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<meta name="DC.Title" content="Magnetization Transfer MR Imaging Demonstrates Degeneration of the Subcortical and Cortical Gray Matter in Huntington Disease" />
<meta name="DC.Identifier" content="10.3174/ajnr.A2225" />
<meta name="DC.Date" content="2010-11-01" />
<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="BACKGROUND AND PURPOSE: GM is typically affected in HD since the presymptomatic stage. Our aim was to investigate with MT MR imaging the microstructural changes of the residual brain subcortical and cortical GM in carriers of the HD gene and to preliminarily assess their correlation with the clinical features.

MATERIALS AND METHODS: Fifteen HD gene carriers with a range of clinical severity and 15 age- and sex-matched healthy controls underwent MT MR imaging on a 1.5T scanner. The MT ratio was measured automatically in several subcortical and cortical GM regions (striatal nuclei; thalami; and the neocortex of the frontal, temporal, parietal, and occipital lobes) by using FLS tools.

RESULTS: The MT ratio was significantly ( P &lt; .05 with Bonferroni correction for multiple comparison) decreased in all subcortical structures except the putamen and decreased diffusely in the cerebral cortex of HD carriers compared with controls. Close correlation was observed between the subcortical and cortical regional MT ratios and several clinical variables, including disease duration, motor disability, and scores in timed neuropsychological tests.

CONCLUSIONS: MT imaging demonstrates degeneration of the subcortical and cortical GM in HD carriers and might serve, along with volumetric assessment, as a surrogate marker in future clinical trials of HD.

CAG
:   cytosine-adenine-guanine
FIRST
:   FMRIB's Integrated Registration and Segmentation Tool
FMRIB
:   Functional MR Imaging of the Brain
FSL
:   FMRIB's Software Library
GM
:   gray matter
HD
:   Huntington disease
MNI
:   Montreal Neurological Institute
MT
:   magnetization transfer
NGMV
:   normalized GM volume
NS
:   not significant
NWMV
:   normalized WM volume
UHDRS
:   Unified Huntington's Disease Rating Scale
WM
:   white matter" />
<meta name="DC.Contributor" content="A. Ginestroni" />
<meta name="DC.Contributor" content="M. Battaglini" />
<meta name="DC.Contributor" content="S. Diciotti" />
<meta name="DC.Contributor" content="R. Della Nave" />
<meta name="DC.Contributor" content="L.N. Mazzoni" />
<meta name="DC.Contributor" content="C. Tessa" />
<meta name="DC.Contributor" content="M. Giannelli" />
<meta name="DC.Contributor" content="S. Piacentini" />
<meta name="DC.Contributor" content="N. De Stefano" />
<meta name="DC.Contributor" content="M. Mascalchi" />
<meta name="article:published_time" content="2010-11-01" />
<meta name="article:section" content="Functional" />
<meta name="citation_title" content="Magnetization Transfer MR Imaging Demonstrates Degeneration of the Subcortical and Cortical Gray Matter in Huntington Disease" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;GM is typically affected in HD since the presymptomatic stage. Our aim was to investigate with MT MR imaging the microstructural changes of the residual brain subcortical and cortical GM in carriers of the HD gene and to preliminarily assess their correlation with the clinical features.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;Fifteen HD gene carriers with a range of clinical severity and 15 age- and sex-matched healthy controls underwent MT MR imaging on a 1.5T scanner. The MT ratio was measured automatically in several subcortical and cortical GM regions (striatal nuclei; thalami; and the neocortex of the frontal, temporal, parietal, and occipital lobes) by using FLS tools.&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;The MT ratio was significantly (&lt;i&gt;P&lt;/i&gt; &amp;lt; .05 with Bonferroni correction for multiple comparison) decreased in all subcortical structures except the putamen and decreased diffusely in the cerebral cortex of HD carriers compared with controls. Close correlation was observed between the subcortical and cortical regional MT ratios and several clinical variables, including disease duration, motor disability, and scores in timed neuropsychological tests.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;MT imaging demonstrates degeneration of the subcortical and cortical GM in HD carriers and might serve, along with volumetric assessment, as a surrogate marker in future clinical trials of HD.&lt;/p&gt;" />
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<meta name="twitter:title" content="Magnetization Transfer MR Imaging Demonstrates Degeneration of the Subcortical and Cortical Gray Matter in Huntington Disease" />
<meta name="twitter:card" content="summary_large_image" />
<meta name="twitter:image" content="http://ajnr-stage2.stage.highwire.org/sites/default/files/highwire/ajnr/31/10.cover.gif" />
<meta name="twitter:description" content="BACKGROUND AND PURPOSE: GM is typically affected in HD since the presymptomatic stage. Our aim was to investigate with MT MR imaging the microstructural changes of the residual brain subcortical and cortical GM in carriers of the HD gene and to preliminarily assess their correlation with the clinical features.

