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G03 Corpus callosal atrophy in Huntington's disease

Identifieur interne : 002E31 ( Istex/Corpus ); précédent : 002E30; suivant : 002E32

G03 Corpus callosal atrophy in Huntington's disease

Auteurs : He Crawford ; Nz Hobbs ; J. Cole ; Em Rees ; G. Owen ; Dr Langbehn ; C. Frost ; B. Landwehrmeyer ; R. Reilmann ; D. Craufurd ; Jc Stout ; A. Durr ; B. Leavitt ; Ra Roos ; Sj Tabrizi ; Ri Scahill

Source :

RBID : ISTEX:F5CA874DE78DE98E65D05D4283D1B3CC98696C71

English descriptors

Abstract

Background Research into Huntington's disease (HD) has revealed white-matter loss in individuals more than 10 years prior to predicted disease onset, focused around the striatum, corpus callosum (CC) and posterior white-matter tracts. Degeneration of the CC is of interest since it provides interhemispheric connections to cortical areas known to be affected in HD. Aims This study aims to investigate the utility of volumetric measurements of the CC in HD using a novel segmentation technique, multiple time-points and a large well-characterised cohort. Structure-function relationship in the CC will also be explored. Methods Volumetric 3T MRI from controls, premanifest gene carriers and early HD subjects enrolled in the TRACK-HD study will be analysed at baseline and 24 months. The CC will be delineated using a semi-automated segmentation protocol. Differences in baseline volumes and atrophy rates between groups will be examined, as well as correlations between volume loss and clinical impairment. Results Preliminary analysis of a subset of subjects indicates that early HD subjects have reduced CC volume compared with controls and premanifest subjects (p<0.001). Increased longitudinal CC volume change was found in early HD subjects, compared with controls (p<0.001). Interestingly there was significant difference in longitudinal change between controls and premanifest subjects close to disease onset (p<0.05). This work will be extended to include multi-site data and correlations between atrophy and clinical and cognitive decline. Conclusions Measurement of CC atrophy may have potential as an imaging biomarker for HD and may prove useful for exploring interhemispheric structure-function relationships. Funding Helen Crawford is supported by the CHDI Foundation, a not for profit organisation dedicated to finding treatments for HD.

