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<meta name="DC.Title" content="Multimodality Imaging of Cortical and White Matter Abnormalities in Sturge-Weber Syndrome" />
<meta name="DC.Date" content="2007-05-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
<meta name="DC.Rights" content="Copyright © American Society of Neuroradiology" />
<meta name="DC.AccessRights" content="restricted" />
<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Impaired cortical venous outflow and abnormal deep venous collaterals are common in Sturge-Weber syndrome (SWS), but their relation to brain metabolism and function is poorly understood. In this study, advanced MR imaging techniques, such as susceptibility-weighted imaging (SWI) and diffusion tensor imaging (DTI), were applied in conjunction with positron-emission tomography (PET), to assess cortical and white matter structural abnormalities and their relation to cortical glucose metabolism and cognitive functions in children with unilateral SWS.

MATERIALS AND METHODS: Thirteen children (age, 1.5–10.3 years) with unilateral SWS underwent MR imaging with SWI and DTI, glucose metabolism PET, and comprehensive neuropsychologic assessment prospectively. The MR imaging and PET images were coregistered and cortical regions showing decreased glucose metabolism were compared with locations of SWI signal intensity abnormalities, changes in white matter water diffusion, and cognitive functions.

RESULTS: SWI detected both cortical abnormalities ( n = 8) and deep transmedullary veins ( n = 9), including those in young children with no cortical SWI signal intensity changes. These veins were often located under cortex adjacent to hypometabolic regions. DTI showed abnormal water diffusion both under hypometabolic cortex and in adjacent white matter with collateral veins. Cognitive dysfunction was associated with abnormal water diffusion in the posterior white matter.

CONCLUSIONS: Transmedullary venous collaterals can be detected early by SWI and persist in white matter adjacent to damaged cortex in children with SWS. Microstructural white matter damage extends beyond cortical abnormalities and may contribute to cognitive impairment. SWI and DTI can be incorporated into clinical MR imaging acquisitions to objectively assess microstructural abnormalities at different stages of SWS." />
<meta name="DC.Contributor" content="C. Juhász" />
<meta name="DC.Contributor" content="E.M. Haacke" />
<meta name="DC.Contributor" content="J. Hu" />
<meta name="DC.Contributor" content="Y. Xuan" />
<meta name="DC.Contributor" content="M. Makki" />
<meta name="DC.Contributor" content="M.E. Behen" />
<meta name="DC.Contributor" content="M. Maqbool" />
<meta name="DC.Contributor" content="O. Muzik" />
<meta name="DC.Contributor" content="D.C. Chugani" />
<meta name="DC.Contributor" content="H.T. Chugani" />
<meta name="article:published_time" content="2007-05-01" />
<meta name="article:section" content="PEDIATRICS" />
<meta name="citation_title" content="Multimodality Imaging of Cortical and White Matter Abnormalities in Sturge-Weber Syndrome" />
<meta name="citation_abstract" lang="en" content="&lt;p&gt;&lt;b&gt;BACKGROUND AND PURPOSE:&lt;/b&gt; Impaired cortical venous outflow and abnormal deep venous collaterals are common in Sturge-Weber syndrome (SWS), but their relation to brain metabolism and function is poorly understood. In this study, advanced MR imaging techniques, such as susceptibility-weighted imaging (SWI) and diffusion tensor imaging (DTI), were applied in conjunction with positron-emission tomography (PET), to assess cortical and white matter structural abnormalities and their relation to cortical glucose metabolism and cognitive functions in children with unilateral SWS.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS:&lt;/b&gt; Thirteen children (age, 1.5–10.3 years) with unilateral SWS underwent MR imaging with SWI and DTI, glucose metabolism PET, and comprehensive neuropsychologic assessment prospectively. The MR imaging and PET images were coregistered and cortical regions showing decreased glucose metabolism were compared with locations of SWI signal intensity abnormalities, changes in white matter water diffusion, and cognitive functions.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS:&lt;/b&gt; SWI detected both cortical abnormalities (&lt;i&gt;n&lt;/i&gt; = 8) and deep transmedullary veins (&lt;i&gt;n&lt;/i&gt; = 9), including those in young children with no cortical SWI signal intensity changes. These veins were often located under cortex &lt;i&gt;adjacent&lt;/i&gt; to hypometabolic regions. DTI showed abnormal water diffusion both under hypometabolic cortex and in adjacent white matter with collateral veins. Cognitive dysfunction was associated with abnormal water diffusion in the posterior white matter.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS:&lt;/b&gt; Transmedullary venous collaterals can be detected early by SWI and persist in white matter adjacent to damaged cortex in children with SWS. Microstructural white matter damage extends beyond cortical abnormalities and may contribute to cognitive impairment. SWI and DTI can be incorporated into clinical MR imaging acquisitions to objectively assess microstructural abnormalities at different stages of SWS.&lt;/p&gt;" />
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<meta name="twitter:title" content="Multimodality Imaging of Cortical and White Matter Abnormalities in Sturge-Weber Syndrome" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Impaired cortical venous outflow and abnormal deep venous collaterals are common in Sturge-Weber syndrome (SWS), but their relation to brain metabolism and function is poorly understood. In this study, advanced MR imaging techniques, such as susceptibility-weighted imaging (SWI) and diffusion tensor imaging (DTI), were applied in conjunction with positron-emission tomography (PET), to assess cortical and white matter structural abnormalities and their relation to cortical glucose metabolism and cognitive functions in children with unilateral SWS.