MATERIALS AND METHODS: Fifteen HD gene carriers with a range of clinical severity and 15 age- and sex-matched healthy controls underwent MT MR imaging on a 1.5T scanner. The MT ratio was measured automatically in several subcortical and cortical GM regions (striatal nuclei; thalami; and the neocortex of the frontal, temporal, parietal, and occipital lobes) by using FLS tools.

RESULTS: The MT ratio was significantly ( P &lt; .05 with Bonferroni correction for multiple comparison) decreased in all subcortical structures except the putamen and decreased diffusely in the cerebral cortex of HD carriers compared with controls. Close correlation was observed between the subcortical and cortical regional MT ratios and several clinical variables, including disease duration, motor disability, and scores in timed neuropsychological tests.

CONCLUSIONS: MT imaging demonstrates degeneration of the subcortical and cortical GM in HD carriers and might serve, along with volumetric assessment, as a surrogate marker in future clinical trials of HD.

CAG
:   cytosine-adenine-guanine
FIRST
:   FMRIB's Integrated Registration and Segmentation Tool
FMRIB
:   Functional MR Imaging of the Brain
FSL
:   FMRIB's Software Library
GM
:   gray matter
HD
:   Huntington disease
MNI
:   Montreal Neurological Institute
MT
:   magnetization transfer
NGMV
:   normalized GM volume
NS
:   not significant
NWMV
:   normalized WM volume
UHDRS
:   Unified Huntington's Disease Rating Scale
WM
:   white matter" />
<meta name="og-title" property="og:title" content="Magnetization Transfer MR Imaging Demonstrates Degeneration of the Subcortical and Cortical Gray Matter in Huntington Disease" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/31/10/1807" />
<meta name="og-site-name" property="og:site_name" content="American Journal of Neuroradiology" />
<meta name="og-description" property="og:description" content="BACKGROUND AND PURPOSE: GM is typically affected in HD since the presymptomatic stage. Our aim was to investigate with MT MR imaging the microstructural changes of the residual brain subcortical and cortical GM in carriers of the HD gene and to preliminarily assess their correlation with the clinical features.

MATERIALS AND METHODS: Fifteen HD gene carriers with a range of clinical severity and 15 age- and sex-matched healthy controls underwent MT MR imaging on a 1.5T scanner. The MT ratio was measured automatically in several subcortical and cortical GM regions (striatal nuclei; thalami; and the neocortex of the frontal, temporal, parietal, and occipital lobes) by using FLS tools.

RESULTS: The MT ratio was significantly ( P &lt; .05 with Bonferroni correction for multiple comparison) decreased in all subcortical structures except the putamen and decreased diffusely in the cerebral cortex of HD carriers compared with controls. Close correlation was observed between the subcortical and cortical regional MT ratios and several clinical variables, including disease duration, motor disability, and scores in timed neuropsychological tests.

CONCLUSIONS: MT imaging demonstrates degeneration of the subcortical and cortical GM in HD carriers and might serve, along with volumetric assessment, as a surrogate marker in future clinical trials of HD.

