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<!DOCTYPE html>
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<meta name="HW.identifier" content="/ajnr/early/2024/12/05/ajnr.A8426.atom" />
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<meta name="DC.Title" content="Alternative Venous Pathways: A Potential Key Imaging Feature for Early Diagnosis of Sturge-Weber Syndrome Type 1" />
<meta name="DC.Identifier" content="10.3174/ajnr.A8426" />
<meta name="DC.Date" content="2024-12-05" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
<meta name="DC.Rights" content="© 2025 by American Journal of Neuroradiology" />
<meta name="DC.AccessRights" content="restricted" />
<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Sturge-Weber syndrome (SWS) is a rare congenital disorder characterized by cortical atrophy and calcifications on late-stage imaging. Understanding the evolution of brain lesions is crucial for effective early interventions, yet the timeline remains unclear. We aimed to evaluate early brain MRI findings and their progression longitudinally on follow-up MRI in children diagnosed with SWS.

MATERIALS AND METHODS: We retrospectively included all children with a confirmed diagnosis of SWS between 2009 and 2023 who had at least 2 available MRIs performed before the age of 2 years. A pediatric radiologist and a pediatric neuroradiologist evaluated all the MRI scans for pial enhancement, choroid plexus enlargement, atrophy, calcifications, a prominent subarachnoid varicose network, transmedullary veins, subependymal veins, and deep extraventricular veins. Descriptive analysis was used for demographic data and brain lesion prevalence. Cumulative incidence curves were used to show the timeline of emerging lesions. K-means clustering was used to categorize the lesions based on their prevalence at 1, 2, 3, 6, 12, 18, and 24 months after birth.

RESULTS: Nine patients met the inclusion criteria. Median ages at the first and last MRIs were 35 days (interquartile range [IQR]: 11–123) and 294 days (IQR: 208–465), respectively. The most prevalent lesions at the first MRI were subarachnoid varicose network (88.9%) and transmedullary veins (77.8%), while prevalence of atrophy and calcifications differed most between the first and last MRIs. The results of the elbow method and K-means clustering showed that we can divide SWS lesions into 3 groups based on their timeline of emergence. The first cluster contained subarachnoid varicose network, transmedullary veins, subependymal veins, and choroid plexus enlargement. The second cluster contained deep extraventricular veins, pial enhancement, accelerated myelination, and atrophy. The last cluster contained calcifications.

CONCLUSIONS: Our findings suggest that dilated venous channels emerge early as a compensatory mechanism, preceding atrophy and calcification. Additionally, these dilated channels precede the appearance of abnormal contrast enhancement of the pia, often termed leptomeningeal angioma. This underscores the importance of early recognition and monitoring of these initial imaging indicators in clinical practice.