Url:
DOI: 10.1136/jnnp-2012-303524.83

Links to Exploration step

ISTEX:F5CA874DE78DE98E65D05D4283D1B3CC98696C71

Le document en format XML

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<div type="abstract">Background Research into Huntington's disease (HD) has revealed white-matter loss in individuals more than 10 years prior to predicted disease onset, focused around the striatum, corpus callosum (CC) and posterior white-matter tracts. Degeneration of the CC is of interest since it provides interhemispheric connections to cortical areas known to be affected in HD. Aims This study aims to investigate the utility of volumetric measurements of the CC in HD using a novel segmentation technique, multiple time-points and a large well-characterised cohort. Structure-function relationship in the CC will also be explored. Methods Volumetric 3T MRI from controls, premanifest gene carriers and early HD subjects enrolled in the TRACK-HD study will be analysed at baseline and 24 months. The CC will be delineated using a semi-automated segmentation protocol. Differences in baseline volumes and atrophy rates between groups will be examined, as well as correlations between volume loss and clinical impairment. Results Preliminary analysis of a subset of subjects indicates that early HD subjects have reduced CC volume compared with controls and premanifest subjects (p<0.001). Increased longitudinal CC volume change was found in early HD subjects, compared with controls (p<0.001). Interestingly there was significant difference in longitudinal change between controls and premanifest subjects close to disease onset (p<0.05). This work will be extended to include multi-site data and correlations between atrophy and clinical and cognitive decline. Conclusions Measurement of CC atrophy may have potential as an imaging biomarker for HD and may prove useful for exploring interhemispheric structure-function relationships. Funding Helen Crawford is supported by the CHDI Foundation, a not for profit organisation dedicated to finding treatments for HD.</div>
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<p>Background Research into Huntington's disease (HD) has revealed white-matter loss in individuals more than 10 years prior to predicted disease onset, focused around the striatum, corpus callosum (CC) and posterior white-matter tracts. Degeneration of the CC is of interest since it provides interhemispheric connections to cortical areas known to be affected in HD. Aims This study aims to investigate the utility of volumetric measurements of the CC in HD using a novel segmentation technique, multiple time-points and a large well-characterised cohort. Structure-function relationship in the CC will also be explored. Methods Volumetric 3T MRI from controls, premanifest gene carriers and early HD subjects enrolled in the TRACK-HD study will be analysed at baseline and 24 months. The CC will be delineated using a semi-automated segmentation protocol. Differences in baseline volumes and atrophy rates between groups will be examined, as well as correlations between volume loss and clinical impairment. Results Preliminary analysis of a subset of subjects indicates that early HD subjects have reduced CC volume compared with controls and premanifest subjects (p<0.001). Increased longitudinal CC volume change was found in early HD subjects, compared with controls (p<0.001). Interestingly there was significant difference in longitudinal change between controls and premanifest subjects close to disease onset (p<0.05). This work will be extended to include multi-site data and correlations between atrophy and clinical and cognitive decline. Conclusions Measurement of CC atrophy may have potential as an imaging biomarker for HD and may prove useful for exploring interhemispheric structure-function relationships. Funding Helen Crawford is supported by the CHDI Foundation, a not for profit organisation dedicated to finding treatments for HD.</p>
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</article-categories>
<title-group>
<article-title>G03 Corpus callosal atrophy in Huntington's disease</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<name>
<surname>Crawford</surname>
<given-names>HE</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Hobbs</surname>
<given-names>NZ</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Cole</surname>
<given-names>J</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Rees</surname>
<given-names>EM</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Owen</surname>
<given-names>G</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Langbehn</surname>
<given-names>DR</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
<xref ref-type="aff" rid="aff3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Frost</surname>
<given-names>C</given-names>
</name>
<xref ref-type="aff" rid="aff4">4</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Landwehrmeyer</surname>
<given-names>B</given-names>
</name>
<xref ref-type="aff" rid="aff5">5</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Reilmann</surname>
<given-names>R</given-names>
</name>
<xref ref-type="aff" rid="aff6">6</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Craufurd</surname>
<given-names>D</given-names>
</name>
<xref ref-type="aff" rid="aff7">7</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Stout</surname>
<given-names>JC</given-names>
</name>
<xref ref-type="aff" rid="aff8">8</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Durr</surname>
<given-names>A</given-names>
</name>
<xref ref-type="aff" rid="aff9">9</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Leavitt</surname>
<given-names>B</given-names>
</name>
<xref ref-type="aff" rid="aff10">10</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Roos</surname>
<given-names>RA</given-names>
</name>
<xref ref-type="aff" rid="aff11">11</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Tabrizi</surname>
<given-names>SJ</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Scahill</surname>
<given-names>RI</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<collab>and the TRACK-HD Investigators</collab>
</contrib>
