Movement Disorders (revue)

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

Identifieur interne : 002B27 ( PascalFrancis/Checkpoint ); précédent : 002B26; suivant : 002B28

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]

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RBID : Pascal:00-0269081

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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.


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Pascal:00-0269081

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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<s1>Division of Medical Psychology, Department of Neuroscience, Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine</s1>
<s2>Baltimore, Maryland</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="05">
<s1>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</s1>
<s2>Baltimore, Maryland</s2>
<s3>USA</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="06">
<s1>Joint Appointment with Department of Neuroscience, Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine</s1>
<s2>Baltimore, Maryland</s2>
<s3>USA</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA20>
<s1>552-560</s1>
</fA20>
<fA21>
<s1>2000</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>20953</s2>
<s5>354000087348900190</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2000 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>38 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>00-0269081</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Movement disorders</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Chorée Huntington</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Huntington disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Corea Huntington</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Noyau caudé</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Caudate nucleus</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Núcleo caudado</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Imagerie RMN</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Nuclear magnetic resonance imaging</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Imageria RMN</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Atrophie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Atrophy</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Atrofia</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Etude longitudinale</s0>
<s5>16</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Follow up study</s0>
<s5>16</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Estudio longitudinal</s0>
<s5>16</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Exploration</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Exploration</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Exploración</s0>
<s5>17</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Evolution</s0>
<s5>18</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Evolution</s0>
<s5>18</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Evolución</s0>
<s5>18</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Asymptomatique</s0>
<s5>23</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Asymptomatic</s0>
<s5>23</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Asintomático</s0>
<s5>23</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Maladie héréditaire</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Genetic disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Enfermedad hereditaria</s0>
<s5>42</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Encéphale</s0>
<s5>45</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Brain (vertebrata)</s0>
<s5>45</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Encéfalo</s0>
<s5>45</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Imagerie médicale</s0>
<s5>53</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Medical imagery</s0>
<s5>53</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Imageneria medical</s0>
<s5>53</s5>
</fC07>
<fN21>
<s1>185</s1>
</fN21>
</pA>
</standard>
</inist>
<affiliations>
<list>
<country>
<li>États-Unis</li>
</country>
<region>
<li>Maryland</li>
<li>Washington (État)</li>
</region>
<settlement>
<li>Seattle</li>
</settlement>
<orgName>
<li>Université de Washington</li>
</orgName>
</list>
<tree>
<country name="États-Unis">
<region name="Maryland">
<name sortKey="Aylward, E H" sort="Aylward, E H" uniqKey="Aylward E" first="E. H." last="Aylward">E. H. Aylward</name>
</region>
<name sortKey="Aylward, E H" sort="Aylward, E H" uniqKey="Aylward E" first="E. H." last="Aylward">E. H. Aylward</name>
<name sortKey="Aylward, E H" sort="Aylward, E H" uniqKey="Aylward E" first="E. H." last="Aylward">E. H. Aylward</name>
<name sortKey="Barta, P E" sort="Barta, P E" uniqKey="Barta P" first="P. E." last="Barta">P. E. Barta</name>
<name sortKey="Brandt, J" sort="Brandt, J" uniqKey="Brandt J" first="J." last="Brandt">J. Brandt</name>
<name sortKey="Codori, A M" sort="Codori, A M" uniqKey="Codori A" first="A.-M." last="Codori">A.-M. Codori</name>
<name sortKey="Pearlson, G D" sort="Pearlson, G D" uniqKey="Pearlson G" first="G. D." last="Pearlson">G. D. Pearlson</name>
<name sortKey="Pearlson, G D" sort="Pearlson, G D" uniqKey="Pearlson G" first="G. D." last="Pearlson">G. D. Pearlson</name>
<name sortKey="Rosenblatt, A" sort="Rosenblatt, A" uniqKey="Rosenblatt A" first="A." last="Rosenblatt">A. Rosenblatt</name>
<name sortKey="Ross, C A" sort="Ross, C A" uniqKey="Ross C" first="C. A." last="Ross">C. A. Ross</name>
<name sortKey="Ross, C A" sort="Ross, C A" uniqKey="Ross C" first="C. A." last="Ross">C. A. Ross</name>
<name sortKey="Sherr, M" sort="Sherr, M" uniqKey="Sherr M" first="M." last="Sherr">M. Sherr</name>
<name sortKey="Stine, O C" sort="Stine, O C" uniqKey="Stine O" first="O. C." last="Stine">O. C. Stine</name>
</country>
</tree>
</affiliations>
</record>

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