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<meta name="DC.Title" content="Venous sinus occlusive disease: MR findings." />
<meta name="DC.Date" content="1994-02-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
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<meta name="DC.Description" content="PURPOSE To study MR patterns of venous sinus occlusive disease and to relate them to the underlying pathophysiology by comparing the appearance and pathophysiologic features of venous sinus occlusive disease with those of arterial ischemic disease.

METHODS The clinical data and MR examinations of 26 patients with venous sinus occlusive disease were retrospectively reviewed with special attention to mass effect, hemorrhage, and T2-weighted image abnormalities as well as to abnormal parenchymal, venous, or arterial enhancement after intravenous gadopentetate dimeglumine administration. Follow-up studies when available were evaluated for atrophy, infarction, chronic mass effect, and hemorrhage.

RESULTS Mass effect was present in 25 of 26 patients. Eleven of the 26 had mass effect without abnormal signal on T2-weighted images. Fifteen patients had abnormal signal on T2-weighted images, but this was much less extensive than the degree of brain swelling in all cases. No patient showed abnormal parenchymal or arterial enhancement. Abnormal venous enhancement was seen in 10 of 13 patients who had contrast-enhanced studies. Intraparenchymal hemorrhage was seen in nine patients with high signal on T2-weighted images predominantly peripheral to the hematoma in eight. Three overall MR patterns were observed in acute sinus thrombosis: 1) mass effect without associated abnormal signal on T2-weighted images, 2) mass effect with associated abnormal signal on T2-weighted images and/or ventricular dilatation that may be reversible, and 3) intraparenchymal hematoma with surrounding edema.

CONCLUSION MR findings of venous sinus occlusive disease are different from those of arterial ischemia and may reflect different underlying pathophysiology. In venous sinus occlusive disease, the breakdown of the blood-brain barrier (vasogenic edema and abnormal parenchymal enhancement) does not always occur, and brain swelling can persist up to 2 years with or without abnormal signal on T2-weighted images. Abnormal signal on T2-weighted images may be reversible and does not always indicate infarction." />
<meta name="DC.Contributor" content="W T Yuh" />
<meta name="DC.Contributor" content="T M Simonson" />
<meta name="DC.Contributor" content="A M Wang" />
<meta name="DC.Contributor" content="T M Koci" />
<meta name="DC.Contributor" content="E T Tali" />
<meta name="DC.Contributor" content="D J Fisher" />
<meta name="DC.Contributor" content="J H Simon" />
<meta name="DC.Contributor" content="J R Jinkins" />
<meta name="DC.Contributor" content="F Tsai" />
<meta name="article:published_time" content="1994-02-01" />
<meta name="citation_title" content="Venous sinus occlusive disease: MR findings." />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;PURPOSE&lt;/h3&gt;
&lt;p&gt;To study MR patterns of venous sinus occlusive disease and to relate them to the underlying pathophysiology by comparing the appearance and pathophysiologic features of venous sinus occlusive disease with those of arterial ischemic disease.&lt;/p&gt;&lt;h3&gt;METHODS&lt;/h3&gt;
&lt;p&gt;The clinical data and MR examinations of 26 patients with venous sinus occlusive disease were retrospectively reviewed with special attention to mass effect, hemorrhage, and T2-weighted image abnormalities as well as to abnormal parenchymal, venous, or arterial enhancement after intravenous gadopentetate dimeglumine administration. Follow-up studies when available were evaluated for atrophy, infarction, chronic mass effect, and hemorrhage.&lt;/p&gt;&lt;h3&gt;RESULTS&lt;/h3&gt;
&lt;p&gt;Mass effect was present in 25 of 26 patients. Eleven of the 26 had mass effect without abnormal signal on T2-weighted images. Fifteen patients had abnormal signal on T2-weighted images, but this was much less extensive than the degree of brain swelling in all cases. No patient showed abnormal parenchymal or arterial enhancement. Abnormal venous enhancement was seen in 10 of 13 patients who had contrast-enhanced studies. Intraparenchymal hemorrhage was seen in nine patients with high signal on T2-weighted images predominantly peripheral to the hematoma in eight. Three overall MR patterns were observed in acute sinus thrombosis: 1) mass effect without associated abnormal signal on T2-weighted images, 2) mass effect with associated abnormal signal on T2-weighted images and/or ventricular dilatation that may be reversible, and 3) intraparenchymal hematoma with surrounding edema.&lt;/p&gt;&lt;h3&gt;CONCLUSION&lt;/h3&gt;
&lt;p&gt;MR findings of venous sinus occlusive disease are different from those of arterial ischemia and may reflect different underlying pathophysiology. In venous sinus occlusive disease, the breakdown of the blood-brain barrier (vasogenic edema and abnormal parenchymal enhancement) does not always occur, and brain swelling can persist up to 2 years with or without abnormal signal on T2-weighted images. Abnormal signal on T2-weighted images may be reversible and does not always indicate infarction.&lt;/p&gt;" />
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<meta name="citation_author" content="W T Yuh" />
<meta name="citation_author_institution" content="Department of Radiology, University of Iowa College of Medicine, Iowa City." />
<meta name="citation_author" content="T M Simonson" />
<meta name="citation_author_institution" content="Department of Radiology, University of Iowa College of Medicine, Iowa City." />
<meta name="citation_author" content="A M Wang" />
<meta name="citation_author_institution" content="Department of Radiology, University of Iowa College of Medicine, Iowa City." />
<meta name="citation_author" content="T M Koci" />
<meta name="citation_author_institution" content="Department of Radiology, University of Iowa College of Medicine, Iowa City." />
<meta name="citation_author" content="E T Tali" />
<meta name="citation_author_institution" content="Department of Radiology, University of Iowa College of Medicine, Iowa City." />
<meta name="citation_author" content="D J Fisher" />
<meta name="citation_author_institution" content="Department of Radiology, University of Iowa College of Medicine, Iowa City." />
<meta name="citation_author" content="J H Simon" />
<meta name="citation_author_institution" content="Department of Radiology, University of Iowa College of Medicine, Iowa City." />
<meta name="citation_author" content="J R Jinkins" />
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<meta name="twitter:title" content="Venous sinus occlusive disease: MR findings." />
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<meta name="twitter:description" content="PURPOSE To study MR patterns of venous sinus occlusive disease and to relate them to the underlying pathophysiology by comparing the appearance and pathophysiologic features of venous sinus occlusive disease with those of arterial ischemic disease.