ASL
:   arterial spin-labeled
IQR
:   interquartile range
MinIP
:   minimum intensity projection
SWS
:   Sturge-Weber syndrome" />
<meta name="DC.Contributor" content="Carmen R. Cerron-Vela" />
<meta name="DC.Contributor" content="Amirreza Manteghinejad" />
<meta name="DC.Contributor" content="Simon M. Clifford" />
<meta name="DC.Contributor" content="Savvas Andronikou" />
<meta name="article:published_time" content="2024-12-05" />
<meta name="article:section" content="PEDIATRIC NEUROIMAGING" />
<meta name="citation_title" content="Alternative Venous Pathways: A Potential Key Imaging Feature for Early Diagnosis of Sturge-Weber Syndrome Type 1" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;Sturge-Weber syndrome (SWS) is a rare congenital disorder characterized by cortical atrophy and calcifications on late-stage imaging. Understanding the evolution of brain lesions is crucial for effective early interventions, yet the timeline remains unclear. We aimed to evaluate early brain MRI findings and their progression longitudinally on follow-up MRI in children diagnosed with SWS.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;We retrospectively included all children with a confirmed diagnosis of SWS between 2009 and 2023 who had at least 2 available MRIs performed before the age of 2 years. A pediatric radiologist and a pediatric neuroradiologist evaluated all the MRI scans for pial enhancement, choroid plexus enlargement, atrophy, calcifications, a prominent subarachnoid varicose network, transmedullary veins, subependymal veins, and deep extraventricular veins. Descriptive analysis was used for demographic data and brain lesion prevalence. Cumulative incidence curves were used to show the timeline of emerging lesions. K-means clustering was used to categorize the lesions based on their prevalence at 1, 2, 3, 6, 12, 18, and 24 months after birth.&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;Nine patients met the inclusion criteria. Median ages at the first and last MRIs were 35 days (interquartile range [IQR]: 11–123) and 294 days (IQR: 208–465), respectively. The most prevalent lesions at the first MRI were subarachnoid varicose network (88.9%) and transmedullary veins (77.8%), while prevalence of atrophy and calcifications differed most between the first and last MRIs. The results of the elbow method and K-means clustering showed that we can divide SWS lesions into 3 groups based on their timeline of emergence. The first cluster contained subarachnoid varicose network, transmedullary veins, subependymal veins, and choroid plexus enlargement. The second cluster contained deep extraventricular veins, pial enhancement, accelerated myelination, and atrophy. The last cluster contained calcifications.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;Our findings suggest that dilated venous channels emerge early as a compensatory mechanism, preceding atrophy and calcification. Additionally, these dilated channels precede the appearance of abnormal contrast enhancement of the pia, often termed leptomeningeal angioma. This underscores the importance of early recognition and monitoring of these initial imaging indicators in clinical practice.&lt;/p&gt;" />
<meta name="citation_journal_title" content="American Journal of Neuroradiology" />
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<meta name="twitter:title" content="Alternative Venous Pathways: A Potential Key Imaging Feature for Early Diagnosis of Sturge-Weber Syndrome Type 1" />
<meta name="twitter:card" content="summary" />
<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Sturge-Weber syndrome (SWS) is a rare congenital disorder characterized by cortical atrophy and calcifications on late-stage imaging. Understanding the evolution of brain lesions is crucial for effective early interventions, yet the timeline remains unclear. We aimed to evaluate early brain MRI findings and their progression longitudinally on follow-up MRI in children diagnosed with SWS.

MATERIALS AND METHODS: We retrospectively included all children with a confirmed diagnosis of SWS between 2009 and 2023 who had at least 2 available MRIs performed before the age of 2 years. A pediatric radiologist and a pediatric neuroradiologist evaluated all the MRI scans for pial enhancement, choroid plexus enlargement, atrophy, calcifications, a prominent subarachnoid varicose network, transmedullary veins, subependymal veins, and deep extraventricular veins. Descriptive analysis was used for demographic data and brain lesion prevalence. Cumulative incidence curves were used to show the timeline of emerging lesions. K-means clustering was used to categorize the lesions based on their prevalence at 1, 2, 3, 6, 12, 18, and 24 months after birth.

RESULTS: Nine patients met the inclusion criteria. Median ages at the first and last MRIs were 35 days (interquartile range [IQR]: 11–123) and 294 days (IQR: 208–465), respectively. The most prevalent lesions at the first MRI were subarachnoid varicose network (88.9%) and transmedullary veins (77.8%), while prevalence of atrophy and calcifications differed most between the first and last MRIs. The results of the elbow method and K-means clustering showed that we can divide SWS lesions into 3 groups based on their timeline of emergence. The first cluster contained subarachnoid varicose network, transmedullary veins, subependymal veins, and choroid plexus enlargement. The second cluster contained deep extraventricular veins, pial enhancement, accelerated myelination, and atrophy. The last cluster contained calcifications.

CONCLUSIONS: Our findings suggest that dilated venous channels emerge early as a compensatory mechanism, preceding atrophy and calcification. Additionally, these dilated channels precede the appearance of abnormal contrast enhancement of the pia, often termed leptomeningeal angioma. This underscores the importance of early recognition and monitoring of these initial imaging indicators in clinical practice.

