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<meta name="DC.Title" content="MR Imaging Quantification of Cerebellar Growth Following Hypoxic-Ischemic Injury to the Neonatal Brain" />
<meta name="DC.Date" content="2004-03-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Cerebellar atrophy may occur as a result of a primary injury, such as infarction or hemorrhage. Impaired growth of a noninjured cerebellum may be seen as a secondary effect related to damage in other remote but connected areas of the brain, or so-called diaschisis. We sought to determine whether perinatal hypoxic-ischemic injury leads to poor cerebellar growth and whether such impairment occurs asymmetrically in infants with predominantly unilateral brain injury.

METHODS: We used a computerized quantification program to measure cerebellar size by using serial MR images. Term-born infants presenting with encephalopathy and/or seizures presumed due to a hypoxic-ischemic insult within 48 hours of delivery were included if they had two or more volume acquisition images obtained at least 3 months apart but within the first 15 months of delivery.

RESULTS: When data were grouped by MR appearances, significant differences in total cerebellum growth were seen between infants with focal infarction and those with basal ganglia and thalamic injury ( P &lt; .001). Unilateral forebrain lesions shown on MR imaging were not predictive of asymmetric cerebellar growth.

CONCLUSION: Infants with focal infarction of the cerebral hemisphere had an apparently normal pattern of growth in both cerebellar hemispheres. However, in infants with severe basal ganglia and thalamic lesions, cerebellar growth was reduced, and the vermis showed little or no growth during the first year after birth." />
<meta name="DC.Contributor" content="Elisabeth Le Strange" />
<meta name="DC.Contributor" content="Nadeem Saeed" />
<meta name="DC.Contributor" content="Frances M. Cowan" />
<meta name="DC.Contributor" content="A. David Edwards" />
<meta name="DC.Contributor" content="Mary A. Rutherford" />
<meta name="article:published_time" content="2004-03-01" />
<meta name="article:section" content="PEDIATRICS" />
<meta name="citation_title" content="MR Imaging Quantification of Cerebellar Growth Following Hypoxic-Ischemic Injury to the Neonatal Brain" />
<meta name="citation_abstract" lang="en" content="&lt;p&gt;&lt;i&gt;BACKGROUND AND PURPOSE:&lt;/i&gt; Cerebellar atrophy may occur as a result of a primary injury, such as infarction or hemorrhage. Impaired growth of a noninjured cerebellum may be seen as a secondary effect related to damage in other remote but connected areas of the brain, or so-called diaschisis. We sought to determine whether perinatal hypoxic-ischemic injury leads to poor cerebellar growth and whether such impairment occurs asymmetrically in infants with predominantly unilateral brain injury.&lt;/p&gt;&lt;p&gt;&lt;i&gt;METHODS:&lt;/i&gt; We used a computerized quantification program to measure cerebellar size by using serial MR images. Term-born infants presenting with encephalopathy and/or seizures presumed due to a hypoxic-ischemic insult within 48 hours of delivery were included if they had two or more volume acquisition images obtained at least 3 months apart but within the first 15 months of delivery.&lt;/p&gt;&lt;p&gt;&lt;i&gt;RESULTS:&lt;/i&gt; When data were grouped by MR appearances, significant differences in total cerebellum growth were seen between infants with focal infarction and those with basal ganglia and thalamic injury (&lt;i&gt;P&lt;/i&gt; &amp;lt; .001). Unilateral forebrain lesions shown on MR imaging were not predictive of asymmetric cerebellar growth.&lt;/p&gt;&lt;p&gt;&lt;i&gt;CONCLUSION:&lt;/i&gt; Infants with focal infarction of the cerebral hemisphere had an apparently normal pattern of growth in both cerebellar hemispheres. However, in infants with severe basal ganglia and thalamic lesions, cerebellar growth was reduced, and the vermis showed little or no growth during the first year after birth.&lt;/p&gt;" />
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<meta name="twitter:title" content="MR Imaging Quantification of Cerebellar Growth Following Hypoxic-Ischemic Injury to the Neonatal Brain" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Cerebellar atrophy may occur as a result of a primary injury, such as infarction or hemorrhage. Impaired growth of a noninjured cerebellum may be seen as a secondary effect related to damage in other remote but connected areas of the brain, or so-called diaschisis. We sought to determine whether perinatal hypoxic-ischemic injury leads to poor cerebellar growth and whether such impairment occurs asymmetrically in infants with predominantly unilateral brain injury.