METHODS The clinical data and MR examinations of 26 patients with venous sinus occlusive disease were retrospectively reviewed with special attention to mass effect, hemorrhage, and T2-weighted image abnormalities as well as to abnormal parenchymal, venous, or arterial enhancement after intravenous gadopentetate dimeglumine administration. Follow-up studies when available were evaluated for atrophy, infarction, chronic mass effect, and hemorrhage.

RESULTS Mass effect was present in 25 of 26 patients. Eleven of the 26 had mass effect without abnormal signal on T2-weighted images. Fifteen patients had abnormal signal on T2-weighted images, but this was much less extensive than the degree of brain swelling in all cases. No patient showed abnormal parenchymal or arterial enhancement. Abnormal venous enhancement was seen in 10 of 13 patients who had contrast-enhanced studies. Intraparenchymal hemorrhage was seen in nine patients with high signal on T2-weighted images predominantly peripheral to the hematoma in eight. Three overall MR patterns were observed in acute sinus thrombosis: 1) mass effect without associated abnormal signal on T2-weighted images, 2) mass effect with associated abnormal signal on T2-weighted images and/or ventricular dilatation that may be reversible, and 3) intraparenchymal hematoma with surrounding edema.

CONCLUSION MR findings of venous sinus occlusive disease are different from those of arterial ischemia and may reflect different underlying pathophysiology. In venous sinus occlusive disease, the breakdown of the blood-brain barrier (vasogenic edema and abnormal parenchymal enhancement) does not always occur, and brain swelling can persist up to 2 years with or without abnormal signal on T2-weighted images. Abnormal signal on T2-weighted images may be reversible and does not always indicate infarction." />
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<meta name="og-site-name" property="og:site_name" content="American Journal of Neuroradiology" />
<meta name="og-description" property="og:description" content="PURPOSE To study MR patterns of venous sinus occlusive disease and to relate them to the underlying pathophysiology by comparing the appearance and pathophysiologic features of venous sinus occlusive disease with those of arterial ischemic disease.

METHODS The clinical data and MR examinations of 26 patients with venous sinus occlusive disease were retrospectively reviewed with special attention to mass effect, hemorrhage, and T2-weighted image abnormalities as well as to abnormal parenchymal, venous, or arterial enhancement after intravenous gadopentetate dimeglumine administration. Follow-up studies when available were evaluated for atrophy, infarction, chronic mass effect, and hemorrhage.

