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<meta name="DC.Title" content="Mechanisms of Bihemispheric Brain Infarctions in the Anterior Circulation on Diffusion-Weighted Images" />
<meta name="DC.Date" content="2005-04-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Multiple acute brain infarctions in both cerebral hemispheres usually suggest an embolic mechanism, particularly one of aortic or cardiac origin. The purpose of this study was to clarify the etiologic mechanisms and topographic features of bihemispheric infarctions depicted on diffusion-weighted imaging (DWI).

METHODS: Among 411 consecutive patients with ischemic stroke who underwent MR imaging in the acute phase, DWI showed bilateral infarctions in 19 (4.6%). In these patients, we analyzed the presence of carotid, aortic or cardiac embolic sources by using ultrasonography, cerebral angiography, and/or transesophageal echocardiography and evaluated the size and topographic distribution of the lesions. We assessed intracranial cross-flow through the anterior communicating artery, mainly on the basis of the anatomic information obatined from angiography or MR angiography.

RESULTS: Bilateral lesions were derived from cardiac and/or aortic embolic sources in 16 (84%) of 19 patients and appeared to originate from unilateral carotid diseases in three (16%). In nine (82%) of 11 patients with cardiac embolic sources, at least one large territorial or subcortical lesion was found in either hemisphere, whereas in all eight patients without a cardiac embolic source, the lesions were small and disseminated bilaterally.

CONCLUSION: Unilateral carotid lesions can cause bihemispheric infarctions through cross-flow in the anterior communicating artery. On DWI, small bihemispheric, disseminated lesions strongly suggest an artery-to-artery embolism. In such cases, aortic and carotid lesions should be assessed as potential embolic sources." />
<meta name="DC.Contributor" content="Kozue Saito" />
<meta name="DC.Contributor" content="Hiroshi Moriwaki" />
<meta name="DC.Contributor" content="Hiroshi Oe" />
<meta name="DC.Contributor" content="Kotaro Miyashita" />
<meta name="DC.Contributor" content="Kazuyuki Nagatsuka" />
<meta name="DC.Contributor" content="Satoshi Ueno" />
<meta name="DC.Contributor" content="Hiroaki Naritomi" />
<meta name="article:published_time" content="2005-04-01" />
<meta name="article:section" content="BRAIN" />
<meta name="citation_title" content="Mechanisms of Bihemispheric Brain Infarctions in the Anterior Circulation on Diffusion-Weighted Images" />
<meta name="citation_abstract" lang="en" content="&lt;p&gt;&lt;i&gt;BACKGROUND AND PURPOSE:&lt;/i&gt; Multiple acute brain infarctions in both cerebral hemispheres usually suggest an embolic mechanism, particularly one of aortic or cardiac origin. The purpose of this study was to clarify the etiologic mechanisms and topographic features of bihemispheric infarctions depicted on diffusion-weighted imaging (DWI).&lt;/p&gt;&lt;p&gt;&lt;i&gt;METHODS:&lt;/i&gt; Among 411 consecutive patients with ischemic stroke who underwent MR imaging in the acute phase, DWI showed bilateral infarctions in 19 (4.6%). In these patients, we analyzed the presence of carotid, aortic or cardiac embolic sources by using ultrasonography, cerebral angiography, and/or transesophageal echocardiography and evaluated the size and topographic distribution of the lesions. We assessed intracranial cross-flow through the anterior communicating artery, mainly on the basis of the anatomic information obatined from angiography or MR angiography.&lt;/p&gt;&lt;p&gt;&lt;i&gt;RESULTS:&lt;/i&gt; Bilateral lesions were derived from cardiac and/or aortic embolic sources in 16 (84%) of 19 patients and appeared to originate from unilateral carotid diseases in three (16%). In nine (82%) of 11 patients with cardiac embolic sources, at least one large territorial or subcortical lesion was found in either hemisphere, whereas in all eight patients without a cardiac embolic source, the lesions were small and disseminated bilaterally.&lt;/p&gt;&lt;p&gt;&lt;i&gt;CONCLUSION:&lt;/i&gt; Unilateral carotid lesions can cause bihemispheric infarctions through cross-flow in the anterior communicating artery. On DWI, small bihemispheric, disseminated lesions strongly suggest an artery-to-artery embolism. In such cases, aortic and carotid lesions should be assessed as potential embolic sources.&lt;/p&gt;" />
<meta name="citation_journal_title" content="American Journal of Neuroradiology" />
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<meta name="citation_publication_date" content="2005/04/01" />
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<meta name="citation_author" content="Kozue Saito" />
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<meta name="citation_author" content="Kotaro Miyashita" />
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<meta name="twitter:title" content="Mechanisms of Bihemispheric Brain Infarctions in the Anterior Circulation on Diffusion-Weighted Images" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Multiple acute brain infarctions in both cerebral hemispheres usually suggest an embolic mechanism, particularly one of aortic or cardiac origin. The purpose of this study was to clarify the etiologic mechanisms and topographic features of bihemispheric infarctions depicted on diffusion-weighted imaging (DWI).

