followed up for 25 (± 1.7) months. Both cross-sectional and longitudinal differences in lesion distribution between RRMS and SPMS patients were analyzed with lesion probability maps (LPMs) and permutation-based inference.
Results:
MS lesions clustered around the lateral ventricles and in the centrum semiovale. Cross-sectionally, compared to RRMS patients, the SPMS patients showed a significantly higher regional probability of T1 hypointense lesions (p≤0.03) in the callosal body, the corticospinal tract, and other tracts adjacent to the lateral ventricles, but not of T2 lesions (peak probabilities were RRMS: T1 9%, T2 18%; SPMS: T1 21%, T2 27%). No longitudinal changes of regional T1 and T2 lesion volumes between baseline and follow-up scan were found.
Conclusion:
The results suggest a particular vulnerability to neurodegeneration during disease progression in a number of WM tracts.</description><identifier>ISSN: 1352-4585</identifier><identifier>EISSN: 1477-0970</identifier><identifier>DOI: 10.1177/1352458512442756</identifier><identifier>PMID: 22495945</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adult ; Analysis of Variance ; Biological and medical sciences ; Brain - pathology ; Chi-Square Distribution ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Disability Evaluation ; Disease Progression ; Europe ; Female ; Humans ; Leukoencephalopathies - pathology ; Magnetic Resonance Imaging ; Male ; Medical sciences ; Middle Aged ; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis ; Multiple Sclerosis, Chronic Progressive - pathology ; Multiple Sclerosis, Relapsing-Remitting - pathology ; Neurology ; Predictive Value of Tests ; Time Factors</subject><ispartof>Multiple sclerosis, 2012-11, Vol.18 (11), p.1577-1584</ispartof><rights>The Author(s) 2012</rights><rights>2015 INIST-CNRS</rights><rights>SAGE Publications © Nov 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-7ab8d8038d6e05cfbaad928dfe71cac8a525b5cc433eccdabd89abc808b7ce143</citedby><cites>FETCH-LOGICAL-c461t-7ab8d8038d6e05cfbaad928dfe71cac8a525b5cc433eccdabd89abc808b7ce143</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/1352458512442756$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/1352458512442756$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,778,782,21802,27907,27908,43604,43605</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26576929$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22495945$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Filli, Lukas</creatorcontrib><creatorcontrib>Hofstetter, Louis</creatorcontrib><creatorcontrib>Kuster, Pascal</creatorcontrib><creatorcontrib>Traud, Stefan</creatorcontrib><creatorcontrib>Mueller-Lenke, Nicole</creatorcontrib><creatorcontrib>Naegelin, Yvonne</creatorcontrib><creatorcontrib>Kappos, Ludwig</creatorcontrib><creatorcontrib>Gass, Achim</creatorcontrib><creatorcontrib>Sprenger, Till</creatorcontrib><creatorcontrib>Nichols, Thomas E</creatorcontrib><creatorcontrib>Vrenken, Hugo</creatorcontrib><creatorcontrib>Barkhof, Frederik</creatorcontrib><creatorcontrib>Polman, Chris</creatorcontrib><creatorcontrib>Radue, Ernst-Wilhelm</creatorcontrib><creatorcontrib>Borgwardt, Stefan J</creatorcontrib><creatorcontrib>Bendfeldt, Kerstin</creatorcontrib><title>Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis</title><title>Multiple sclerosis</title><addtitle>Mult Scler</addtitle><description>Background:
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. MS lesions show a typical distribution pattern and primarily affect the white matter (WM) in the periventricular zone and in the centrum semiovale.
Objective:
To track lesion development during disease progression, we compared the spatiotemporal distribution patterns of lesions in relapsing–remitting MS (RRMS) and secondary progressive MS (SPMS).
Methods:
We used T1 and T2 weighted MR images of 209 RRMS and 62 SPMS patients acquired on two different 1.5 Tesla MR scanners in two clinical centers followed up for 25 (± 1.7) months. Both cross-sectional and longitudinal differences in lesion distribution between RRMS and SPMS patients were analyzed with lesion probability maps (LPMs) and permutation-based inference.