CAG
:   cytosine-adenine-guanine
FIRST
:   FMRIB's Integrated Registration and Segmentation Tool
FMRIB
:   Functional MR Imaging of the Brain
FSL
:   FMRIB's Software Library
GM
:   gray matter
HD
:   Huntington disease
MNI
:   Montreal Neurological Institute
MT
:   magnetization transfer
NGMV
:   normalized GM volume
NS
:   not significant
NWMV
:   normalized WM volume
UHDRS
:   Unified Huntington's Disease Rating Scale
WM
:   white matter" />
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    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-volume highwire-cite-metadata">vol. 31 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">no. 10 </span><span  class="highwire-cite-metadata-page-string highwire-cite-metadata">1807-1812 </span></div>
  
  
  
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    <div class="highwire-markup"><div xmlns="http://www.w3.org/1999/xhtml" class="content-block-markup" xmlns:xhtml="http://www.w3.org/1999/xhtml"><div xmlns:xhtml="http://www.w3.org/1999/xhtml" class="contributors"><ol class="contributor-list" id="contrib-group-1"><li class="contributor" id="contrib-1"><span class="name">A. Ginestroni</span><a id="xref-aff-1-1" class="xref-aff" href="#aff-1">a</a>, </li><li class="contributor" id="contrib-2"><span class="name">M. Battaglini</span><a id="xref-aff-3-1" class="xref-aff" href="#aff-3">c</a>, </li><li class="contributor" id="contrib-3"><span class="name">S. Diciotti</span><a id="xref-aff-1-2" class="xref-aff" href="#aff-1">a</a>, </li><li class="contributor" id="contrib-4"><span class="name">R. Della Nave</span><a id="xref-aff-1-3" class="xref-aff" href="#aff-1">a</a>, </li><li class="contributor" id="contrib-5"><span class="name">L.N. Mazzoni</span><a id="xref-aff-1-4" class="xref-aff" href="#aff-1">a</a>, </li><li class="contributor" id="contrib-6"><span class="name">C. Tessa</span><a id="xref-aff-4-1" class="xref-aff" href="#aff-4">d</a>, </li><li class="contributor" id="contrib-7"><span class="name">M. Giannelli</span><a id="xref-aff-5-1" class="xref-aff" href="#aff-5">e</a>, </li><li class="contributor" id="contrib-8"><span class="name">S. Piacentini</span><a id="xref-aff-2-1" class="xref-aff" href="#aff-2">b</a>, </li><li class="contributor" id="contrib-9"><span class="name">N. De Stefano</span><a id="xref-aff-3-2" class="xref-aff" href="#aff-3">c</a> and </li><li class="last" id="contrib-10"><span class="name">M. Mascalchi</span><a id="xref-aff-1-5" class="xref-aff" href="#aff-1">a</a></li></ol><ol class="affiliation-list"><li class="aff"><a id="aff-1" name="aff-1"></a><address><sup>a</sup>From the Radiodiagnostic Section, Department of Clinical Physiopathology (A.G., S.D., R.D.N., M.M., C.I.R.M., L.N.M.)</address></li><li class="aff"><a id="aff-2" name="aff-2"></a><address><sup>b</sup>Department of Neurological and Psychiatric Sciences (S.P.), University of Florence, Florence, Italy</address></li><li class="aff"><a id="aff-3" name="aff-3"></a><address><sup>c</sup>Department of Neurological and Behavioral Sciences (M.B., N.D.S.), University of Siena, Siena, Italy</address></li><li class="aff"><a id="aff-4" name="aff-4"></a><address><sup>d</sup>Radiology Unit (C.T.), Versilia Hospital, Pietrasanta (Lucca), Italy</address></li><li class="aff"><a id="aff-5" name="aff-5"></a><address><sup>e</sup>Department of Medical Physics (M.G.), Santa Chiara Hospital, Pisa, Italy.</address></li></ol><ol class="corresp-list"><li class="corresp" id="corresp-1">Please address correspondence to Mario Mascalchi, MD, PhD, <span class="addr-line">Radiodiagnostic Section, Department of Clinical Physiopathology, University of Florence, Viale Morgagni 85, 50134 Florence, Italy</span>; e-mail: <span class="em-link"><span class="em-addr">m.mascalchi{at}dfc.unifi.it</span></span></li></ol></div></div><a href="http://ajnr-stage2.stage.highwire.org/content/31/10/1807.full" class="hw-link hw-link-article-full-text" data-icon-position="" data-hide-link-title="0">View Full Text</a></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">Nov 2010, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">31 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(10) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1807-1812; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A2225 </span></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">Nov 2010, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">31 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(10) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1807-1812; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A2225 </span></div>
  
  
  
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