RESULTS Mass effect was present in 25 of 26 patients. Eleven of the 26 had mass effect without abnormal signal on T2-weighted images. Fifteen patients had abnormal signal on T2-weighted images, but this was much less extensive than the degree of brain swelling in all cases. No patient showed abnormal parenchymal or arterial enhancement. Abnormal venous enhancement was seen in 10 of 13 patients who had contrast-enhanced studies. Intraparenchymal hemorrhage was seen in nine patients with high signal on T2-weighted images predominantly peripheral to the hematoma in eight. Three overall MR patterns were observed in acute sinus thrombosis: 1) mass effect without associated abnormal signal on T2-weighted images, 2) mass effect with associated abnormal signal on T2-weighted images and/or ventricular dilatation that may be reversible, and 3) intraparenchymal hematoma with surrounding edema.

CONCLUSION MR findings of venous sinus occlusive disease are different from those of arterial ischemia and may reflect different underlying pathophysiology. In venous sinus occlusive disease, the breakdown of the blood-brain barrier (vasogenic edema and abnormal parenchymal enhancement) does not always occur, and brain swelling can persist up to 2 years with or without abnormal signal on T2-weighted images. Abnormal signal on T2-weighted images may be reversible and does not always indicate infarction." />
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      <h1 class="highwire-cite-title" id="page-title">Venous sinus occlusive disease: MR findings.</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">W T Yuh</span>, <span class="highwire-citation-author" data-delta="1">T M Simonson</span>, <span class="highwire-citation-author" data-delta="2">A M Wang</span>, <span class="highwire-citation-author" data-delta="3">T M Koci</span>, <span class="highwire-citation-author" data-delta="4">E T Tali</span>, <span class="highwire-citation-author" data-delta="5">D J Fisher</span>, <span class="highwire-citation-author" data-delta="6">J H Simon</span>, <span class="highwire-citation-author" data-delta="7">J R Jinkins</span> and <span class="highwire-citation-author" data-delta="8">F Tsai</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">February 1994,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">15 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(2) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">309-316; </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-5935--6127770189" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">W T Yuh </div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'>Department of Radiology, University of Iowa College of Medicine, Iowa City.</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=W%2BT%2BYuh%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=Yuh%20WT&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%3AW%2BT%2BYuh%2B" rel="nofollow" class="" 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          <p id="p-1"><strong>PURPOSE</strong> To study MR patterns of venous sinus occlusive disease and to relate them to the underlying pathophysiology by comparing the appearance and pathophysiologic features of venous sinus occlusive disease with those of arterial ischemic disease.</p>
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          <p id="p-2"><strong>METHODS</strong> The clinical data and MR examinations of 26 patients with venous sinus occlusive disease were retrospectively reviewed with special attention to mass effect, hemorrhage, and T2-weighted image abnormalities as well as to abnormal parenchymal, venous, or arterial enhancement after intravenous gadopentetate dimeglumine administration. Follow-up studies when available were evaluated for atrophy, infarction, chronic mass effect, and hemorrhage.</p>
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          <p id="p-3"><strong>RESULTS</strong> Mass effect was present in 25 of 26 patients. Eleven of the 26 had mass effect without abnormal signal on T2-weighted images. Fifteen patients had abnormal signal on T2-weighted images, but this was much less extensive than the degree of brain swelling in all cases. No patient showed abnormal parenchymal or arterial enhancement. Abnormal venous enhancement was seen in 10 of 13 patients who had contrast-enhanced studies. Intraparenchymal hemorrhage was seen in nine patients with high signal on T2-weighted images predominantly peripheral to the hematoma in eight. Three overall MR patterns were observed in acute sinus thrombosis: 1) mass effect without associated abnormal signal on T2-weighted images, 2) mass effect with associated abnormal signal on T2-weighted images and/or ventricular dilatation that may be reversible, and 3) intraparenchymal hematoma with surrounding edema.</p>
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          <p id="p-4"><strong>CONCLUSION</strong> MR findings of venous sinus occlusive disease are different from those of arterial ischemia and may reflect different underlying pathophysiology. In venous sinus occlusive disease, the breakdown of the blood-brain barrier (vasogenic edema and abnormal parenchymal enhancement) does not always occur, and brain swelling can persist up to 2 years with or without abnormal signal on T2-weighted images. Abnormal signal on T2-weighted images may be reversible and does not always indicate infarction.</p>
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        	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">Vol. 15</span>, <span  class="highwire-cite-metadata-issue highwire-cite-metadata">Issue 2 </span><div  class="highwire-cite-metadata-pubdate highwire-cite-metadata">1 Feb 1994 </div></div>
      
      
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    	<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">Feb 1994, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">15 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(2) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">309-316; </span></div>
  
  
  
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