MovDisordV3, Main, Exploration, bibRecord, 001A64

Rate and acceleration of whole‐brain atrophy in premanifest and early Huntington's disease

Identifieur interne : 001A64 ( Main/Exploration ); précédent : 001A63; suivant : 001A65

Rate and acceleration of whole‐brain atrophy in premanifest and early Huntington's disease

Auteurs : Edward J. Wild [Royaume-Uni] ; Susie M. D. Henley [Royaume-Uni] ; Nicola Z. Hobbs [Royaume-Uni] ; Chris Frost [Royaume-Uni] ; David G. Macmanus [Royaume-Uni] ; Roger A. Barker [Royaume-Uni] ; Nick C. Fox [Royaume-Uni] ; Sarah J. Tabrizi [Royaume-Uni]

Source :

Movement Disorders [ 0885-3185 ] ; 2010-05-15.

RBID : ISTEX:F3C4FCE8D751C4EEDBFF14C6213BB3C8F6B13ABD

Descripteurs français

Pascal (Inist)
- Atrophie, Chorée de Huntington, Encéphale, Imagerie RMN, Pathologie du système nerveux, Volumétrie.

English descriptors

KwdEn :
- Adult, Age of Onset, Atrophy, Atrophy (epidemiology), Atrophy (pathology), Brain (pathology), Cohort Studies, Disease Progression, Encephalon, Female, Humans, Huntington Disease (epidemiology), Huntington Disease (genetics), Huntington Disease (pathology), Huntington disease, Huntington's disease, Magnetic Resonance Imaging, Male, Middle Aged, Nervous system diseases, Nuclear magnetic resonance imaging, Point Mutation (genetics), Prospective Studies, Severity of Illness Index, Volumetric analysis, volumetric MRI, whole‐brain atrophy.
MESH :
- epidemiology : Atrophy, Huntington Disease.
- genetics : Huntington Disease, Point Mutation.
- pathology : Atrophy, Brain, Huntington Disease.
- Adult, Age of Onset, Cohort Studies, Disease Progression, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Prospective Studies, Severity of Illness Index.

Abstract

Huntington's disease (HD) produces progressive and ultimately widespread impairment of brain function. Neostriatal atrophy alone cannot account for whole‐brain losses seen postmortem, and the mutant huntingtin protein and its neuropathologic sequelae are evident throughout the brain. Whole‐brain atrophy quantification encompasses the totality of mutant huntingtin's effects on brain volume and may be useful in tracking progression in trials. We studied whole‐brain atrophy in HD using a 2‐year follow‐up design, with three annual MRI scans. We recruited 20 control subjects, 21 premanifest mutation carriers, and 40 patients with early HD and used the brain boundary shift integral to study rate and acceleration of atrophy. Among subjects with an acceptable quality 2‐year scan pair, age‐ and gender‐standardized mean brain atrophy rate was greater (P < 0.001) in the patients with HD (n = 21; 0.88%/yr; 95% confidence interval: 0.62–1.13%/yr) than that in controls (n = 13; 0.16%/yr; 0.00–0.32%/yr). In the 12 patients with early HD in whom acceleration could be directly assessed there was evidence (P= 0.048) of acceleration year‐on‐year (mean acceleration = 0.69% yr−2; 95% confidence interval: 0.01% yr−2 to 1.37% yr−2), although this was not formally significantly different from that in controls (n = 7, P = 0.055). Statistically significantly increased atrophy rates and acceleration were not seen overall in the premanifest group, who were on average 18 years from predicted disease onset. We conclude that the study of whole‐brain atrophy has the potential to inform our understanding of the neurobiology of HD and warrants further study as one means of assessing the outcomes of future clinical trials. © 2009 Movement Disorder Society

Url:

https://api.istex.fr/document/F3C4FCE8D751C4EEDBFF14C6213BB3C8F6B13ABD/fulltext/pdf

DOI: 10.1002/mds.22969

Affiliations:

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
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<term>Atrophy (pathology)</term>
<term>Brain (pathology)</term>
<term>Cohort Studies</term>
<term>Disease Progression</term>
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<term>Humans</term>
<term>Huntington Disease (epidemiology)</term>
<term>Huntington Disease (genetics)</term>
<term>Huntington Disease (pathology)</term>
<term>Huntington disease</term>
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<term>Male</term>
<term>Middle Aged</term>
<term>Nervous system diseases</term>
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<term>Huntington Disease</term>
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<term>Point Mutation</term>
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<term>Huntington Disease</term>
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<term>Age of Onset</term>
<term>Cohort Studies</term>
<term>Disease Progression</term>
<term>Female</term>
<term>Humans</term>
<term>Magnetic Resonance Imaging</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Prospective Studies</term>
<term>Severity of Illness Index</term>
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<term>Chorée de Huntington</term>
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<front><div type="abstract" xml:lang="en">Huntington's disease (HD) produces progressive and ultimately widespread impairment of brain function. Neostriatal atrophy alone cannot account for whole‐brain losses seen postmortem, and the mutant huntingtin protein and its neuropathologic sequelae are evident throughout the brain. Whole‐brain atrophy quantification encompasses the totality of mutant huntingtin's effects on brain volume and may be useful in tracking progression in trials. We studied whole‐brain atrophy in HD using a 2‐year follow‐up design, with three annual MRI scans. We recruited 20 control subjects, 21 premanifest mutation carriers, and 40 patients with early HD and used the brain boundary shift integral to study rate and acceleration of atrophy. Among subjects with an acceptable quality 2‐year scan pair, age‐ and gender‐standardized mean brain atrophy rate was greater (P < 0.001) in the patients with HD (n = 21; 0.88%/yr; 95% confidence interval: 0.62–1.13%/yr) than that in controls (n = 13; 0.16%/yr; 0.00–0.32%/yr). In the 12 patients with early HD in whom acceleration could be directly assessed there was evidence (P= 0.048) of acceleration year‐on‐year (mean acceleration = 0.69% yr−2; 95% confidence interval: 0.01% yr−2 to 1.37% yr−2), although this was not formally significantly different from that in controls (n = 7, P = 0.055). Statistically significantly increased atrophy rates and acceleration were not seen overall in the premanifest group, who were on average 18 years from predicted disease onset. We conclude that the study of whole‐brain atrophy has the potential to inform our understanding of the neurobiology of HD and warrants further study as one means of assessing the outcomes of future clinical trials. © 2009 Movement Disorder Society</div>
</front>
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<name sortKey="Henley, Susie M D" sort="Henley, Susie M D" uniqKey="Henley S" first="Susie M. D." last="Henley">Susie M. D. Henley</name>
<name sortKey="Henley, Susie M D" sort="Henley, Susie M D" uniqKey="Henley S" first="Susie M. D." last="Henley">Susie M. D. Henley</name>
<name sortKey="Hobbs, Nicola Z" sort="Hobbs, Nicola Z" uniqKey="Hobbs N" first="Nicola Z." last="Hobbs">Nicola Z. Hobbs</name>
<name sortKey="Hobbs, Nicola Z" sort="Hobbs, Nicola Z" uniqKey="Hobbs N" first="Nicola Z." last="Hobbs">Nicola Z. Hobbs</name>
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Movement Disorders (revue)

Rate and acceleration of whole‐brain atrophy in premanifest and early Huntington's disease

Rate and acceleration of whole‐brain atrophy in premanifest and early Huntington's disease

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

	Movement Disorders (revue)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.