Movement Disorders (revue)

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Rate of caudate atrophy in presymptomatic and symptomatic stages of Huntington's disease

Identifieur interne : 000105 ( PascalFrancis/Curation ); précédent : 000104; suivant : 000106

Rate of caudate atrophy in presymptomatic and symptomatic stages of Huntington's disease

Auteurs : E. H. Aylward [États-Unis] ; A.-M. Codori [États-Unis] ; A. Rosenblatt [États-Unis] ; M. Sherr [États-Unis] ; J. Brandt [États-Unis] ; O. C. Stine [États-Unis] ; P. E. Barta [États-Unis] ; G. D. Pearlson [États-Unis] ; C. A. Ross [États-Unis]

Source :

RBID : Pascal:00-0269081

Descripteurs français

English descriptors

Abstract

Previous research by our group demonstrated a longitudinal change in caudate volume for symptomatic subjects with Huntington's disease (HD), and suggested that volume of the caudate may be a useful outcome measure for therapeutic studies in symptomatic patients. The current study was designed to determine whether longitudinal change in caudate atrophy could be documented in presymptomatic carriers of the HD gene mutation, and to compare rate of change in these subjects with rate of change in mildly and moderately affected symptomatic patients. We measured caudate volumes on serial magnetic resonance image scans from 30 patients at three stages of HD: 10 presymptomatic; 10 with mild symptoms, as indicated by scores on the Quantified Neurological Exam (QNE) ≤35; and 10 with moderate symptoms (QNE >45). The mean interscan interval was 36 months. When analyzed separately, both symptomatic groups and the presymptomatic group demonstrated a significant change in caudate volume over time. Amount of change over time did not differ significantly among the three groups. We conclude that change in caudate volume may be a useful outcome measure for assessing treatment effectiveness in both presymptomatic and symptomatic subjects.
pA  
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A08 01  1  ENG  @1 Rate of caudate atrophy in presymptomatic and symptomatic stages of Huntington's disease
A11 01  1    @1 AYLWARD (E. H.)
A11 02  1    @1 CODORI (A.-M.)
A11 03  1    @1 ROSENBLATT (A.)
A11 04  1    @1 SHERR (M.)
A11 05  1    @1 BRANDT (J.)
A11 06  1    @1 STINE (O. C.)
A11 07  1    @1 BARTA (P. E.)
A11 08  1    @1 PEARLSON (G. D.)
A11 09  1    @1 ROSS (C. A.)
A14 01      @1 Division of Psychiatric Neuroimaging, Johns Hopkins University School of Medicine @2 Baltimore, Maryland @3 USA @Z 1 aut. @Z 7 aut. @Z 8 aut.
A14 02      @1 Division of Neurobiology, Johns Hopkins University School of Medicine @2 Baltimore, Maryland @3 USA @Z 1 aut. @Z 3 aut. @Z 4 aut. @Z 6 aut. @Z 9 aut.
A14 03      @1 Departments of Radiology and Psychiatry, University of Washington @2 Seattle, Washington @3 USA @Z 1 aut.
A14 04      @1 Division of Medical Psychology, Department of Neuroscience, Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine @2 Baltimore, Maryland @3 USA @Z 2 aut. @Z 5 aut.
A14 05      @1 Joint Appointment with School of Hygiene and Public Health, Department of Neuroscience, Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine @2 Baltimore, Maryland @3 USA @Z 8 aut.
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C01 01    ENG  @0 Previous research by our group demonstrated a longitudinal change in caudate volume for symptomatic subjects with Huntington's disease (HD), and suggested that volume of the caudate may be a useful outcome measure for therapeutic studies in symptomatic patients. The current study was designed to determine whether longitudinal change in caudate atrophy could be documented in presymptomatic carriers of the HD gene mutation, and to compare rate of change in these subjects with rate of change in mildly and moderately affected symptomatic patients. We measured caudate volumes on serial magnetic resonance image scans from 30 patients at three stages of HD: 10 presymptomatic; 10 with mild symptoms, as indicated by scores on the Quantified Neurological Exam (QNE) ≤35; and 10 with moderate symptoms (QNE >45). The mean interscan interval was 36 months. When analyzed separately, both symptomatic groups and the presymptomatic group demonstrated a significant change in caudate volume over time. Amount of change over time did not differ significantly among the three groups. We conclude that change in caudate volume may be a useful outcome measure for assessing treatment effectiveness in both presymptomatic and symptomatic subjects.
C02 01  X    @0 002B17G
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C03 01  X  SPA  @0 Corea Huntington @5 01
C03 02  X  FRE  @0 Noyau caudé @5 04
C03 02  X  ENG  @0 Caudate nucleus @5 04
C03 02  X  SPA  @0 Núcleo caudado @5 04
C03 03  X  FRE  @0 Imagerie RMN @5 07
C03 03  X  ENG  @0 Nuclear magnetic resonance imaging @5 07
C03 03  X  SPA  @0 Imageria RMN @5 07
C03 04  X  FRE  @0 Atrophie @5 10
C03 04  X  ENG  @0 Atrophy @5 10
C03 04  X  SPA  @0 Atrofia @5 10
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C03 08  X  ENG  @0 Human @5 20
C03 08  X  SPA  @0 Hombre @5 20
C03 09  X  FRE  @0 Asymptomatique @5 23
C03 09  X  ENG  @0 Asymptomatic @5 23
C03 09  X  SPA  @0 Asintomático @5 23
C07 01  X  FRE  @0 Système nerveux pathologie @5 37
C07 01  X  ENG  @0 Nervous system diseases @5 37
C07 01  X  SPA  @0 Sistema nervioso patología @5 37
C07 02  X  FRE  @0 Système nerveux central pathologie @5 38
C07 02  X  ENG  @0 Central nervous system disease @5 38
C07 02  X  SPA  @0 Sistema nervosio central patología @5 38
C07 03  X  FRE  @0 Encéphale pathologie @5 39
C07 03  X  ENG  @0 Cerebral disorder @5 39
C07 03  X  SPA  @0 Encéfalo patología @5 39
C07 04  X  FRE  @0 Extrapyramidal syndrome @5 40
C07 04  X  ENG  @0 Extrapyramidal syndrome @5 40
C07 04  X  SPA  @0 Extrapiramidal síndrome @5 40
C07 05  X  FRE  @0 Maladie dégénérative @5 41
C07 05  X  ENG  @0 Degenerative disease @5 41
C07 05  X  SPA  @0 Enfermedad degenerativa @5 41
C07 06  X  FRE  @0 Maladie héréditaire @5 42
C07 06  X  ENG  @0 Genetic disease @5 42
C07 06  X  SPA  @0 Enfermedad hereditaria @5 42
C07 07  X  FRE  @0 Encéphale @5 45
C07 07  X  ENG  @0 Brain (vertebrata) @5 45
C07 07  X  SPA  @0 Encéfalo @5 45
C07 08  X  FRE  @0 Imagerie médicale @5 53
C07 08  X  ENG  @0 Medical imagery @5 53
C07 08  X  SPA  @0 Imageneria medical @5 53
N21       @1 185

