Diffusion tensor imaging in presymptomatic and early huntington's disease : Selective white matter pathology and its relationship to clinical measures
Identifieur interne : 001A15 ( PascalFrancis/Corpus ); précédent : 001A14; suivant : 001A16Diffusion tensor imaging in presymptomatic and early huntington's disease : Selective white matter pathology and its relationship to clinical measures
Auteurs : H. Diana Rosas ; David S. Tuch ; Nathanael D. Hevelone ; Alexandra K. Zaleta ; Mark Vangel ; Steven M. Hersch ; David H. SalatSource :
- Movement disorders [ 0885-3185 ] ; 2006.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Atrophy of cortical and subcortical gray matter is apparent in Huntington's disease (HD) before symptoms manifest. We hypothesized that the white matter (WM) connecting cortical and subcortical regions must also be affected early and that select clinical symptoms were related to systems degeneration. We used diffusion tensor magnetic resonance imaging (DTI) to examine the regional nature of WM abnormalities in early HD, including the preclinical period, and to determine whether regional changes correlated with clinical features. We studied individuals in early stages (HD), presymptomatic individuals known to carry the genetic mutation that causes HD (Pre-HD), and matched healthy controls. DTI indices of tissue integrity were obtained from several regions of interest, including the corpus callosum (CC), internal capsule (IC), and basal ganglia, were compared across groups by t tests, and were correlated to cognitive and clinical measures. WM alterations were found throughout the CC, in the anterior and posterior limbs of the IC, and in frontal subcortical WM in HD subjects, supporting the selective involvement of the pyramidal tracts in HD; a similar distribution of changes was seen in Pre-HD subjects, supporting presymptomatic alterations. There was a significant relationship between select DTI measures and cognitive performance. Alterations in diffusion indices were also seen in the striatum that were independent of atrophy. Our findings support that WM alterations occur very early in HD. The distribution of the changes suggests that these changes contribute to the disruption of pyramidal and extrapyramidal circuits and also support a role of compromised cortical circuitry in early cognitive and subtle motor impairment during the preclinical stages of HD.
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Format Inist (serveur)
NO : | PASCAL 06-0518081 INIST |
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ET : | Diffusion tensor imaging in presymptomatic and early huntington's disease : Selective white matter pathology and its relationship to clinical measures |
AU : | ROSAS (H. Diana); TUCH (David S.); HEVELONE (Nathanael D.); ZALETA (Alexandra K.); VANGEL (Mark); HERSCH (Steven M.); SALAT (David H.) |
AF : | Department of Neurology, Massachusetts General Hospital and Harvard Medical School/Boston, Massachusetts/Etats-Unis (1 aut., 6 aut.); Center for Neuroimaging of Aging and Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School/Boston, Massachusetts/Etats-Unis (1 aut., 3 aut., 4 aut., 7 aut.); Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital/Harvard Medical School/Charlestown, Massachusetts/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2006; Vol. 21; No. 9; Pp. 1317-1325; Bibl. 42 ref. |
LA : | Anglais |
EA : | Atrophy of cortical and subcortical gray matter is apparent in Huntington's disease (HD) before symptoms manifest. We hypothesized that the white matter (WM) connecting cortical and subcortical regions must also be affected early and that select clinical symptoms were related to systems degeneration. We used diffusion tensor magnetic resonance imaging (DTI) to examine the regional nature of WM abnormalities in early HD, including the preclinical period, and to determine whether regional changes correlated with clinical features. We studied individuals in early stages (HD), presymptomatic individuals known to carry the genetic mutation that causes HD (Pre-HD), and matched healthy controls. DTI indices of tissue integrity were obtained from several regions of interest, including the corpus callosum (CC), internal capsule (IC), and basal ganglia, were compared across groups by t tests, and were correlated to cognitive and clinical measures. WM alterations were found throughout the CC, in the anterior and posterior limbs of the IC, and in frontal subcortical WM in HD subjects, supporting the selective involvement of the pyramidal tracts in HD; a similar distribution of changes was seen in Pre-HD subjects, supporting presymptomatic alterations. There was a significant relationship between select DTI measures and cognitive performance. Alterations in diffusion indices were also seen in the striatum that were independent of atrophy. Our findings support that WM alterations occur very early in HD. The distribution of the changes suggests that these changes contribute to the disruption of pyramidal and extrapyramidal circuits and also support a role of compromised cortical circuitry in early cognitive and subtle motor impairment during the preclinical stages of HD. |
CC : | 002B17; 002B17G; 002B24A06 |
FD : | Système nerveux pathologie; Chorée Huntington; Tenseur de diffusion; Substance blanche; Anatomopathologie; Imagerie de diffusion |
FG : | Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Maladie héréditaire; Système nerveux central pathologie |
ED : | Nervous system diseases; Huntington disease; Diffusion tensor; White matter; Anatomic pathology; Diffusion imaging |
EG : | Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Central nervous system disease |
SD : | Sistema nervioso patología; Corea Huntington; Tensor de difusión; Substancia blanca; Anatomía patológica |
LO : | INIST-20953.354000158780860030 |
ID : | 06-0518081 |
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Pascal:06-0518081Le document en format XML
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<series><title level="j" type="main">Movement disorders</title>