ASL
:   arterial spin-labeled
IQR
:   interquartile range
MinIP
:   minimum intensity projection
SWS
:   Sturge-Weber syndrome" />
<meta name="og-title" property="og:title" content="Alternative Venous Pathways: A Potential Key Imaging Feature for Early Diagnosis of Sturge-Weber Syndrome Type 1" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/early/2024/12/05/ajnr.A8426" />
<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: Sturge-Weber syndrome (SWS) is a rare congenital disorder characterized by cortical atrophy and calcifications on late-stage imaging. Understanding the evolution of brain lesions is crucial for effective early interventions, yet the timeline remains unclear. We aimed to evaluate early brain MRI findings and their progression longitudinally on follow-up MRI in children diagnosed with SWS.

MATERIALS AND METHODS: We retrospectively included all children with a confirmed diagnosis of SWS between 2009 and 2023 who had at least 2 available MRIs performed before the age of 2 years. A pediatric radiologist and a pediatric neuroradiologist evaluated all the MRI scans for pial enhancement, choroid plexus enlargement, atrophy, calcifications, a prominent subarachnoid varicose network, transmedullary veins, subependymal veins, and deep extraventricular veins. Descriptive analysis was used for demographic data and brain lesion prevalence. Cumulative incidence curves were used to show the timeline of emerging lesions. K-means clustering was used to categorize the lesions based on their prevalence at 1, 2, 3, 6, 12, 18, and 24 months after birth.

RESULTS: Nine patients met the inclusion criteria. Median ages at the first and last MRIs were 35 days (interquartile range [IQR]: 11–123) and 294 days (IQR: 208–465), respectively. The most prevalent lesions at the first MRI were subarachnoid varicose network (88.9%) and transmedullary veins (77.8%), while prevalence of atrophy and calcifications differed most between the first and last MRIs. The results of the elbow method and K-means clustering showed that we can divide SWS lesions into 3 groups based on their timeline of emergence. The first cluster contained subarachnoid varicose network, transmedullary veins, subependymal veins, and choroid plexus enlargement. The second cluster contained deep extraventricular veins, pial enhancement, accelerated myelination, and atrophy. The last cluster contained calcifications.

CONCLUSIONS: Our findings suggest that dilated venous channels emerge early as a compensatory mechanism, preceding atrophy and calcification. Additionally, these dilated channels precede the appearance of abnormal contrast enhancement of the pia, often termed leptomeningeal angioma. This underscores the importance of early recognition and monitoring of these initial imaging indicators in clinical practice.

ASL
:   arterial spin-labeled
IQR
:   interquartile range
MinIP
:   minimum intensity projection
SWS
:   Sturge-Weber syndrome" />
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    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">Carmen R. Cerron-Vela</span>, <span class="highwire-citation-author" data-delta="1">Amirreza Manteghinejad</span>, <span class="highwire-citation-author" data-delta="2">Simon M. Clifford</span> and <span class="highwire-citation-author" data-delta="3">Savvas Andronikou</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">December 2024,  </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata">DOI: https://doi.org/10.3174/ajnr.A8426 </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-112178--61977195174" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">Carmen R. 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Cerron-Vela</a></li></ul></div><div class="author-tooltip-1"><div class="author-tooltip-name">Amirreza Manteghinejad </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania</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=Amirreza%2BManteghinejad%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=Manteghinejad%20A&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%3AAmirreza%2BManteghinejad%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/0000-0002-3847-5496" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for Amirreza Manteghinejad</a></li></ul></div><div class="author-tooltip-2"><div class="author-tooltip-name">Simon M. Clifford </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania</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=Simon%2BM.%2BClifford%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=Clifford%20SM&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%3ASimon%2BM.%2BClifford%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/0000-0002-2793-4159" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for Simon M. Clifford</a></li></ul></div><div class="author-tooltip-3"><div class="author-tooltip-name">Savvas Andronikou </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'><span class='nlm-sup'>a</span>From the Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania</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=Savvas%2BAndronikou%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=Andronikou%20S&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%3ASavvas%2BAndronikou%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/0000-0002-1015-9790" target="_blank" class="" data-icon-position="" data-hide-link-title="0">ORCID record for Savvas Andronikou</a></li></ul></div></div></div>  </div>

  
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