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<meta name="DC.Title" content="The Impact of Intracortical Lesions on Volumes of Subcortical Structures in Multiple Sclerosis" />
<meta name="DC.Identifier" content="10.3174/ajnr.A6513" />
<meta name="DC.Date" content="2020-05-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Recent studies showed thalamic atrophy in the early stages of MS. We investigated the impact of intracortical lesions on the volumes of subcortical structures (especially the thalamus) compared with other lesions in MS.

MATERIALS AND METHODS: Seventy-one patients with MS were included. The volumes of intracortical lesions and white matter lesions were identified on double inversion recovery and FLAIR, respectively, by using 3D Slicer. Volumes of white matter T1 hypointensities and subcortical gray matter, thalamus, caudate, putamen, and pallidum volumes were calculated using FreeSurfer. Age, MS duration, and the Expanded Disability Status Scale score were assessed.

RESULTS: Patients with intracortical lesions were older ( P  = .003), had longer disease duration ( P  &lt; .001), and higher Expanded Disability Status Scale scores ( P  = .02). The presence of intracortical lesions was associated with a significant decrease of subcortical gray matter volume ( P  = .02). In our multiple regression model, intracortical lesion volume was the only predictor of thalamic volume ( R 2 = 0.4, b * = –0.28, P  = .03) independent of white matter lesion volume and T1 hypointensity volume. White matter lesion volume showed an impact on subcortical gray matter volume in patients with relapsing-remitting MS ( P  = .04) and those with disease duration of &lt;5 years ( P  = .04) and on thalamic volume in patients with Expanded Disability Status Scale scores of &lt;4.0 ( P  = .01). By contrast, intracortical lesion volume showed an impact on subcortical gray matter and thalamic volumes in the secondary-progressive MS subgroup ( P  = .02 and P  &lt; .001) in patients with a long-standing disease course ( P  &lt; .001 and P  = .001) and more profound disability ( P  &lt; .001 and P  &lt; .001).

CONCLUSIONS: Thalamic atrophy was explained better by intracortical lesions than by white matter lesion and T1 hypointensity volumes, especially in patients with more profound disability.

DIR
:   double inversion recovery
EDSS
:   Expanded Disability Status Scale
iCL
:   intracortical lesion
ICV
:   intracranial volume
PPMS
:   primary-progressive MS
RRMS
:   relapsing-remitting MS
SPMS
:   secondary-progressive MS
T1H
:   T1 hypointensities
WMH
:   white matter hypointensities
WML
:   white matter lesions
SGMS
:   subcortical grey matter structures
b *
:   standartized regression coefficients" />
<meta name="DC.Contributor" content="I. Kalinin" />
<meta name="DC.Contributor" content="G. Makshakov" />
<meta name="DC.Contributor" content="E. Evdoshenko" />
<meta name="article:published_time" content="2020-05-01" />
<meta name="article:section" content="Adult Brain" />
<meta name="citation_title" content="The Impact of Intracortical Lesions on Volumes of Subcortical Structures in Multiple Sclerosis" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;Recent studies showed thalamic atrophy in the early stages of MS. We investigated the impact of intracortical lesions on the volumes of subcortical structures (especially the thalamus) compared with other lesions in MS.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;Seventy-one patients with MS were included. The volumes of intracortical lesions and white matter lesions were identified on double inversion recovery and FLAIR, respectively, by using 3D Slicer. Volumes of white matter T1 hypointensities and subcortical gray matter, thalamus, caudate, putamen, and pallidum volumes were calculated using FreeSurfer. Age, MS duration, and the Expanded Disability Status Scale score were assessed.&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;Patients with intracortical lesions were older (&lt;i&gt;P &lt;/i&gt;= .003), had longer disease duration (&lt;i&gt;P &lt;/i&gt;&amp;lt; .001), and higher Expanded Disability Status Scale scores (&lt;i&gt;P &lt;/i&gt;= .02). The presence of intracortical lesions was associated with a significant decrease of subcortical gray matter volume (&lt;i&gt;P &lt;/i&gt;= .02). In our multiple regression model, intracortical lesion volume was the only predictor of thalamic volume (&lt;i&gt;R&lt;/i&gt;&lt;sup&gt;2&lt;/sup&gt; = 0.4, &lt;i&gt;b&lt;/i&gt;* = –0.28, &lt;i&gt;P &lt;/i&gt;= .03) independent of white matter lesion volume and T1 hypointensity volume. White matter lesion volume showed an impact on subcortical gray matter volume in patients with relapsing-remitting MS (&lt;i&gt;P &lt;/i&gt;= .04) and those with disease duration of &amp;lt;5 years (&lt;i&gt;P &lt;/i&gt;= .04) and on thalamic volume in patients with Expanded Disability Status Scale scores of &amp;lt;4.0 (&lt;i&gt;P &lt;/i&gt;= .01). By contrast, intracortical lesion volume showed an impact on subcortical gray matter and thalamic volumes in the secondary-progressive MS subgroup (&lt;i&gt;P &lt;/i&gt;= .02 and &lt;i&gt;P &lt;/i&gt;&amp;lt; .001) in patients with a long-standing disease course (&lt;i&gt;P &lt;/i&gt;&amp;lt; .001 and &lt;i&gt;P &lt;/i&gt;= .001) and more profound disability (&lt;i&gt;P &lt;/i&gt;&amp;lt; .001 and &lt;i&gt;P &lt;/i&gt;&amp;lt; .001).&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;Thalamic atrophy was explained better by intracortical lesions than by white matter lesion and T1 hypointensity volumes, especially in patients with more profound disability.&lt;/p&gt;" />
<meta name="citation_journal_title" content="American Journal of Neuroradiology" />
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<meta name="citation_publication_date" content="2020/05/01" />
<meta name="citation_mjid" content="ajnr;41/5/804" />
<meta name="citation_id" content="41/5/804" />
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<meta name="citation_issn" content="0195-6108" />
<meta name="citation_issn" content="1936-959X" />
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<meta name="citation_author" content="I. Kalinin" />
<meta name="citation_author_institution" content="aFrom the SPb Center of Multiple Sclerosis and AID (SBIH City Clinical Hospital No. 31), St. Petersburg, Russia." />
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<meta name="citation_author" content="G. Makshakov" />
<meta name="citation_author_institution" content="aFrom the SPb Center of Multiple Sclerosis and AID (SBIH City Clinical Hospital No. 31), St. Petersburg, Russia." />
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<meta name="citation_author" content="E. Evdoshenko" />
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<meta name="twitter:title" content="The Impact of Intracortical Lesions on Volumes of Subcortical Structures in Multiple Sclerosis" />
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<meta name="twitter:image" content="http://ajnr-stage2.stage.highwire.org/sites/default/files/highwire/ajnr/41/5.cover-source.jpg" />
<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Recent studies showed thalamic atrophy in the early stages of MS. We investigated the impact of intracortical lesions on the volumes of subcortical structures (especially the thalamus) compared with other lesions in MS.

