Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease
Identifieur interne : 002D57 ( Main/Curation ); précédent : 002D56; suivant : 002D58Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease
Auteurs : Richard M. Camicioli [Canada] ; Christopher C. Hanstock [Canada] ; Thomas P. Bouchard [Canada] ; Myrlene Gee [Canada] ; Nancy J. Fisher [Canada] ; W. R. Wayne Martin [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2007-02-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Analysis of Variance, Dysfunction, Evaluation scale, Female, Hoehn and Yahr Rating, Humans, Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy, Male, Motor Cortex (pathology), NMR spectrometry, Nervous system diseases, Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Sign, Unified Parkinson's Disease Rating Scale, magnetic resonance spectroscopy, motor signs.
- MESH :
- pathology : Motor Cortex, Parkinson Disease.
- physiopathology : Parkinson Disease.
- Aged, Aged, 80 and over, Analysis of Variance, Female, Humans, Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy, Male.
Abstract
The anterior cingulate (AC) gyrus and the presupplementary motor area (pre‐SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD. © 2006 Movement Disorder Society
Url:
DOI: 10.1002/mds.21288
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<front><div type="abstract" xml:lang="en">The anterior cingulate (AC) gyrus and the presupplementary motor area (pre‐SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD. © 2006 Movement Disorder Society</div>
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<front><div type="abstract" xml:lang="en">The anterior cingulate (AC) gyrus and the presupplementary motor area (pre-SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre-SMA, or posterior cingulate (PC). Forty-four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini-Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid-sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre-SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre-SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD.</div>
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<ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease</title>
<author><name sortKey="Camicioli, Richard M" sort="Camicioli, Richard M" uniqKey="Camicioli R" first="Richard M." last="Camicioli">Richard M. Camicioli</name>
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<author><name sortKey="Hanstock, Christopher C" sort="Hanstock, Christopher C" uniqKey="Hanstock C" first="Christopher C." last="Hanstock">Christopher C. Hanstock</name>
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<author><name sortKey="Bouchard, Thomas P" sort="Bouchard, Thomas P" uniqKey="Bouchard T" first="Thomas P." last="Bouchard">Thomas P. Bouchard</name>
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<author><name sortKey="Gee, Myrlene" sort="Gee, Myrlene" uniqKey="Gee M" first="Myrlene" last="Gee">Myrlene Gee</name>
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<author><name sortKey="Fisher, Nancy J" sort="Fisher, Nancy J" uniqKey="Fisher N" first="Nancy J." last="Fisher">Nancy J. Fisher</name>
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<author><name sortKey="Martin, W R Wayne" sort="Martin, W R Wayne" uniqKey="Martin W" first="W. R. Wayne" last="Martin">W. R. Wayne Martin</name>
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<idno type="doi">10.1002/mds.21288</idno>
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<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson's disease</title>
<author><name sortKey="Camicioli, Richard M" sort="Camicioli, Richard M" uniqKey="Camicioli R" first="Richard M." last="Camicioli">Richard M. Camicioli</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta</wicri:regionArea>
<wicri:noRegion>Alberta</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Hanstock, Christopher C" sort="Hanstock, Christopher C" uniqKey="Hanstock C" first="Christopher C." last="Hanstock">Christopher C. Hanstock</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta</wicri:regionArea>
<wicri:noRegion>Alberta</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Bouchard, Thomas P" sort="Bouchard, Thomas P" uniqKey="Bouchard T" first="Thomas P." last="Bouchard">Thomas P. Bouchard</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta</wicri:regionArea>
<wicri:noRegion>Alberta</wicri:noRegion>
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<author><name sortKey="Gee, Myrlene" sort="Gee, Myrlene" uniqKey="Gee M" first="Myrlene" last="Gee">Myrlene Gee</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta</wicri:regionArea>
<wicri:noRegion>Alberta</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Fisher, Nancy J" sort="Fisher, Nancy J" uniqKey="Fisher N" first="Nancy J." last="Fisher">Nancy J. Fisher</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Division of Neurosciences, University of Alberta, Edmonton, Alberta</wicri:regionArea>
<wicri:noRegion>Alberta</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Martin, W R Wayne" sort="Martin, W R Wayne" uniqKey="Martin W" first="W. R. Wayne" last="Martin">W. R. Wayne Martin</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta</wicri:regionArea>
<wicri:noRegion>Alberta</wicri:noRegion>
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<series><title level="j">Movement Disorders</title>
<title level="j" type="sub">Official Journal of the Movement Disorder Society</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2007-02-15">2007-02-15</date>
<biblScope unit="vol">22</biblScope>
<biblScope unit="issue">3</biblScope>
<biblScope unit="page" from="382">382</biblScope>
<biblScope unit="page" to="386">386</biblScope>
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<idno type="DOI">10.1002/mds.21288</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term>
<term>Aged, 80 and over</term>
<term>Analysis of Variance</term>
<term>Female</term>
<term>Hoehn and Yahr Rating</term>
<term>Humans</term>
<term>Magnetic Resonance Imaging</term>
<term>Magnetic Resonance Spectroscopy</term>
<term>Male</term>
<term>Motor Cortex (pathology)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Parkinson's disease</term>
<term>Unified Parkinson's Disease Rating Scale</term>
<term>magnetic resonance spectroscopy</term>
<term>motor signs</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Motor Cortex</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Aged, 80 and over</term>
<term>Analysis of Variance</term>
<term>Female</term>
<term>Humans</term>
<term>Magnetic Resonance Imaging</term>
<term>Magnetic Resonance Spectroscopy</term>
<term>Male</term>
</keywords>
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<front><div type="abstract" xml:lang="en">The anterior cingulate (AC) gyrus and the presupplementary motor area (pre‐SMA) show pathological changes in Parkinson's disease (PD). We examined if PD patients show magnetic resonance spectroscopy (MRS) changes in NAA/Cr in the AC, pre‐SMA, or posterior cingulate (PC). Forty‐four (27 male, 17 female) healthy nondemented PD patients and 38 controls (18 male, 20 female) 65 years of age and older were examined using the Unified Parkinson's Disease Rating Scale (UPDRS), Mini‐Mental State Examination, Frontal Assessment Battery, and Geriatric Depression Scale. MRS was performed at 1.5 T. Voxels (8 cc; PRESS; TE = 80; TR = 1,600 ms) were placed mid‐sagittally. Gray matter and white matter volumes were measured within voxels using SPM2. Spectra were analyzed using LC model to yield NAA/Cr and Cho/Cr. Demographic and cognitive measures did not differ between groups. Motor UPDRS was 17.7 ± 8.8 for PD. Pre‐SMA NAA/Cr was lower in PD (PD: 1.39 ± 0.17; control: 1.47 ± 0.16; P = 0.045) and correlated negatively with age (r = 0.39; P = 0.01), but not with UPDRS, disease duration, or dopamine equivalents. AC and PC NAA/Cr and Cho/Cr in any region did not differ (P > 0.05). In conclusion, pre‐SMA NAA/Cr was selectively decreased in PD, consistent with neuronal dysfunction. This should be further examined as a biomarker of disease in PD. © 2006 Movement Disorder Society</div>
</front>
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