METHODS: Among 411 consecutive patients with ischemic stroke who underwent MR imaging in the acute phase, DWI showed bilateral infarctions in 19 (4.6%). In these patients, we analyzed the presence of carotid, aortic or cardiac embolic sources by using ultrasonography, cerebral angiography, and/or transesophageal echocardiography and evaluated the size and topographic distribution of the lesions. We assessed intracranial cross-flow through the anterior communicating artery, mainly on the basis of the anatomic information obatined from angiography or MR angiography.

RESULTS: Bilateral lesions were derived from cardiac and/or aortic embolic sources in 16 (84%) of 19 patients and appeared to originate from unilateral carotid diseases in three (16%). In nine (82%) of 11 patients with cardiac embolic sources, at least one large territorial or subcortical lesion was found in either hemisphere, whereas in all eight patients without a cardiac embolic source, the lesions were small and disseminated bilaterally.

CONCLUSION: Unilateral carotid lesions can cause bihemispheric infarctions through cross-flow in the anterior communicating artery. On DWI, small bihemispheric, disseminated lesions strongly suggest an artery-to-artery embolism. In such cases, aortic and carotid lesions should be assessed as potential embolic sources." />
<meta name="og-title" property="og:title" content="Mechanisms of Bihemispheric Brain Infarctions in the Anterior Circulation on Diffusion-Weighted Images" />
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<meta name="og-description" property="og:description" content="BACKGROUND AND PURPOSE: Multiple acute brain infarctions in both cerebral hemispheres usually suggest an embolic mechanism, particularly one of aortic or cardiac origin. The purpose of this study was to clarify the etiologic mechanisms and topographic features of bihemispheric infarctions depicted on diffusion-weighted imaging (DWI).

METHODS: Among 411 consecutive patients with ischemic stroke who underwent MR imaging in the acute phase, DWI showed bilateral infarctions in 19 (4.6%). In these patients, we analyzed the presence of carotid, aortic or cardiac embolic sources by using ultrasonography, cerebral angiography, and/or transesophageal echocardiography and evaluated the size and topographic distribution of the lesions. We assessed intracranial cross-flow through the anterior communicating artery, mainly on the basis of the anatomic information obatined from angiography or MR angiography.

RESULTS: Bilateral lesions were derived from cardiac and/or aortic embolic sources in 16 (84%) of 19 patients and appeared to originate from unilateral carotid diseases in three (16%). In nine (82%) of 11 patients with cardiac embolic sources, at least one large territorial or subcortical lesion was found in either hemisphere, whereas in all eight patients without a cardiac embolic source, the lesions were small and disseminated bilaterally.

CONCLUSION: Unilateral carotid lesions can cause bihemispheric infarctions through cross-flow in the anterior communicating artery. On DWI, small bihemispheric, disseminated lesions strongly suggest an artery-to-artery embolism. In such cases, aortic and carotid lesions should be assessed as potential embolic sources." />
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        	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">Vol. 26</span>, <span  class="highwire-cite-metadata-issue highwire-cite-metadata">Issue 4 </span><div  class="highwire-cite-metadata-pubdate highwire-cite-metadata">1 Apr 2005 </div></div>
      
      
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      <div class="highwire-cite-title">Mechanisms of Bihemispheric Brain Infarctions in the Anterior Circulation on Diffusion-Weighted Images</div>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0"><span class="nlm-given-names">Kozue</span> <span class="nlm-surname">Saito</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">Hiroshi</span> <span class="nlm-surname">Moriwaki</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">Hiroshi</span> <span class="nlm-surname">Oe</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">Kotaro</span> <span class="nlm-surname">Miyashita</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">Kazuyuki</span> <span class="nlm-surname">Nagatsuka</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">Satoshi</span> <span class="nlm-surname">Ueno</span></span>, <span class="highwire-citation-author" data-delta="6"><span class="nlm-given-names">Hiroaki</span> <span class="nlm-surname">Naritomi</span></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">Apr 2005, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">26 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(4) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">809-814; </span></div>
  
  
  
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      <div class="highwire-cite-title">Mechanisms of Bihemispheric Brain Infarctions in the Anterior Circulation on Diffusion-Weighted Images</div>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0"><span class="nlm-given-names">Kozue</span> <span class="nlm-surname">Saito</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">Hiroshi</span> <span class="nlm-surname">Moriwaki</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">Hiroshi</span> <span class="nlm-surname">Oe</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">Kotaro</span> <span class="nlm-surname">Miyashita</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">Kazuyuki</span> <span class="nlm-surname">Nagatsuka</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">Satoshi</span> <span class="nlm-surname">Ueno</span></span>, <span class="highwire-citation-author" data-delta="6"><span class="nlm-given-names">Hiroaki</span> <span class="nlm-surname">Naritomi</span></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">Apr 2005, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">26 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(4) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">809-814; </span></div>
  
  
  
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