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<meta name="DC.Title" content="Magnetization transfer effects in MR imaging of in vivo intracranial hemorrhage." />
<meta name="DC.Date" content="1993-07-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
<meta name="DC.Rights" content="Copyright © American Society of Neuroradiology" />
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<meta name="DC.Description" content="PURPOSE Recent papers have hypothesized that diamagnetic effects of clotting and conformational changes in aging red blood cells immobilize the hemoglobin protein and thus are responsible for the marked hypointensity of acute hematomas on T2-weighted spin-echo MR images. To test that hypothesis, the authors evaluated 24 hemorrhagic components of intracranial hemorrhagic lesions using accepted criteria based on spin-echo images as the definitions of the stage of the hemorrhage.

METHODS As a measure of the effects of macromolecular (hemoglobin protein) immobility, magnetization transfer contrast was elicited using a pulsed saturation magnetization transfer experiment. The apparent magnetization transfer contrast (AMTC) was determined by comparing the signal intensities of saturated with unsaturated images and quantified for acute isolated hemorrhages, acute nonisolated hemorrhagic lesions, and subacute-to-chronic hemorrhages.

RESULTS The AMTC of isolated acute hemorrhage was significantly less than that of normal, white matter and gray matter, indicating the lack of significant magnetization transfer and therefore the lack of effects of restriction of hemoglobin mobility on the signal intensity of acute hemorrhage. Acutely hemorrhagic tissue (nonisolated acute hemorrhage) has significantly more AMTC than isolated acute hemorrhage, but still not exceeding that of brain parenchyma.

CONCLUSION This in vivo data concurs with in vitro data and reinforces the concept that the marked hypointensity of acute hematomas is mainly a magnetic susceptibility effect." />
<meta name="DC.Contributor" content="R L Mittl" />
<meta name="DC.Contributor" content="J M Gomori" />
<meta name="DC.Contributor" content="M D Schnall" />
<meta name="DC.Contributor" content="G A Holland" />
<meta name="DC.Contributor" content="R I Grossman" />
<meta name="DC.Contributor" content="S W Atlas" />
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<meta name="citation_title" content="Magnetization transfer effects in MR imaging of in vivo intracranial hemorrhage." />
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&lt;p&gt;Recent papers have hypothesized that diamagnetic effects of clotting and conformational changes in aging red blood cells immobilize the hemoglobin protein and thus are responsible for the marked hypointensity of acute hematomas on T2-weighted spin-echo MR images. To test that hypothesis, the authors evaluated 24 hemorrhagic components of intracranial hemorrhagic lesions using accepted criteria based on spin-echo images as the definitions of the stage of the hemorrhage.&lt;/p&gt;&lt;h3&gt;METHODS&lt;/h3&gt;
&lt;p&gt;As a measure of the effects of macromolecular (hemoglobin protein) immobility, magnetization transfer contrast was elicited using a pulsed saturation magnetization transfer experiment. The apparent magnetization transfer contrast (AMTC) was determined by comparing the signal intensities of saturated with unsaturated images and quantified for acute isolated hemorrhages, acute nonisolated hemorrhagic lesions, and subacute-to-chronic hemorrhages.&lt;/p&gt;&lt;h3&gt;RESULTS&lt;/h3&gt;
&lt;p&gt;The AMTC of isolated acute hemorrhage was significantly less than that of normal, white matter and gray matter, indicating the lack of significant magnetization transfer and therefore the lack of effects of restriction of hemoglobin mobility on the signal intensity of acute hemorrhage. Acutely hemorrhagic tissue (nonisolated acute hemorrhage) has significantly more AMTC than isolated acute hemorrhage, but still not exceeding that of brain parenchyma.&lt;/p&gt;&lt;h3&gt;CONCLUSION&lt;/h3&gt;
&lt;p&gt;This in vivo data concurs with in vitro data and reinforces the concept that the marked hypointensity of acute hematomas is mainly a magnetic susceptibility effect.&lt;/p&gt;" />
<meta name="citation_journal_title" content="American Journal of Neuroradiology" />
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<meta name="citation_author" content="R L Mittl" />
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<meta name="citation_author" content="J M Gomori" />
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<meta name="citation_author" content="M D Schnall" />
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<meta name="citation_author" content="G A Holland" />
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<meta name="citation_author" content="R I Grossman" />
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<meta name="twitter:title" content="Magnetization transfer effects in MR imaging of in vivo intracranial hemorrhage." />
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<meta name="twitter:description" content="PURPOSE Recent papers have hypothesized that diamagnetic effects of clotting and conformational changes in aging red blood cells immobilize the hemoglobin protein and thus are responsible for the marked hypointensity of acute hematomas on T2-weighted spin-echo MR images. To test that hypothesis, the authors evaluated 24 hemorrhagic components of intracranial hemorrhagic lesions using accepted criteria based on spin-echo images as the definitions of the stage of the hemorrhage.