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<aff id="aff1">
<label>1</label>
UCL Institute of Neurology, University College London, London, UK</aff>
<aff id="aff2">
<label>2</label>
Department of Psychiatry, University of Iowa, Iowa City, Iowa, USA</aff>
<aff id="aff3">
<label>3</label>
Department of Biostatistics (Secondary), University of Iowa, Iowa City, Iowa, USA</aff>
<aff id="aff4">
<label>4</label>
Department of Medical Statistics, London School of Hygiene and Tropical Medicine, London, UK</aff>
<aff id="aff5">
<label>5</label>
Department of Neurology, Ulm University, Ulm, Germany</aff>
<aff id="aff6">
<label>6</label>
Department of Neurology, University of Münster, Münster, Germany</aff>
<aff id="aff7">
<label>7</label>
Genetic Medicine, University of Manchester, Manchester Academic Health Sciences Centre and Central Manchester University Hospitals NHS Foundation Trust, St Mary's Hospital, Manchester, UK</aff>
<aff id="aff8">
<label>8</label>
School of Psychology and Psychiatry, Monash University, Victoria, Australia</aff>
<aff id="aff9">
<label>9</label>
Department of Genetics and Cytogenetics, and INSERM UMR S679, APHP Hôpital de la Salpêtrière, Paris, France</aff>
<aff id="aff10">
<label>10</label>
Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</aff>
<aff id="aff11">
<label>11</label>
Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands</aff>
<pub-date pub-type="ppub">
<month>9</month>
<year>2012</year>
</pub-date>
<volume>83</volume>
<volume-id pub-id-type="other">83</volume-id>
<volume-id pub-id-type="other">83</volume-id>
<issue>Suppl 1</issue>
<issue-id pub-id-type="other">jnnp;83/Suppl_1</issue-id>
<issue-id pub-id-type="other" content-type="supplement">Suppl_1</issue-id>
<issue-id pub-id-type="other">83/Suppl_1</issue-id>
<issue-title>European Huntington's Disease Network 2012 plenary meeting, Stockholm, Sweden, 14—16 September 2012</issue-title>
<fpage seq="1">A27</fpage>
<permissions>
<copyright-statement>© 2012, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</copyright-statement>
<copyright-year>2012</copyright-year>
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<abstract>
<sec>
<title>Background</title>
<p>Research into Huntington's disease (HD) has revealed white-matter loss in individuals more than 10 years prior to predicted disease onset, focused around the striatum, corpus callosum (CC) and posterior white-matter tracts. Degeneration of the CC is of interest since it provides interhemispheric connections to cortical areas known to be affected in HD.</p>
</sec>
<sec>
<title>Aims</title>
<p>This study aims to investigate the utility of volumetric measurements of the CC in HD using a novel segmentation technique, multiple time-points and a large well-characterised cohort. Structure-function relationship in the CC will also be explored.</p>
</sec>
<sec>
<title>Methods</title>
<p>Volumetric 3T MRI from controls, premanifest gene carriers and early HD subjects enrolled in the TRACK-HD study will be analysed at baseline and 24 months. The CC will be delineated using a semi-automated segmentation protocol. Differences in baseline volumes and atrophy rates between groups will be examined, as well as correlations between volume loss and clinical impairment.</p>
</sec>
<sec>
<title>Results</title>
<p>Preliminary analysis of a subset of subjects indicates that early HD subjects have reduced CC volume compared with controls and premanifest subjects (p<0.001). Increased longitudinal CC volume change was found in early HD subjects, compared with controls (p<0.001). Interestingly there was significant difference in longitudinal change between controls and premanifest subjects close to disease onset (p<0.05). This work will be extended to include multi-site data and correlations between atrophy and clinical and cognitive decline.</p>
</sec>
<sec>
<title>Conclusions</title>
<p>Measurement of CC atrophy may have potential as an imaging biomarker for HD and may prove useful for exploring interhemispheric structure-function relationships.</p>
</sec>
<sec>
<title>Funding</title>
<p>Helen Crawford is supported by the CHDI Foundation, a not for profit organisation dedicated to finding treatments for HD.</p>
</sec>
</abstract>
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<abstract>Background Research into Huntington's disease (HD) has revealed white-matter loss in individuals more than 10 years prior to predicted disease onset, focused around the striatum, corpus callosum (CC) and posterior white-matter tracts. Degeneration of the CC is of interest since it provides interhemispheric connections to cortical areas known to be affected in HD. Aims This study aims to investigate the utility of volumetric measurements of the CC in HD using a novel segmentation technique, multiple time-points and a large well-characterised cohort. Structure-function relationship in the CC will also be explored. Methods Volumetric 3T MRI from controls, premanifest gene carriers and early HD subjects enrolled in the TRACK-HD study will be analysed at baseline and 24 months. The CC will be delineated using a semi-automated segmentation protocol. Differences in baseline volumes and atrophy rates between groups will be examined, as well as correlations between volume loss and clinical impairment. Results Preliminary analysis of a subset of subjects indicates that early HD subjects have reduced CC volume compared with controls and premanifest subjects (p<0.001). Increased longitudinal CC volume change was found in early HD subjects, compared with controls (p<0.001). Interestingly there was significant difference in longitudinal change between controls and premanifest subjects close to disease onset (p<0.05). This work will be extended to include multi-site data and correlations between atrophy and clinical and cognitive decline. Conclusions Measurement of CC atrophy may have potential as an imaging biomarker for HD and may prove useful for exploring interhemispheric structure-function relationships. Funding Helen Crawford is supported by the CHDI Foundation, a not for profit organisation dedicated to finding treatments for HD.</abstract>
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