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Movement Disorders (revue)

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Evidence of Thalamic Dysfunction in Huntington Disease by Proton Magnetic Resonance Spectroscopy

Identifieur interne : 001839 ( PascalFrancis/Curation ); précédent : 001838; suivant : 001840

Evidence of Thalamic Dysfunction in Huntington Disease by Proton Magnetic Resonance Spectroscopy

Auteurs : Heloisa H. Ruocco [Brésil] ; Iscia Lopes-Cendes [Brésil] ; Li M. Li [Brésil] ; Fernando Cendes [Brésil]

Source :

RBID : Pascal:08-0069695

Descripteurs français

English descriptors

Abstract

Our objective was to investigate thalamic neuronal dysfunction in patients with Huntington disease (HD). We performed localized single-voxel proton magnetic resonance spectroscopy (MRS) of the thalamus in 22 HD patients and 25 healthy individuals. The mean age of patients was 48.5 years (ranging from 32 to 71 years). Age at onset varied between 20 and 66 years (mean 38.9 years). The expanded CAG repeat ranged from 40 to 52 (mean 45.2) CAGs. The mean age of control group was 35.4 years, ranging from 19 to 67 years. N-acetylaspartate (NAA) relative to creatine (NAA/Cr) values in the thalamus of HD patients were decreased when compared with controls (P = 0.0001). The spectroscopic findings were not correlated with motor impairment. However, there was a positive correlation between duration of disease and motor impairment (P = 0.02, r = 0.48), and a tendency for positive correlation between duration of disease and NAA/Cr (P = 0.059, r = 0.4). We found decreased NAA/Cr values in the thalamus of patients with HD, indicating neuronal loss or dysfunction. This is in agreement with previous studies that indicated the involvement of mitochondrial dysfunction in the neurodegenerative process of HD.
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A11 02  1    @1 LOPES-CENDES (Iscia)
A11 03  1    @1 LI (Li M.)
A11 04  1    @1 CENDES (Fernando)
A14 01      @1 Department of Neurology, University of Campinas @2 Campinas, São Paulo @3 BRA @Z 1 aut. @Z 3 aut. @Z 4 aut.
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C01 01    ENG  @0 Our objective was to investigate thalamic neuronal dysfunction in patients with Huntington disease (HD). We performed localized single-voxel proton magnetic resonance spectroscopy (MRS) of the thalamus in 22 HD patients and 25 healthy individuals. The mean age of patients was 48.5 years (ranging from 32 to 71 years). Age at onset varied between 20 and 66 years (mean 38.9 years). The expanded CAG repeat ranged from 40 to 52 (mean 45.2) CAGs. The mean age of control group was 35.4 years, ranging from 19 to 67 years. N-acetylaspartate (NAA) relative to creatine (NAA/Cr) values in the thalamus of HD patients were decreased when compared with controls (P = 0.0001). The spectroscopic findings were not correlated with motor impairment. However, there was a positive correlation between duration of disease and motor impairment (P = 0.02, r = 0.48), and a tendency for positive correlation between duration of disease and NAA/Cr (P = 0.059, r = 0.4). We found decreased NAA/Cr values in the thalamus of patients with HD, indicating neuronal loss or dysfunction. This is in agreement with previous studies that indicated the involvement of mitochondrial dysfunction in the neurodegenerative process of HD.
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C07 03  X  FRE  @0 Maladie dégénérative @5 39
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C07 03  X  SPA  @0 Enfermedad degenerativa @5 39
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N21       @1 035
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Pascal:08-0069695

Le document en format XML

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</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>Pathologie du système nerveux central</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>
<fC07 i1="06" i2="X" l="FRE">
<s0>Encéphale</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Encephalon</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Encéfalo</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Système nerveux central</s0>
<s5>44</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>44</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>44</s5>
</fC07>
<fN21>
<s1>035</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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