MATERIALS AND METHODS: Thirteen children (age, 1.5–10.3 years) with unilateral SWS underwent MR imaging with SWI and DTI, glucose metabolism PET, and comprehensive neuropsychologic assessment prospectively. The MR imaging and PET images were coregistered and cortical regions showing decreased glucose metabolism were compared with locations of SWI signal intensity abnormalities, changes in white matter water diffusion, and cognitive functions.

RESULTS: SWI detected both cortical abnormalities ( n = 8) and deep transmedullary veins ( n = 9), including those in young children with no cortical SWI signal intensity changes. These veins were often located under cortex adjacent to hypometabolic regions. DTI showed abnormal water diffusion both under hypometabolic cortex and in adjacent white matter with collateral veins. Cognitive dysfunction was associated with abnormal water diffusion in the posterior white matter.

CONCLUSIONS: Transmedullary venous collaterals can be detected early by SWI and persist in white matter adjacent to damaged cortex in children with SWS. Microstructural white matter damage extends beyond cortical abnormalities and may contribute to cognitive impairment. SWI and DTI can be incorporated into clinical MR imaging acquisitions to objectively assess microstructural abnormalities at different stages of SWS." />
<meta name="og-title" property="og:title" content="Multimodality Imaging of Cortical and White Matter Abnormalities in Sturge-Weber Syndrome" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/28/5/900" />
<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: Impaired cortical venous outflow and abnormal deep venous collaterals are common in Sturge-Weber syndrome (SWS), but their relation to brain metabolism and function is poorly understood. In this study, advanced MR imaging techniques, such as susceptibility-weighted imaging (SWI) and diffusion tensor imaging (DTI), were applied in conjunction with positron-emission tomography (PET), to assess cortical and white matter structural abnormalities and their relation to cortical glucose metabolism and cognitive functions in children with unilateral SWS.

MATERIALS AND METHODS: Thirteen children (age, 1.5–10.3 years) with unilateral SWS underwent MR imaging with SWI and DTI, glucose metabolism PET, and comprehensive neuropsychologic assessment prospectively. The MR imaging and PET images were coregistered and cortical regions showing decreased glucose metabolism were compared with locations of SWI signal intensity abnormalities, changes in white matter water diffusion, and cognitive functions.

RESULTS: SWI detected both cortical abnormalities ( n = 8) and deep transmedullary veins ( n = 9), including those in young children with no cortical SWI signal intensity changes. These veins were often located under cortex adjacent to hypometabolic regions. DTI showed abnormal water diffusion both under hypometabolic cortex and in adjacent white matter with collateral veins. Cognitive dysfunction was associated with abnormal water diffusion in the posterior white matter.

CONCLUSIONS: Transmedullary venous collaterals can be detected early by SWI and persist in white matter adjacent to damaged cortex in children with SWS. Microstructural white matter damage extends beyond cortical abnormalities and may contribute to cognitive impairment. SWI and DTI can be incorporated into clinical MR imaging acquisitions to objectively assess microstructural abnormalities at different stages of SWS." />
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      <h1 class="highwire-cite-title" id="page-title">Multimodality Imaging of Cortical and White Matter Abnormalities in Sturge-Weber Syndrome</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">C. Juhász</span>, <span class="highwire-citation-author" data-delta="1">E.M. Haacke</span>, <span class="highwire-citation-author" data-delta="2">J. Hu</span>, <span class="highwire-citation-author" data-delta="3">Y. Xuan</span>, <span class="highwire-citation-author" data-delta="4">M. Makki</span>, <span class="highwire-citation-author" data-delta="5">M.E. Behen</span>, <span class="highwire-citation-author" data-delta="6">M. Maqbool</span>, <span class="highwire-citation-author" data-delta="7">O. Muzik</span>, <span class="highwire-citation-author" data-delta="8">D.C. Chugani</span> and <span class="highwire-citation-author" data-delta="9">H.T. Chugani</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 2007,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">28 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(5) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">900-906; </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-6955--61207993274" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">C. Juhász </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=C.%2BJuh%C3%A1sz%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=Juh%C3%A1sz%20C&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 last"><a href="/search/author1%3AC.%2BJuh%25C3%25A1sz%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li></ul></div><div class="author-tooltip-1"><div class="author-tooltip-name">E.M. 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