000006369 001__ 6369
000006369 005__ 20240523043342.0
000006369 02470 $$ahttps://doi.org/10.1371/journal.pone.0209326$$2doi
000006369 037__ $$aTEXTUAL$$bArticle
000006369 041__ $$aeng
000006369 245__ $$aGray matter atrophy in multiple sclerosis despite clinical and lesion stability during natalizumab treatment
000006369 269__ $$a2018-12-21
000006369 336__ $$aArticle
000006369 520__ $$a&lt;p&gt;Background: Brain volume loss is an important surrogate marker for assessing disability in MS; however, contribution of gray and white matter to the whole brain volume loss needs further examination in the context of specific MS treatment.&lt;/p&gt; &lt;p&gt;Objectives: To examine whole and segmented gray, white, thalamic, and corpus callosum volume loss in stable patients receiving natalizumab for 2–5 years.&lt;/p&gt; &lt;p&gt;Methods: This was a retrospective study of 20 patients undergoing treatment with natalizumab for 24–68 months. Whole brain volume loss was determined with SIENA. Gray and white matter segmentation was done using FAST. Thalamic and corpus callosum volumes were determined using Freesurfer. T1 relaxation values of chronic hypointense lesions (black holes) were determined using a quantitative, in-house developed method to assess lesion evolution.&lt;/p&gt; &lt;p&gt;Results: Over a mean of 36.6 months, median percent brain volume change (PBVC) was -2.0% (IQR 0.99–2.99). There was decline in gray (p = 0.001) but not white matter (p = 0.6), and thalamic (p = 0.01) but not corpus callosum volume (p = 0.09). Gray matter loss correlated with PBVC (Spearman’s r = 0.64, p = 0.003) but not white matter (Spearman’s r = 0.42, p = 0.07). Age significantly influenced whole brain volume loss (p = 0.010, multivariate regression), but disease duration and baseline T2 lesion volume did not. There was no change in T1 relaxation values of lesions or T2 lesion volume over time. All patients remained clinically stable.&lt;/p&gt; &lt;p&gt;Conclusions: These results demonstrate that brain volume loss in MS is primarily driven by gray matter changes and may be independent of clinically effective treatment.&lt;/p&gt;
000006369 536__ $$oTurku University Hospital
000006369 540__ $$a&lt;p&gt;© 2018 Koskimäki et al.&lt;/p&gt; &lt;p&gt;This is an open access article distributed under the terms of the &lt;a href="http://creativecommons.org/licenses/by/4.0/" target="_blank"&gt;Creative Commons Attribution License&lt;/a&gt;, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.&lt;/p&gt;
000006369 542__ $$fCC BY
000006369 594__ $$aAll relevant data are within the paper and its Supporting Information files.
000006369 690__ $$aBiological Sciences Division
000006369 691__ $$aNeurology
000006369 691__ $$aRadiology
000006369 7001_ $$1http://orcid.org/0000-0001-7171-3217$$2ORCID$$aKoskimäki, Fredrika$$uUniversity of Turku
000006369 7001_ $$aBernard, Jacqueline$$uOregon Health Science University
000006369 7001_ $$1http://orcid.org/0000-0002-6418-0309$$2ORCID$$aYong, Jeong$$uNorthwestern University
000006369 7001_ $$aArndt, Nancy$$uUniversity of Chicago
000006369 7001_ $$aCarroll, Timothy$$uUniversity of Chicago
000006369 7001_ $$aLee, Seon-Kyu$$uUniversity of Chicago
000006369 7001_ $$aReder, Anthony T.$$uUniversity of Chicago
000006369 7001_ $$aJaved, Adil$$uUniversity of Chicago
000006369 773__ $$tPLOS ONE
000006369 8564_ $$yArticle$$9feadba3d-136e-4822-881e-0f65abe72829$$s791019$$uhttps://knowledge.uchicago.edu/record/6369/files/journal.pone.0209326.pdf$$ePublic
000006369 8564_ $$yAppendix$$94549ba27-d8d6-4432-a95c-b4f4b5a3ae53$$s32256$$uhttps://knowledge.uchicago.edu/record/6369/files/pone.0209326.s001.xls$$ePublic
000006369 908__ $$aI agree
000006369 909CO $$ooai:uchicago.tind.io:6369$$pGLOBAL_SET
000006369 983__ $$aArticle