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<front><div type="abstract" xml:lang="en">Atrophy of cortical and subcortical gray matter is apparent in Huntington's disease (HD) before symptoms manifest. We hypothesized that the white matter (WM) connecting cortical and subcortical regions must also be affected early and that select clinical symptoms were related to systems degeneration. We used diffusion tensor magnetic resonance imaging (DTI) to examine the regional nature of WM abnormalities in early HD, including the preclinical period, and to determine whether regional changes correlated with clinical features. We studied individuals in early stages (HD), presymptomatic individuals known to carry the genetic mutation that causes HD (Pre-HD), and matched healthy controls. DTI indices of tissue integrity were obtained from several regions of interest, including the corpus callosum (CC), internal capsule (IC), and basal ganglia, were compared across groups by t tests, and were correlated to cognitive and clinical measures. WM alterations were found throughout the CC, in the anterior and posterior limbs of the IC, and in frontal subcortical WM in HD subjects, supporting the selective involvement of the pyramidal tracts in HD; a similar distribution of changes was seen in Pre-HD subjects, supporting presymptomatic alterations. There was a significant relationship between select DTI measures and cognitive performance. Alterations in diffusion indices were also seen in the striatum that were independent of atrophy. Our findings support that WM alterations occur very early in HD. The distribution of the changes suggests that these changes contribute to the disruption of pyramidal and extrapyramidal circuits and also support a role of compromised cortical circuitry in early cognitive and subtle motor impairment during the preclinical stages of HD.</div>
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<fC02 i1="03" i2="X"><s0>002B24A06</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Chorée Huntington</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Huntington disease</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Corea Huntington</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Tenseur de diffusion</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Diffusion tensor</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Tensor de difusión</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Substance blanche</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>White matter</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Substancia blanca</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Anatomopathologie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Anatomic pathology</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Anatomía patológica</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Imagerie de diffusion</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Diffusion imaging</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Genetic disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>41</s5>
</fC07>
<fN21><s1>338</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
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<server><NO>PASCAL 06-0518081 INIST</NO>
<ET>Diffusion tensor imaging in presymptomatic and early huntington's disease : Selective white matter pathology and its relationship to clinical measures</ET>
<AU>ROSAS (H. Diana); TUCH (David S.); HEVELONE (Nathanael D.); ZALETA (Alexandra K.); VANGEL (Mark); HERSCH (Steven M.); SALAT (David H.)</AU>
<AF>Department of Neurology, Massachusetts General Hospital and Harvard Medical School/Boston, Massachusetts/Etats-Unis (1 aut., 6 aut.); Center for Neuroimaging of Aging and Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School/Boston, Massachusetts/Etats-Unis (1 aut., 3 aut., 4 aut., 7 aut.); Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital/Harvard Medical School/Charlestown, Massachusetts/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2006; Vol. 21; No. 9; Pp. 1317-1325; Bibl. 42 ref.</SO>
<LA>Anglais</LA>
<EA>Atrophy of cortical and subcortical gray matter is apparent in Huntington's disease (HD) before symptoms manifest. We hypothesized that the white matter (WM) connecting cortical and subcortical regions must also be affected early and that select clinical symptoms were related to systems degeneration. We used diffusion tensor magnetic resonance imaging (DTI) to examine the regional nature of WM abnormalities in early HD, including the preclinical period, and to determine whether regional changes correlated with clinical features. We studied individuals in early stages (HD), presymptomatic individuals known to carry the genetic mutation that causes HD (Pre-HD), and matched healthy controls. DTI indices of tissue integrity were obtained from several regions of interest, including the corpus callosum (CC), internal capsule (IC), and basal ganglia, were compared across groups by t tests, and were correlated to cognitive and clinical measures. WM alterations were found throughout the CC, in the anterior and posterior limbs of the IC, and in frontal subcortical WM in HD subjects, supporting the selective involvement of the pyramidal tracts in HD; a similar distribution of changes was seen in Pre-HD subjects, supporting presymptomatic alterations. There was a significant relationship between select DTI measures and cognitive performance. Alterations in diffusion indices were also seen in the striatum that were independent of atrophy. Our findings support that WM alterations occur very early in HD. The distribution of the changes suggests that these changes contribute to the disruption of pyramidal and extrapyramidal circuits and also support a role of compromised cortical circuitry in early cognitive and subtle motor impairment during the preclinical stages of HD.</EA>
<CC>002B17; 002B17G; 002B24A06</CC>
<FD>Système nerveux pathologie; Chorée Huntington; Tenseur de diffusion; Substance blanche; Anatomopathologie; Imagerie de diffusion</FD>
<FG>Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Maladie héréditaire; Système nerveux central pathologie</FG>
<ED>Nervous system diseases; Huntington disease; Diffusion tensor; White matter; Anatomic pathology; Diffusion imaging</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Central nervous system disease</EG>
<SD>Sistema nervioso patología; Corea Huntington; Tensor de difusión; Substancia blanca; Anatomía patológica</SD>
<LO>INIST-20953.354000158780860030</LO>
<ID>06-0518081</ID>
</server>
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