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<meta name="DC.Title" content="Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study" />
<meta name="DC.Identifier" content="10.3174/ajnr.A2128" />
<meta name="DC.Date" content="2010-10-01" />
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<meta name="DC.Description" content="BACKGROUND AND PURPOSE: HD entails damage of the WM. Our aim was to explore in vivo the regional volume and microstructure of the brain WM in HD and to correlate such findings with clinical status of the patients.

MATERIALS AND METHODS: Fifteen HD gene carriers in different clinical stages of the disease and 15 healthy controls were studied with T1-weighted images for VBM and DTI for TBSS. Maps of FA, MD, and λ∥ and λ⊥ were reconstructed.

RESULTS: Compared with controls, in addition to neostriatum and cortical GM volume loss, individuals with HD showed volume loss in the genu of the internal capsule and subcortical frontal WM bilaterally, the right splenium of the corpus callosum, and the left corona radiata. TBSS revealed symmetrically decreased FA in the corpus callosum, fornix, external/extreme capsule, inferior fronto-occipital fasciculus, and inferior longitudinal fasciculus. Areas of increased MD were more extensive and included arciform fibers of the cerebral hemispheres and cerebral peduncles. Increase of the λ∥ and a comparatively more pronounced increase of the λ⊥ underlay the decreased FA of the WM in HD. Areas of WM atrophy, decreased FA, and increased MD correlated with the severity of the motor and cognitive dysfunction, whereas only the areas with increased MD correlated with disease duration.

CONCLUSIONS: Microstructural damage accompanies volume decrease of the WM in HD and is correlated with the clinical deficits and disease duration. MR imaging−based measures could be considered as a biomarker of neurodegeneration in HD gene carriers.

corr
:   corrected
DTI
:   diffusion tensor imaging
FA
:   fractional anisotropy
FDR
:   false discovery rate
FMRIB
:   Oxford Centre for Functional MRI of the Brain
FSL
:   FMRIB Software Library
GM
:   gray matter
HD
:   Huntington disease
L
:   left
λ∥
:   axial diffusivity
λ⊥
:   radial diffusivity
MD
:   mean diffusivity
SPM
:   Statistical Parametric Mapping
TBSS
:   Tract-Based Spatial Statistics
UHDRS
:   Unified Huntington's Disease Rating Scale
VBM
:   voxel-based morphometry
WM
:   white matter
R
:   right" />
<meta name="DC.Contributor" content="R. Della Nave" />
<meta name="DC.Contributor" content="A. Ginestroni" />
<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="M. Filippi" />
<meta name="DC.Contributor" content="M. Mascalchi" />
<meta name="article:published_time" content="2010-10-01" />
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<meta name="citation_title" content="Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;HD entails damage of the WM.  Our aim was to explore in vivo the regional volume and microstructure of the brain WM in HD and to correlate such findings with clinical status of the  patients.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;Fifteen HD gene carriers in different clinical stages of the disease and 15 healthy controls were studied with T1-weighted images for VBM and DTI for TBSS. Maps of FA, MD, and λ∥ and λ⊥ were  reconstructed.&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;Compared with controls, in addition to neostriatum and cortical GM volume loss, individuals with HD showed volume loss in the genu of the internal capsule and subcortical frontal WM bilaterally, the right splenium of the corpus callosum, and the left corona radiata. TBSS revealed symmetrically decreased FA in the corpus callosum, fornix, external/extreme capsule, inferior fronto-occipital fasciculus, and inferior longitudinal fasciculus. Areas of increased MD were more extensive and included arciform fibers of the cerebral hemispheres and cerebral peduncles. Increase of the λ∥ and a comparatively more pronounced increase of the λ⊥ underlay the decreased FA of the WM in HD. Areas of WM atrophy, decreased FA, and increased MD correlated with the severity of the motor and cognitive dysfunction, whereas only the areas with increased MD correlated with disease  duration.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;Microstructural damage accompanies volume decrease of the WM in HD and is correlated with the clinical deficits and disease duration. MR imaging−based measures could be considered as a biomarker of neurodegeneration in HD gene carriers.&lt;/p&gt;" />
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<meta name="twitter:title" content="Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: HD entails damage of the WM. Our aim was to explore in vivo the regional volume and microstructure of the brain WM in HD and to correlate such findings with clinical status of the patients.

MATERIALS AND METHODS: Fifteen HD gene carriers in different clinical stages of the disease and 15 healthy controls were studied with T1-weighted images for VBM and DTI for TBSS. Maps of FA, MD, and λ∥ and λ⊥ were reconstructed.

RESULTS: Compared with controls, in addition to neostriatum and cortical GM volume loss, individuals with HD showed volume loss in the genu of the internal capsule and subcortical frontal WM bilaterally, the right splenium of the corpus callosum, and the left corona radiata. TBSS revealed symmetrically decreased FA in the corpus callosum, fornix, external/extreme capsule, inferior fronto-occipital fasciculus, and inferior longitudinal fasciculus. Areas of increased MD were more extensive and included arciform fibers of the cerebral hemispheres and cerebral peduncles. Increase of the λ∥ and a comparatively more pronounced increase of the λ⊥ underlay the decreased FA of the WM in HD. Areas of WM atrophy, decreased FA, and increased MD correlated with the severity of the motor and cognitive dysfunction, whereas only the areas with increased MD correlated with disease duration.