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Pascal:00-0269081

Le document en format XML

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<term>Caudate nucleus</term>
<term>Evolution</term>
<term>Exploration</term>
<term>Follow up study</term>
<term>Human</term>
<term>Huntington disease</term>
<term>Nuclear magnetic resonance imaging</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Chorée Huntington</term>
<term>Noyau caudé</term>
<term>Imagerie RMN</term>
<term>Atrophie</term>
<term>Etude longitudinale</term>
<term>Exploration</term>
<term>Evolution</term>
<term>Homme</term>
<term>Asymptomatique</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr">
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<div type="abstract" xml:lang="en">Previous research by our group demonstrated a longitudinal change in caudate volume for symptomatic subjects with Huntington's disease (HD), and suggested that volume of the caudate may be a useful outcome measure for therapeutic studies in symptomatic patients. The current study was designed to determine whether longitudinal change in caudate atrophy could be documented in presymptomatic carriers of the HD gene mutation, and to compare rate of change in these subjects with rate of change in mildly and moderately affected symptomatic patients. We measured caudate volumes on serial magnetic resonance image scans from 30 patients at three stages of HD: 10 presymptomatic; 10 with mild symptoms, as indicated by scores on the Quantified Neurological Exam (QNE) ≤35; and 10 with moderate symptoms (QNE >45). The mean interscan interval was 36 months. When analyzed separately, both symptomatic groups and the presymptomatic group demonstrated a significant change in caudate volume over time. Amount of change over time did not differ significantly among the three groups. We conclude that change in caudate volume may be a useful outcome measure for assessing treatment effectiveness in both presymptomatic and symptomatic subjects.</div>
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