MATERIALS AND METHODS: Seventy-one patients with MS were included. The volumes of intracortical lesions and white matter lesions were identified on double inversion recovery and FLAIR, respectively, by using 3D Slicer. Volumes of white matter T1 hypointensities and subcortical gray matter, thalamus, caudate, putamen, and pallidum volumes were calculated using FreeSurfer. Age, MS duration, and the Expanded Disability Status Scale score were assessed.

RESULTS: Patients with intracortical lesions were older ( P  = .003), had longer disease duration ( P  &lt; .001), and higher Expanded Disability Status Scale scores ( P  = .02). The presence of intracortical lesions was associated with a significant decrease of subcortical gray matter volume ( P  = .02). In our multiple regression model, intracortical lesion volume was the only predictor of thalamic volume ( R 2 = 0.4, b * = –0.28, P  = .03) independent of white matter lesion volume and T1 hypointensity volume. White matter lesion volume showed an impact on subcortical gray matter volume in patients with relapsing-remitting MS ( P  = .04) and those with disease duration of &lt;5 years ( P  = .04) and on thalamic volume in patients with Expanded Disability Status Scale scores of &lt;4.0 ( P  = .01). By contrast, intracortical lesion volume showed an impact on subcortical gray matter and thalamic volumes in the secondary-progressive MS subgroup ( P  = .02 and P  &lt; .001) in patients with a long-standing disease course ( P  &lt; .001 and P  = .001) and more profound disability ( P  &lt; .001 and P  &lt; .001).

CONCLUSIONS: Thalamic atrophy was explained better by intracortical lesions than by white matter lesion and T1 hypointensity volumes, especially in patients with more profound disability.

DIR
:   double inversion recovery
EDSS
:   Expanded Disability Status Scale
iCL
:   intracortical lesion
ICV
:   intracranial volume
PPMS
:   primary-progressive MS
RRMS
:   relapsing-remitting MS
SPMS
:   secondary-progressive MS
T1H
:   T1 hypointensities
WMH
:   white matter hypointensities
WML
:   white matter lesions
SGMS
:   subcortical grey matter structures
b *
:   standartized regression coefficients" />
<meta name="og-title" property="og:title" content="The Impact of Intracortical Lesions on Volumes of Subcortical Structures in Multiple Sclerosis" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/41/5/804" />
<meta name="og-site-name" property="og:site_name" content="American Journal of Neuroradiology" />
<meta name="og-description" property="og:description" content="BACKGROUND AND PURPOSE: Recent studies showed thalamic atrophy in the early stages of MS. We investigated the impact of intracortical lesions on the volumes of subcortical structures (especially the thalamus) compared with other lesions in MS.

MATERIALS AND METHODS: Seventy-one patients with MS were included. The volumes of intracortical lesions and white matter lesions were identified on double inversion recovery and FLAIR, respectively, by using 3D Slicer. Volumes of white matter T1 hypointensities and subcortical gray matter, thalamus, caudate, putamen, and pallidum volumes were calculated using FreeSurfer. Age, MS duration, and the Expanded Disability Status Scale score were assessed.