CONCLUSIONS: Microstructural damage accompanies volume decrease of the WM in HD and is correlated with the clinical deficits and disease duration. MR imaging−based measures could be considered as a biomarker of neurodegeneration in HD gene carriers.

corr
:   corrected
DTI
:   diffusion tensor imaging
FA
:   fractional anisotropy
FDR
:   false discovery rate
FMRIB
:   Oxford Centre for Functional MRI of the Brain
FSL
:   FMRIB Software Library
GM
:   gray matter
HD
:   Huntington disease
L
:   left
λ∥
:   axial diffusivity
λ⊥
:   radial diffusivity
MD
:   mean diffusivity
SPM
:   Statistical Parametric Mapping
TBSS
:   Tract-Based Spatial Statistics
UHDRS
:   Unified Huntington's Disease Rating Scale
VBM
:   voxel-based morphometry
WM
:   white matter
R
:   right" />
<meta name="og-title" property="og:title" content="Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/31/9/1675" />
<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: HD entails damage of the WM. Our aim was to explore in vivo the regional volume and microstructure of the brain WM in HD and to correlate such findings with clinical status of the patients.

MATERIALS AND METHODS: Fifteen HD gene carriers in different clinical stages of the disease and 15 healthy controls were studied with T1-weighted images for VBM and DTI for TBSS. Maps of FA, MD, and λ∥ and λ⊥ were reconstructed.

RESULTS: Compared with controls, in addition to neostriatum and cortical GM volume loss, individuals with HD showed volume loss in the genu of the internal capsule and subcortical frontal WM bilaterally, the right splenium of the corpus callosum, and the left corona radiata. TBSS revealed symmetrically decreased FA in the corpus callosum, fornix, external/extreme capsule, inferior fronto-occipital fasciculus, and inferior longitudinal fasciculus. Areas of increased MD were more extensive and included arciform fibers of the cerebral hemispheres and cerebral peduncles. Increase of the λ∥ and a comparatively more pronounced increase of the λ⊥ underlay the decreased FA of the WM in HD. Areas of WM atrophy, decreased FA, and increased MD correlated with the severity of the motor and cognitive dysfunction, whereas only the areas with increased MD correlated with disease duration.

CONCLUSIONS: Microstructural damage accompanies volume decrease of the WM in HD and is correlated with the clinical deficits and disease duration. MR imaging−based measures could be considered as a biomarker of neurodegeneration in HD gene carriers.

corr
:   corrected
DTI
:   diffusion tensor imaging
FA
:   fractional anisotropy
FDR
:   false discovery rate
FMRIB
:   Oxford Centre for Functional MRI of the Brain
FSL
:   FMRIB Software Library
GM
:   gray matter
HD
:   Huntington disease
L
:   left
λ∥
:   axial diffusivity
λ⊥
:   radial diffusivity
MD
:   mean diffusivity
SPM
:   Statistical Parametric Mapping
TBSS
:   Tract-Based Spatial Statistics
UHDRS
:   Unified Huntington's Disease Rating Scale
VBM
:   voxel-based morphometry
WM
:   white matter
R
:   right" />
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      <h1 class="highwire-cite-title" id="page-title">Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">R. Della Nave</span>, <span class="highwire-citation-author" data-delta="1">A. Ginestroni</span>, <span class="highwire-citation-author" data-delta="2">C. Tessa</span>, <span class="highwire-citation-author" data-delta="3">M. Giannelli</span>, <span class="highwire-citation-author" data-delta="4">S. Piacentini</span>, <span class="highwire-citation-author" data-delta="5">M. Filippi</span> and <span class="highwire-citation-author" data-delta="6">M. Mascalchi</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">October 2010,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">31 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(9) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1675-1681; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata">DOI: https://doi.org/10.3174/ajnr.A2128 </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-9830--61689028284" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">R. Della Nave </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.%2BDella%2BNave%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=Della%20Nave%20R&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%3AR.%2BDella%2BNave%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">A. 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        <h2 class="pane-title">Data supplements</h2>
    
