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<meta name="DC.Title" content="Proton MR spectroscopy in patients with neurofibromatosis type 1: evaluation of hamartomas and clinical correlation." />
<meta name="DC.Date" content="1995-01-01" />
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<meta name="DC.Description" content="PURPOSE To use proton MR spectroscopy in patients with neurofibromatosis type 1 to determine: (a) the spectroscopic characteristics of hamartomas and compare them with that of gliomas; (b) whether differences exist between patients with and without learning disabilities; and (c) spectroscopic patterns in normal-appearing brain (by MR imaging) in patients with and without focal lesions.

METHODS Seventeen proton MR spectroscopy volumes were obtained in 10 patients with neurofibromatosis type 1 (including hamartomas, N = 7; normal-appearing brain, N = 10). Seven patients had learning disorders, and 3 were mentally normal. Ten healthy volunteers and 10 patients with pathologically proved gliomas (all grades) were also examined. N-Acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were calculated for all samples.

RESULTS (a) Hamartomas showed higher N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios than gliomas. Hamartomas showed N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios similar to those of healthy volunteers. (b) No significant differences in N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were found in patients who had neurofibromatosis type 1 with and without learning disabilities. (c) N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were similar for patients who had neurofibromatosis type 1 with and without focal hamartomas and in healthy volunteers.

CONCLUSIONS (a) Hamartomas have a proton MR spectroscopy pattern different from that of glioma and similar to that of normal brain. (b) As performed in this study, proton MR spectroscopy did not show significant differences in patients who had neurofibromatosis type 1 with and without learning disabilities. (c) Patients who have neurofibromatosis type 1 with and without hamartomas seem to have normal intervening brain by proton MR spectroscopy when compared with healthy volunteers." />
<meta name="DC.Contributor" content="M Castillo" />
<meta name="DC.Contributor" content="C Green" />
<meta name="DC.Contributor" content="L Kwock" />
<meta name="DC.Contributor" content="K Smith" />
<meta name="DC.Contributor" content="D Wilson" />
<meta name="DC.Contributor" content="S Schiro" />
<meta name="DC.Contributor" content="R Greenwood" />
<meta name="article:published_time" content="1995-01-01" />
<meta name="citation_title" content="Proton MR spectroscopy in patients with neurofibromatosis type 1: evaluation of hamartomas and clinical correlation." />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;PURPOSE&lt;/h3&gt;
&lt;p&gt;To use proton MR spectroscopy in patients with neurofibromatosis type 1 to determine: (a) the spectroscopic characteristics of hamartomas and compare them with that of gliomas; (b) whether differences exist between patients with and without learning disabilities; and (c) spectroscopic patterns in normal-appearing brain (by MR imaging) in patients with and without focal lesions.&lt;/p&gt;&lt;h3&gt;METHODS&lt;/h3&gt;
&lt;p&gt;Seventeen proton MR spectroscopy volumes were obtained in 10 patients with neurofibromatosis type 1 (including hamartomas, N = 7; normal-appearing brain, N = 10). Seven patients had learning disorders, and 3 were mentally normal. Ten healthy volunteers and 10 patients with pathologically proved gliomas (all grades) were also examined. N-Acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were calculated for all samples.&lt;/p&gt;&lt;h3&gt;RESULTS&lt;/h3&gt;
&lt;p&gt;(a) Hamartomas showed higher N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios than gliomas. Hamartomas showed N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios similar to those of healthy volunteers. (b) No significant differences in N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were found in patients who had neurofibromatosis type 1 with and without learning disabilities. (c) N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were similar for patients who had neurofibromatosis type 1 with and without focal hamartomas and in healthy volunteers.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS&lt;/h3&gt;
&lt;p&gt;(a) Hamartomas have a proton MR spectroscopy pattern different from that of glioma and similar to that of normal brain. (b) As performed in this study, proton MR spectroscopy did not show significant differences in patients who had neurofibromatosis type 1 with and without learning disabilities. (c) Patients who have neurofibromatosis type 1 with and without hamartomas seem to have normal intervening brain by proton MR spectroscopy when compared with healthy volunteers.&lt;/p&gt;" />
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<meta name="citation_author" content="M Castillo" />
<meta name="citation_author" content="C Green" />
<meta name="citation_author" content="L Kwock" />
<meta name="citation_author" content="K Smith" />
<meta name="citation_author" content="D Wilson" />
<meta name="citation_author" content="S Schiro" />
<meta name="citation_author" content="R Greenwood" />
<meta name="twitter:title" content="Proton MR spectroscopy in patients with neurofibromatosis type 1: evaluation of hamartomas and clinical correlation." />
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<meta name="twitter:description" content="PURPOSE To use proton MR spectroscopy in patients with neurofibromatosis type 1 to determine: (a) the spectroscopic characteristics of hamartomas and compare them with that of gliomas; (b) whether differences exist between patients with and without learning disabilities; and (c) spectroscopic patterns in normal-appearing brain (by MR imaging) in patients with and without focal lesions.