Results:
MS lesions clustered around the lateral ventricles and in the centrum semiovale. Cross-sectionally, compared to RRMS patients, the SPMS patients showed a significantly higher regional probability of T1 hypointense lesions (p≤0.03) in the callosal body, the corticospinal tract, and other tracts adjacent to the lateral ventricles, but not of T2 lesions (peak probabilities were RRMS: T1 9%, T2 18%; SPMS: T1 21%, T2 27%). No longitudinal changes of regional T1 and T2 lesion volumes between baseline and follow-up scan were found.
Conclusion:
The results suggest a particular vulnerability to neurodegeneration during disease progression in a number of WM tracts.</description><subject>Adult</subject><subject>Analysis of Variance</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Chi-Square Distribution</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Disability Evaluation</subject><subject>Disease Progression</subject><subject>Europe</subject><subject>Female</subject><subject>Humans</subject><subject>Leukoencephalopathies - pathology</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</subject><subject>Multiple Sclerosis, Chronic Progressive - pathology</subject><subject>Multiple Sclerosis, Relapsing-Remitting - pathology</subject><subject>Neurology</subject><subject>Predictive Value of Tests</subject><subject>Time Factors</subject><issn>1352-4585</issn><issn>1477-0970</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kU1rFjEQxxdRbK3ePUlABC9bk2yyyR6l-AaFHtTzMpvMPqZkX8xkK735HfyGfpKmPI9aCp5mmPnNf_7DVNVzwU-FMOaNaLRU2mohlZJGtw-qY6GMqXln-MOSl3Z92z-qnhBdcs6NafTj6khK1elO6ePq-vMKOSwZp3VJEJkPlFMYtlKb2TKyH99CRjZBzphYRCplYmFmCSOsFObd75-_Ek4h55IzmD0jdMvsIV2zNS27hEThqihsMYc1IiMXMS0U6Gn1aIRI-OwQT6qv7999OftYn198-HT29rx2qhW5NjBYb3ljfYtcu3EA8J20fkQjHDgLWupBO6eaBp3zMHjbweAst4NxKFRzUr3e6xY73zek3E-BHMYIMy4b9UIIrRtuJC_oy3vo5bKlubgrlOGtaDWXheJ7ypU7KOHYrylM5eBe8FvO9PffUkZeHIS3YUL_d-DPHwrw6gAAOYhjgtkF-se12rSd7ApX7zmCHd5x97_FN476prw</recordid><startdate>20121101</startdate><enddate>20121101</enddate><creator>Filli, Lukas</creator><creator>Hofstetter, Louis</creator><creator>Kuster, Pascal</creator><creator>Traud, Stefan</creator><creator>Mueller-Lenke, Nicole</creator><creator>Naegelin, Yvonne</creator><creator>Kappos, Ludwig</creator><creator>Gass, Achim</creator><creator>Sprenger, Till</creator><creator>Nichols, Thomas E</creator><creator>Vrenken, Hugo</creator><creator>Barkhof, Frederik</creator><creator>Polman, Chris</creator><creator>Radue, Ernst-Wilhelm</creator><creator>Borgwardt, Stefan J</creator><creator>Bendfeldt, Kerstin</creator><general>SAGE Publications</general><general>Sage Publications</general><general>Sage Publications Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20121101</creationdate><title>Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis</title><author>Filli, Lukas ; Hofstetter, Louis ; Kuster, Pascal ; Traud, Stefan ; Mueller-Lenke, Nicole ; Naegelin, Yvonne ; Kappos, Ludwig ; Gass, Achim ; Sprenger, Till ; Nichols, Thomas E ; Vrenken, Hugo ; Barkhof, Frederik ; Polman, Chris ; Radue, Ernst-Wilhelm ; Borgwardt, Stefan J ; Bendfeldt, Kerstin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-7ab8d8038d6e05cfbaad928dfe71cac8a525b5cc433eccdabd89abc808b7ce143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Analysis of Variance</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Chi-Square Distribution</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Disability Evaluation</topic><topic>Disease Progression</topic><topic>Europe</topic><topic>Female</topic><topic>Humans</topic><topic>Leukoencephalopathies - pathology</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Multiple Sclerosis, Chronic Progressive - pathology</topic><topic>Multiple Sclerosis, Relapsing-Remitting - pathology</topic><topic>Neurology</topic><topic>Predictive Value of