RESULTS: Patients with intracortical lesions were older ( P  = .003), had longer disease duration ( P  &lt; .001), and higher Expanded Disability Status Scale scores ( P  = .02). The presence of intracortical lesions was associated with a significant decrease of subcortical gray matter volume ( P  = .02). In our multiple regression model, intracortical lesion volume was the only predictor of thalamic volume ( R 2 = 0.4, b * = –0.28, P  = .03) independent of white matter lesion volume and T1 hypointensity volume. White matter lesion volume showed an impact on subcortical gray matter volume in patients with relapsing-remitting MS ( P  = .04) and those with disease duration of &lt;5 years ( P  = .04) and on thalamic volume in patients with Expanded Disability Status Scale scores of &lt;4.0 ( P  = .01). By contrast, intracortical lesion volume showed an impact on subcortical gray matter and thalamic volumes in the secondary-progressive MS subgroup ( P  = .02 and P  &lt; .001) in patients with a long-standing disease course ( P  &lt; .001 and P  = .001) and more profound disability ( P  &lt; .001 and P  &lt; .001).

CONCLUSIONS: Thalamic atrophy was explained better by intracortical lesions than by white matter lesion and T1 hypointensity volumes, especially in patients with more profound disability.

DIR
:   double inversion recovery
EDSS
:   Expanded Disability Status Scale
iCL
:   intracortical lesion
ICV
:   intracranial volume
PPMS
:   primary-progressive MS
RRMS
:   relapsing-remitting MS
SPMS
:   secondary-progressive MS
T1H
:   T1 hypointensities
WMH
:   white matter hypointensities
WML
:   white matter lesions
SGMS
:   subcortical grey matter structures
b *
:   standartized regression coefficients" />
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    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">I. Kalinin</span>, <span class="highwire-citation-author" data-delta="1">G. Makshakov</span> and <span class="highwire-citation-author" data-delta="2">E. Evdoshenko</span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">May 2020,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">41 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(5) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">804-808; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata">DOI: https://doi.org/10.3174/ajnr.A6513 </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-75171--61861580749" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">I. Kalinin </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the SPb Center of Multiple Sclerosis and AID (SBIH City Clinical Hospital No. 31), St. Petersburg, Russia.</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=I.%2BKalinin%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Kalinin%20I&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AI.%2BKalinin%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="https://orcid.org/0000-0001-8297-1529" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for I. Kalinin</a></li></ul></div><div class="author-tooltip-1"><div class="author-tooltip-name">G. Makshakov </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the SPb Center of Multiple Sclerosis and AID (SBIH City Clinical Hospital No. 31), St. Petersburg, Russia.</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=G.%2BMakshakov%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Makshakov%20G&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AG.%2BMakshakov%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="https://orcid.org/0000-0001-6831-0441" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for G. Makshakov</a></li></ul></div><div class="author-tooltip-2"><div class="author-tooltip-name">E. Evdoshenko </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the SPb Center of Multiple Sclerosis and AID (SBIH City Clinical Hospital No. 31), St. Petersburg, Russia.</div></span></div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=E.%2BEvdoshenko%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Evdoshenko%20E&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link"><a href="/search/author1%3AE.%2BEvdoshenko%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li><li class="author-orcid-link last"><a href="https://orcid.org/0000-0002-8006-237X" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for E. Evdoshenko</a></li></ul></div></div></div>  </div>

  
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    <div class="highwire-markup"><div xmlns="http://www.w3.org/1999/xhtml" xmlns:xhtml="http://www.w3.org/1999/xhtml" class="section ref-list" id="ref-list-1"><h2 class="">References</h2><ol class="cit-list ref-use-labels"><li><span class="ref-label">1.</span><a class="rev-xref-ref" href="#xref-ref-1-1" title="View reference 1. in text" id="ref-1">↵</a><div class="cit ref-cit ref-journal" id="cit-41.5.804.1" data-doi="10.1177/1352458519851247"><div class="cit-metadata"><ol class="cit-auth-list"><li><span class="cit-auth"><span class="cit-name-surname">Capone</span>  <span class="cit-name-given-names">F</span></span>, </li><li><span class="cit-auth"><span class="cit-name-surname">Collorone</span>  <span class="cit-name-given-names">S</span></span>, </li><li><span class="cit-auth"><span class="cit-name-surname">Cortese</span>  <span class="cit-name-given-names">R</span></span>, <span class="cit-etal">et al</span></li></ol><cite>. <span class="cit-article-title">Fatigue in multiple 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        	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">Vol. 41</span>, <span  class="highwire-cite-metadata-issue highwire-cite-metadata">Issue 5 </span><div  class="highwire-cite-metadata-pubdate highwire-cite-metadata">1 May 2020 </div></div>
      
      
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      <div class="highwire-cite-title">The Impact of Intracortical Lesions on Volumes of Subcortical Structures in Multiple Sclerosis</div>  
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