Movement Disorders (revue)

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

Identifieur interne : 004977 ( Main/Curation ); précédent : 004976; suivant : 004978

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

Auteurs : Elizabeth H. Aylward [États-Unis] ; Ann Marie Codori [États-Unis] ; Adam Rosenblatt [États-Unis] ; Meeia Sherr [États-Unis] ; Jason Brandt [États-Unis] ; Oscar C. Stine [États-Unis] ; Patrick E. Barta [États-Unis] ; Godfrey D. Pearlson [États-Unis] ; Christopher A. Ross [États-Unis]

Source :

RBID : ISTEX:13E5EA42CC313299FA90380C3B80DF1555A8B269

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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.

Url:
DOI: 10.1002/1531-8257(200005)15:3<552::AID-MDS1020>3.0.CO;2-P

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ISTEX:13E5EA42CC313299FA90380C3B80DF1555A8B269

Le document en format XML

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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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<name sortKey="Codori, A M" sort="Codori, A M" uniqKey="Codori A" first="A M" last="Codori">A M Codori</name>
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<name sortKey="Rosenblatt, A" sort="Rosenblatt, A" uniqKey="Rosenblatt A" first="A" last="Rosenblatt">A. Rosenblatt</name>
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<name sortKey="Sherr, M" sort="Sherr, M" uniqKey="Sherr M" first="M" last="Sherr">M. Sherr</name>
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<name sortKey="Brandt, J" sort="Brandt, J" uniqKey="Brandt J" first="J" last="Brandt">J. Brandt</name>
</author>
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<name sortKey="Stine, O C" sort="Stine, O C" uniqKey="Stine O" first="O C" last="Stine">O C Stine</name>
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<name sortKey="Ross, C A" sort="Ross, C A" uniqKey="Ross C" first="C A" last="Ross">C A Ross</name>
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<title xml:lang="en">Rate of caudate atrophy in presymptomatic and symptomatic stages of Huntington's disease.</title>
<author>
<name sortKey="Aylward, E H" sort="Aylward, E H" uniqKey="Aylward E" first="E H" last="Aylward">E H Aylward</name>
<affiliation wicri:level="2">
<nlm:affiliation>Division of Psychiatric Neuroimaging, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Psychiatric Neuroimaging, Johns Hopkins University School of Medicine, Baltimore, Maryland</wicri:regionArea>
<placeName>
<region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author>
<name sortKey="Codori, A M" sort="Codori, A M" uniqKey="Codori A" first="A M" last="Codori">A M Codori</name>
</author>
<author>
<name sortKey="Rosenblatt, A" sort="Rosenblatt, A" uniqKey="Rosenblatt A" first="A" last="Rosenblatt">A. Rosenblatt</name>
</author>
<author>
<name sortKey="Sherr, M" sort="Sherr, M" uniqKey="Sherr M" first="M" last="Sherr">M. Sherr</name>
</author>
<author>
<name sortKey="Brandt, J" sort="Brandt, J" uniqKey="Brandt J" first="J" last="Brandt">J. Brandt</name>
</author>
<author>
<name sortKey="Stine, O C" sort="Stine, O C" uniqKey="Stine O" first="O C" last="Stine">O C Stine</name>
</author>
<author>
<name sortKey="Barta, P E" sort="Barta, P E" uniqKey="Barta P" first="P E" last="Barta">P E Barta</name>
</author>
<author>
<name sortKey="Pearlson, G D" sort="Pearlson, G D" uniqKey="Pearlson G" first="G D" last="Pearlson">G D Pearlson</name>
</author>
<author>
<name sortKey="Ross, C A" sort="Ross, C A" uniqKey="Ross C" first="C A" last="Ross">C A Ross</name>
</author>
</analytic>
<series>
<title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
<idno type="ISSN">0885-3185</idno>
<imprint>
<date when="2000" type="published">2000</date>
</imprint>
</series>
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<keywords scheme="KwdEn" xml:lang="en">
<term>Adult</term>
<term>Aged</term>
<term>Atrophy</term>
<term>Caudate Nucleus (pathology)</term>
<term>Female</term>
<term>Genetic Testing</term>
<term>Heterozygote Detection</term>
<term>Humans</term>
<term>Huntington Disease (diagnosis)</term>
<term>Huntington Disease (genetics)</term>
<term>Longitudinal Studies</term>
<term>Magnetic Resonance Imaging</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Neurologic Examination</term>
</keywords>
<keywords scheme="MESH" qualifier="diagnosis" xml:lang="en">
<term>Huntington Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Huntington Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Caudate Nucleus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Adult</term>
<term>Aged</term>
<term>Atrophy</term>
<term>Female</term>
<term>Genetic Testing</term>
<term>Heterozygote Detection</term>
<term>Humans</term>
<term>Longitudinal Studies</term>
<term>Magnetic Resonance Imaging</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Neurologic Examination</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<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) < or =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>
</front>
</TEI>
</PubMed>
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