METHODS Seventeen proton MR spectroscopy volumes were obtained in 10 patients with neurofibromatosis type 1 (including hamartomas, N = 7; normal-appearing brain, N = 10). Seven patients had learning disorders, and 3 were mentally normal. Ten healthy volunteers and 10 patients with pathologically proved gliomas (all grades) were also examined. N-Acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were calculated for all samples.

RESULTS (a) Hamartomas showed higher N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios than gliomas. Hamartomas showed N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios similar to those of healthy volunteers. (b) No significant differences in N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were found in patients who had neurofibromatosis type 1 with and without learning disabilities. (c) N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were similar for patients who had neurofibromatosis type 1 with and without focal hamartomas and in healthy volunteers.

CONCLUSIONS (a) Hamartomas have a proton MR spectroscopy pattern different from that of glioma and similar to that of normal brain. (b) As performed in this study, proton MR spectroscopy did not show significant differences in patients who had neurofibromatosis type 1 with and without learning disabilities. (c) Patients who have neurofibromatosis type 1 with and without hamartomas seem to have normal intervening brain by proton MR spectroscopy when compared with healthy volunteers." />
<meta name="og-title" property="og:title" content="Proton MR spectroscopy in patients with neurofibromatosis type 1: evaluation of hamartomas and clinical correlation." />
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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 use proton MR spectroscopy in patients with neurofibromatosis type 1 to determine: (a) the spectroscopic characteristics of hamartomas and compare them with that of gliomas; (b) whether differences exist between patients with and without learning disabilities; and (c) spectroscopic patterns in normal-appearing brain (by MR imaging) in patients with and without focal lesions.

METHODS Seventeen proton MR spectroscopy volumes were obtained in 10 patients with neurofibromatosis type 1 (including hamartomas, N = 7; normal-appearing brain, N = 10). Seven patients had learning disorders, and 3 were mentally normal. Ten healthy volunteers and 10 patients with pathologically proved gliomas (all grades) were also examined. N-Acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were calculated for all samples.

RESULTS (a) Hamartomas showed higher N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios than gliomas. Hamartomas showed N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios similar to those of healthy volunteers. (b) No significant differences in N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were found in patients who had neurofibromatosis type 1 with and without learning disabilities. (c) N-acetyl aspartate/creatine, creatine/choline, and N-acetyl aspartate/choline ratios were similar for patients who had neurofibromatosis type 1 with and without focal hamartomas and in healthy volunteers.

CONCLUSIONS (a) Hamartomas have a proton MR spectroscopy pattern different from that of glioma and similar to that of normal brain. (b) As performed in this study, proton MR spectroscopy did not show significant differences in patients who had neurofibromatosis type 1 with and without learning disabilities. (c) Patients who have neurofibromatosis type 1 with and without hamartomas seem to have normal intervening brain by proton MR spectroscopy when compared with healthy volunteers." />
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      <h1 class="highwire-cite-title" id="page-title">Proton MR spectroscopy in patients with neurofibromatosis type 1: evaluation of hamartomas and clinical correlation.</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">M Castillo</span>, <span class="highwire-citation-author" data-delta="1">C Green</span>, <span class="highwire-citation-author" data-delta="2">L Kwock</span>, <span class="highwire-citation-author" data-delta="3">K Smith</span>, <span class="highwire-citation-author" data-delta="4">D Wilson</span>, <span class="highwire-citation-author" data-delta="5">S Schiro</span> and <span class="highwire-citation-author" data-delta="6">R Greenwood</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">January 1995,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">16 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(1) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">141-147; </span></div>
  
  
  
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        	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">Vol. 16</span>, <span  class="highwire-cite-metadata-issue highwire-cite-metadata">Issue 1 </span><div  class="highwire-cite-metadata-pubdate highwire-cite-metadata">1 Jan 1995 </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">Jan 1995, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">16 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(1) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">141-147; </span></div>
  
  
  
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