METHODS As a measure of the effects of macromolecular (hemoglobin protein) immobility, magnetization transfer contrast was elicited using a pulsed saturation magnetization transfer experiment. The apparent magnetization transfer contrast (AMTC) was determined by comparing the signal intensities of saturated with unsaturated images and quantified for acute isolated hemorrhages, acute nonisolated hemorrhagic lesions, and subacute-to-chronic hemorrhages.

RESULTS The AMTC of isolated acute hemorrhage was significantly less than that of normal, white matter and gray matter, indicating the lack of significant magnetization transfer and therefore the lack of effects of restriction of hemoglobin mobility on the signal intensity of acute hemorrhage. Acutely hemorrhagic tissue (nonisolated acute hemorrhage) has significantly more AMTC than isolated acute hemorrhage, but still not exceeding that of brain parenchyma.

CONCLUSION This in vivo data concurs with in vitro data and reinforces the concept that the marked hypointensity of acute hematomas is mainly a magnetic susceptibility effect." />
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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 Recent papers have hypothesized that diamagnetic effects of clotting and conformational changes in aging red blood cells immobilize the hemoglobin protein and thus are responsible for the marked hypointensity of acute hematomas on T2-weighted spin-echo MR images. To test that hypothesis, the authors evaluated 24 hemorrhagic components of intracranial hemorrhagic lesions using accepted criteria based on spin-echo images as the definitions of the stage of the hemorrhage.

METHODS As a measure of the effects of macromolecular (hemoglobin protein) immobility, magnetization transfer contrast was elicited using a pulsed saturation magnetization transfer experiment. The apparent magnetization transfer contrast (AMTC) was determined by comparing the signal intensities of saturated with unsaturated images and quantified for acute isolated hemorrhages, acute nonisolated hemorrhagic lesions, and subacute-to-chronic hemorrhages.

RESULTS The AMTC of isolated acute hemorrhage was significantly less than that of normal, white matter and gray matter, indicating the lack of significant magnetization transfer and therefore the lack of effects of restriction of hemoglobin mobility on the signal intensity of acute hemorrhage. Acutely hemorrhagic tissue (nonisolated acute hemorrhage) has significantly more AMTC than isolated acute hemorrhage, but still not exceeding that of brain parenchyma.

CONCLUSION This in vivo data concurs with in vitro data and reinforces the concept that the marked hypointensity of acute hematomas is mainly a magnetic susceptibility effect." />
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      <h1 class="highwire-cite-title" id="page-title">Magnetization transfer effects in MR imaging of in vivo intracranial hemorrhage.</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">R L Mittl</span>, <span class="highwire-citation-author" data-delta="1">J M Gomori</span>, <span class="highwire-citation-author" data-delta="2">M D Schnall</span>, <span class="highwire-citation-author" data-delta="3">G A Holland</span>, <span class="highwire-citation-author" data-delta="4">R I Grossman</span> and <span class="highwire-citation-author" data-delta="5">S W Atlas</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">July 1993,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">14 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(4) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">881-891; </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-5797--61457331461" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">R L Mittl <span class="nlm-suffix">Jr</span></div><div class="author-tooltip-affiliation"><span class="author-tooltip-text"><div class='author-affiliation'>Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, PA 19104.</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=R%2BL%2BMittl%2B%3Cspan%2Bclass%3D%22nlm-suffix%22%3EJr%3C/span%3E" 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=Mittl%20RL&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li 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        	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">Vol. 14</span>, <span  class="highwire-cite-metadata-issue highwire-cite-metadata">Issue 4 </span><div  class="highwire-cite-metadata-pubdate highwire-cite-metadata">1 Jul 1993 </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">Jul 1993, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">14 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(4) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">881-891; </span></div>
  
  
  
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      <div class="highwire-cite-title">Magnetization transfer effects in MR imaging of in vivo intracranial hemorrhage.</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">R L</span> <span class="nlm-surname">Mittl</span></span>, <span class="highwire-citation-author" data-delta="1"><span class="nlm-given-names">J M</span> <span class="nlm-surname">Gomori</span></span>, <span class="highwire-citation-author" data-delta="2"><span class="nlm-given-names">M D</span> <span class="nlm-surname">Schnall</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">G A</span> <span class="nlm-surname">Holland</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">R I</span> <span class="nlm-surname">Grossman</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">S W</span> <span class="nlm-surname">Atlas</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">Jul 1993, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">14 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(4) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">881-891; </span></div>
  
  
  
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