METHODS: We used a computerized quantification program to measure cerebellar size by using serial MR images. Term-born infants presenting with encephalopathy and/or seizures presumed due to a hypoxic-ischemic insult within 48 hours of delivery were included if they had two or more volume acquisition images obtained at least 3 months apart but within the first 15 months of delivery.

RESULTS: When data were grouped by MR appearances, significant differences in total cerebellum growth were seen between infants with focal infarction and those with basal ganglia and thalamic injury ( P &lt; .001). Unilateral forebrain lesions shown on MR imaging were not predictive of asymmetric cerebellar growth.

CONCLUSION: Infants with focal infarction of the cerebral hemisphere had an apparently normal pattern of growth in both cerebellar hemispheres. However, in infants with severe basal ganglia and thalamic lesions, cerebellar growth was reduced, and the vermis showed little or no growth during the first year after birth." />
<meta name="og-title" property="og:title" content="MR Imaging Quantification of Cerebellar Growth Following Hypoxic-Ischemic Injury to the Neonatal Brain" />
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<meta name="og-description" property="og:description" content="BACKGROUND AND PURPOSE: Cerebellar atrophy may occur as a result of a primary injury, such as infarction or hemorrhage. Impaired growth of a noninjured cerebellum may be seen as a secondary effect related to damage in other remote but connected areas of the brain, or so-called diaschisis. We sought to determine whether perinatal hypoxic-ischemic injury leads to poor cerebellar growth and whether such impairment occurs asymmetrically in infants with predominantly unilateral brain injury.

METHODS: We used a computerized quantification program to measure cerebellar size by using serial MR images. Term-born infants presenting with encephalopathy and/or seizures presumed due to a hypoxic-ischemic insult within 48 hours of delivery were included if they had two or more volume acquisition images obtained at least 3 months apart but within the first 15 months of delivery.

RESULTS: When data were grouped by MR appearances, significant differences in total cerebellum growth were seen between infants with focal infarction and those with basal ganglia and thalamic injury ( P &lt; .001). Unilateral forebrain lesions shown on MR imaging were not predictive of asymmetric cerebellar growth.

CONCLUSION: Infants with focal infarction of the cerebral hemisphere had an apparently normal pattern of growth in both cerebellar hemispheres. However, in infants with severe basal ganglia and thalamic lesions, cerebellar growth was reduced, and the vermis showed little or no growth during the first year after birth." />
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<div id="hw-article-author-popups-top-node-10411--6945180378" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">Elisabeth Le Strange </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=Elisabeth%2BLe%2BStrange%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=Le%20Strange%20E&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%3AElisabeth%2BLe%2BStrange%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">Nadeem Saeed </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=Nadeem%2BSaeed%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=Saeed%20N&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%3ANadeem%2BSaeed%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-2"><div class="author-tooltip-name">Frances M. Cowan </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=Frances%2BM.%2BCowan%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=Cowan%20FM&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%3AFrances%2BM.%2BCowan%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-3"><div class="author-tooltip-name">A. David Edwards </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=A.%2BDavid%2BEdwards%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=Edwards%20AD&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%3AA.%2BDavid%2BEdwards%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-4"><div class="author-tooltip-name">Mary A. Rutherford </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=Mary%2BA.%2BRutherford%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=Rutherford%20MA&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%3AMary%2BA.%2BRutherford%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li></ul></div></div></div>  </div>

  
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        	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">Vol. 25</span>, <span  class="highwire-cite-metadata-issue highwire-cite-metadata">Issue 3 </span><div  class="highwire-cite-metadata-pubdate highwire-cite-metadata">1 Mar 2004 </div></div>
      
      
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