Tests</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Filli, Lukas</creatorcontrib><creatorcontrib>Hofstetter, Louis</creatorcontrib><creatorcontrib>Kuster, Pascal</creatorcontrib><creatorcontrib>Traud, Stefan</creatorcontrib><creatorcontrib>Mueller-Lenke, Nicole</creatorcontrib><creatorcontrib>Naegelin, Yvonne</creatorcontrib><creatorcontrib>Kappos, Ludwig</creatorcontrib><creatorcontrib>Gass, Achim</creatorcontrib><creatorcontrib>Sprenger, Till</creatorcontrib><creatorcontrib>Nichols, Thomas E</creatorcontrib><creatorcontrib>Vrenken, Hugo</creatorcontrib><creatorcontrib>Barkhof, Frederik</creatorcontrib><creatorcontrib>Polman, Chris</creatorcontrib><creatorcontrib>Radue, Ernst-Wilhelm</creatorcontrib><creatorcontrib>Borgwardt, Stefan J</creatorcontrib><creatorcontrib>Bendfeldt, Kerstin</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Multiple sclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Filli, Lukas</au><au>Hofstetter, Louis</au><au>Kuster, Pascal</au><au>Traud, Stefan</au><au>Mueller-Lenke, Nicole</au><au>Naegelin, Yvonne</au><au>Kappos, Ludwig</au><au>Gass, Achim</au><au>Sprenger, Till</au><au>Nichols, Thomas E</au><au>Vrenken, Hugo</au><au>Barkhof, Frederik</au><au>Polman, Chris</au><au>Radue, Ernst-Wilhelm</au><au>Borgwardt, Stefan J</au><au>Bendfeldt, Kerstin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis</atitle><jtitle>Multiple sclerosis</jtitle><addtitle>Mult Scler</addtitle><date>2012-11-01</date><risdate>2012</risdate><volume>18</volume><issue>11</issue><spage>1577</spage><epage>1584</epage><pages>1577-1584</pages><issn>1352-4585</issn><eissn>1477-0970</eissn><abstract>Background:
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. MS lesions show a typical distribution pattern and primarily affect the white matter (WM) in the periventricular zone and in the centrum semiovale.
Objective:
To track lesion development during disease progression, we compared the spatiotemporal distribution patterns of lesions in relapsing–remitting MS (RRMS) and secondary progressive MS (SPMS).
Methods:
We used T1 and T2 weighted MR images of 209 RRMS and 62 SPMS patients acquired on two different 1.5 Tesla MR scanners in two clinical centers followed up for 25 (± 1.7) months. Both cross-sectional and longitudinal differences in lesion distribution between RRMS and SPMS patients were analyzed with lesion probability maps (LPMs) and permutation-based inference.
Results:
MS lesions clustered around the lateral ventricles and in the centrum semiovale. Cross-sectionally, compared to RRMS patients, the SPMS patients showed a significantly higher regional probability of T1 hypointense lesions (p≤0.03) in the callosal body, the corticospinal tract, and other tracts adjacent to the lateral ventricles, but not of T2 lesions (peak probabilities were RRMS: T1 9%, T2 18%; SPMS: T1 21%, T2 27%). No longitudinal changes of regional T1 and T2 lesion volumes between baseline and follow-up scan were found.
Conclusion:
The results suggest a particular vulnerability to neurodegeneration during disease progression in a number of WM tracts.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>22495945</pmid><doi>10.1177/1352458512442756</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1352-4585 |
| ispartof | Multiple sclerosis, 2012-11, Vol.18 (11), p.1577-1584 |
| issn | 1352-4585 1477-0970 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1115530720 |
| source | MEDLINE; SAGE Complete |
| subjects | Adult Analysis of Variance Biological and medical sciences Brain - pathology Chi-Square Distribution Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disability Evaluation Disease Progression Europe Female Humans Leukoencephalopathies - pathology Magnetic Resonance Imaging Male Medical sciences Middle Aged Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Multiple Sclerosis, Chronic Progressive - pathology Multiple Sclerosis, Relapsing-Remitting - pathology Neurology Predictive Value of Tests Time Factors |
| title | Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis |
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