  
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            <h2>Supplemental Online Materials</h2>
            <p><strong>Files in this Data Supplement:</strong></p>
            <ul><li><a href="/highwire/filestream/52264/field_highwire_adjunct_files/0/2128_tables_figures.pdf" class="rewritten" data-icon-position="" data-hide-link-title="0">Online Tables 1-6 and Figures 1-9 (PDF)</a> -
                  		<br/><br/>
                  <em>Online Table 1:</em> VBM results for volumes of GM and WM in 15 patients with HD (P &lt; .05 FDR corrected)
                  <br/><br/>
                  <em>Online Table 2:</em>  VBM results showing the significant (P &lt; .05 FDR corrected) correlation between individual scores of motor deficit and cognitive
                  tests and the areas of GM and WM losses in 15 HD gene carriers
                  <br/><br/>
                  <em>Online Table 3:</em>  TBSS results: areas of increased MD in 15 patients with HD versus 15 healthy controls
                  <br/><br/>
                  <em>Online Table 4:</em>  TBSS results:  correlation between decreased FA and Motor Scale score in 15 patients with HD
                  <br/><br/>
                  <em>Online Table 5:</em>  TBSS results:  correlation between decreased FA and Stroop Color-Word interference test score in 15 patients with HD
                  <br/><br/>
                  <em>Online Table 6:</em>  TBSS results:  correlation between decreased FA and Symbol Digit test score in 15 patients with HD
                  <br/><br/>
                  <em>Online Figure 1:</em>  VBM analysis in HD gene carriers vs healthy controls. Maps of the t-value (voxel analysis at p &lt; 0.05 corrected for multiple
                  comparisons) represented as glass brain (A,B) showing areas of GM (A) and WM (B) losses in HD gene carriers as compared to
                  healthy controls. See Supplementary Table 1 for details.
                  <br/><br/>
                  <em>Online Figure 2:</em>  TBSS analysis of FA, λ||, �λ⊥ and MD maps in HD gene carriers vs healthy controls. Maps of the t-value (t &gt;3 with p &lt; 0.05
                  corrected for multiple comparisons) at a mid-ventricular level showing in red the areas of significantly decreased FA in the
                  lateral portions of the posteriors corpus callosum and anterior fornix and in green the areas of significantly increased FA
                  in the supralenticular frontal WM comprising the corticospinal tracts, anterior thalamic radiations and superior fronto-occipital
                  fasciculus. A corresponding increase of the greatest eigenvalue is shown in pink by λ|| map, while the λ⊥ map shows its increase
                  in sky blue only in the areas of decreased FA and elsewhere. The map of MD shows in yellow the areas of increased MD which
                  are widespread and corresponds to those of altered FA and beyond.
                  <br/><br/>
                  <em>Online Figure 3:</em>  TBSS analysis of MD maps. Maps of the t-value (t &gt;3 with p &lt; 0.05 corrected for multiple comparisons) showing in yellow
                  the areas of significantly increased in WM in HD gene carriers as compared to controls. These include multiple association
                  tracts and the corpus callosum. Note the involvement of arciform fibres and of the cerebral peduncles (B,C) (colour bar indicates
                  1-p values).
                  <br/><br/>
                  <em>Online Figure 4:</em>  TTBSS correlation results in HD gene carriers. Blue shows the areas where FA inversely correlates (t &gt;3 with p &lt; 0.05 corrected
                  for multiple comparisons) with the motor scale of the UHDRS. Note the predominant location within (head, body and splenium)
                  (U) and beside the corpus callosum (colour bar indicates 1-p values) of the significant clusters. 
                  <br/><br/>
                  <em>Online Figure 5:</em>  TBSS correlation results in HD gene carriers. Blue shows the areas where FA correlates (t &gt;3 with p &lt; 0.05 corrected for
                  multiple comparisons) with the Stroop test results. Note the restriction of the areas to the frontal lobes and to the anterior
                  portion of the corpus callosum body (U) �(colour bar indicates 1-p values).
                  <br/><br/>
                  <em>Online Figure 6:</em> TBSS correlation results in HD gene carriers. Blue shows the areas where FA correlates (t &gt;3 with p &lt; 0.05 corrected for
                  multiple comparisons) with the individual scores in the Symbol Digit test (colour bar indicates 1-p values). The clusters
                  in the corpus callosum (U) are localized in the anterior and posterior portion of the body and in the head.
                  <br/><br/>
                  <em>Online Figure 7:</em>  TBSS correlation results in HD gene carriers. Green shows the areas where MD correlates (t &gt;3 with p &lt; 0.05 corrected for
                  multiple comparisons) with the individual motor score (colour bar indicates 1-p values). The clusters in the corpus callosum
                  (U) are localized in the body. 
                  <br/><br/>
                  <em>Online Figure 8:</em>  TBSS correlation results in HD gene carriers. Green shows the areas where MD inversely correlates (t &gt;3 with p &lt; 0.05 corrected
                  for multiple comparisons) with the individual scores in the Verbal Fluency test (colour bar indicates 1-p values).
                  <br/><br/>
                  <em>Online Figure 9:</em>  TBSS correlation results in HD gene carriers. Green shows the areas where MD inversely correlates (t &gt;3 with p &lt; 0.05 corrected
                  for multiple comparisons) with the individual scores in the Symbol Digit test (colour bar indicates 1-p values).
               </li></ul>
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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">Oct 2010, </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">31 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(9) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1675-1681; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata"><span class="label">DOI:</span> 10.3174/ajnr.A2128 </span></div>
  
  
  
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