Brain structural damage in spinocerebellar ataxia type 2. A voxel‐based morphometry study
Identifieur interne : 002C71 ( Istex/Curation ); précédent : 002C70; suivant : 002C72Brain structural damage in spinocerebellar ataxia type 2. A voxel‐based morphometry study
Auteurs : Riccardo Della Nave [Italie] ; Andrea Ginestroni [Italie] ; Carlo Tessa [Italie] ; Mirco Cosottini [Italie] ; Marco Giannelli [Italie] ; Elena Salvatore [Italie] ; Ferdinando Sartucci [Italie] ; Giuseppe De Michele [Italie] ; Maria Teresa Dotti [Italie] ; Silvia Piacentini [Italie] ; Mario Mascalchi [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-04-30.
English descriptors
Abstract
Voxel‐based morphometry (VBM) enables an unbiased in‐vivo whole‐brain quantitative analysis of differences in gray matter (GM), white matter (WM) and cerebro‐spinal fluid (CSF) volumes. We assessed with VBM 20 spinocerebellar ataxia Type 2 (SCA2) patients with mild or moderate cerebellar deficit and 20 age and sex‐matched healthy controls. SCA2 patients showed a significant (P < 0.05 corrected for multiple comparison) symmetric loss of GM in the cerebellar vermis and hemispheres sparing lobules I,II, Crus II,VII, and X, and of the WM in the peridentate region, middle cerebellar peduncles, dorsal pons, and cerebral peduncles. The CSF volume was increased in the posterior cranial fossa. No GM, WM or CSF volume changes were observed in the supratentorial compartment. A mild (P < 0.05, >0.01) correlation was observed between the GM and WM loss and severity of the neurological deficit. In SCA2 patients with mild to moderate cerebellar deficit, GM and WM volume loss and CSF volume increase are confined to the posterior cranial fossa. © 2008 Movement Disorder Society
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DOI: 10.1002/mds.21982
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A voxel‐based morphometry study</title><author><name sortKey="Nave, Riccardo Della" sort="Nave, Riccardo Della" uniqKey="Nave R" first="Riccardo Della" last="Nave">Riccardo Della Nave</name><affiliation wicri:level="1"><mods:affiliation>Radiodiagnostic Section, Department of Clinical Physiopathology, University of Florence, Florence, Italy</mods:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Radiodiagnostic Section, Department of Clinical Physiopathology, University of Florence, Florence</wicri:regionArea></affiliation></author><author><name sortKey="Ginestroni, Andrea" sort="Ginestroni, Andrea" uniqKey="Ginestroni A" first="Andrea" last="Ginestroni">Andrea Ginestroni</name><affiliation wicri:level="1"><mods:affiliation>Radiodiagnostic Section, Department of Clinical Physiopathology, University of Florence, Florence, Italy</mods:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Radiodiagnostic Section, Department of Clinical Physiopathology, 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sortKey="Mascalchi, Mario" sort="Mascalchi, Mario" uniqKey="Mascalchi M" first="Mario" last="Mascalchi">Mario Mascalchi</name><affiliation wicri:level="1"><mods:affiliation>Radiodiagnostic Section, Department of Clinical Physiopathology, University of Florence, Florence, Italy</mods:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Radiodiagnostic Section, Department of Clinical Physiopathology, University of Florence, Florence</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</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="2008-04-30">2008-04-30</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="899">899</biblScope><biblScope unit="page" to="903">903</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">27EAF0D80C242217DB4A7148709310C1F89D1595</idno><idno type="DOI">10.1002/mds.21982</idno><idno type="ArticleID">MDS21982</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>MR imaging</term><term>ataxia</term><term>spinocerebellar ataxia type 2</term><term>voxel‐based morphometry</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Voxel‐based morphometry (VBM) enables an unbiased in‐vivo whole‐brain quantitative analysis of differences in gray matter (GM), white matter (WM) and cerebro‐spinal fluid (CSF) volumes. We assessed with VBM 20 spinocerebellar ataxia Type 2 (SCA2) patients with mild or moderate cerebellar deficit and 20 age and sex‐matched healthy controls. SCA2 patients showed a significant (P < 0.05 corrected for multiple comparison) symmetric loss of GM in the cerebellar vermis and hemispheres sparing lobules I,II, Crus II,VII, and X, and of the WM in the peridentate region, middle cerebellar peduncles, dorsal pons, and cerebral peduncles. The CSF volume was increased in the posterior cranial fossa. No GM, WM or CSF volume changes were observed in the supratentorial compartment. A mild (P < 0.05, >0.01) correlation was observed between the GM and WM loss and severity of the neurological deficit. In SCA2 patients with mild to moderate cerebellar deficit, GM and WM volume loss and CSF volume increase are confined to the posterior cranial fossa. © 2008 Movement Disorder Society</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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