Morphometric changes of sensorimotor structures in focal dystonia
Identifieur interne : 001323 ( Istex/Corpus ); précédent : 001322; suivant : 001324Morphometric changes of sensorimotor structures in focal dystonia
Auteurs : Mark Obermann ; Ozguer Yaldizli ; Armin De Greiff ; Martin Lenard Lachenmayer ; Anna Rebecca Buhl ; Felicitus Tumczak ; Elke Ruth Gizewski ; Hans-Christoph Diener ; Matthias MaschkeSource :
- Movement Disorders [ 0885-3185 ] ; 2007-06-15.
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Abstract
Idiopathic cervical dystonia (CD) and benign essential blepharospasm (BEB) are the most common forms of focal dystonia. Previous autopsy and imaging studies suggested that these disorders are not accompanied by structural brain abnormalities. However, recent brain voxel‐based morphometry (VBM) studies of these conditions suggest that there actually may be changes in gray matter. The objective of this stdy was to detect possible gray matter abnormalities in patients with CD and BEB using VBM and to compare the results between the two conditions and with age‐ and gender‐matched controls. High‐resolution MRI was employed to evaluate healthy controls and individuals with BEB and CD. Eleven BEB, 9 CD, and 14 healthy control subjects were imaged. VBM revealed alterations of gray matter structures involved in sensorimotor processing in the individuals with focal dystonia. In CD subjects there was increased gray matter in the thalamus, caudate head bilaterally, superior temporal lobe, and left cerebellum, while gray matter was decreased in the putamen bilaterally. BEB subjects had increased gray matter in the caudate head and cerebellum bilaterally as well as decrease in the putamen and thalamus bilaterally. These findings strongly underline the recent notion that idiopathic focal dystonias might have a detectable structural correlate. They also demonstrate structural similarities of the investigated focal dystonias, possibly reflecting a shared common pathophysiological origin. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21495
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Greiff">Armin De Greiff</name><affiliation><mods:affiliation>Department of Neuroradiology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lachenmayer, Martin Lenard" sort="Lachenmayer, Martin Lenard" uniqKey="Lachenmayer M" first="Martin Lenard" last="Lachenmayer">Martin Lenard Lachenmayer</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Buhl, Anna Rebecca" sort="Buhl, Anna Rebecca" uniqKey="Buhl A" first="Anna Rebecca" last="Buhl">Anna Rebecca Buhl</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Tumczak, Felicitus" sort="Tumczak, Felicitus" uniqKey="Tumczak F" first="Felicitus" last="Tumczak">Felicitus Tumczak</name><affiliation><mods:affiliation>Department of Neurology, University 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Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Hufelandstr. 55, 45122 Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Yaldizli, Ozguer" sort="Yaldizli, Ozguer" uniqKey="Yaldizli O" first="Ozguer" last="Yaldizli">Ozguer Yaldizli</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="De Greiff, Armin" sort="De Greiff, Armin" uniqKey="De Greiff A" first="Armin" last="De Greiff">Armin De Greiff</name><affiliation><mods:affiliation>Department of Neuroradiology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lachenmayer, Martin Lenard" sort="Lachenmayer, Martin Lenard" uniqKey="Lachenmayer M" first="Martin Lenard" last="Lachenmayer">Martin Lenard Lachenmayer</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Buhl, Anna Rebecca" sort="Buhl, Anna Rebecca" uniqKey="Buhl A" first="Anna Rebecca" last="Buhl">Anna Rebecca Buhl</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Tumczak, Felicitus" sort="Tumczak, Felicitus" uniqKey="Tumczak F" first="Felicitus" last="Tumczak">Felicitus Tumczak</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Gizewski, Elke Ruth" sort="Gizewski, Elke Ruth" uniqKey="Gizewski E" first="Elke Ruth" last="Gizewski">Elke Ruth Gizewski</name><affiliation><mods:affiliation>Department of Neuroradiology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Diener, Hans Hristoph" sort="Diener, Hans Hristoph" uniqKey="Diener H" first="Hans-Christoph" last="Diener">Hans-Christoph Diener</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Maschke, Matthias" sort="Maschke, Matthias" uniqKey="Maschke M" first="Matthias" last="Maschke">Matthias Maschke</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg—Essen, Essen, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Germany</mods:affiliation></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="2007-06-15">2007-06-15</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1117">1117</biblScope><biblScope unit="page" to="1123">1123</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">09540BE5AD2D8AE73ABAB2C67E300EC9D590B8FF</idno><idno type="DOI">10.1002/mds.21495</idno><idno type="ArticleID">MDS21495</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>basal ganglia.</term><term>blepharospasm</term><term>cervical dystonia</term><term>focal dystonia</term><term>sensorimotor integration</term><term>torticollis</term><term>voxel‐based morphometry</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Idiopathic cervical dystonia (CD) and benign essential blepharospasm (BEB) are the most common forms of focal dystonia. Previous autopsy and imaging studies suggested that these disorders are not accompanied by structural brain abnormalities. However, recent brain voxel‐based morphometry (VBM) studies of these conditions suggest that there actually may be changes in gray matter. The objective of this stdy was to detect possible gray matter abnormalities in patients with CD and BEB using VBM and to compare the results between the two conditions and with age‐ and gender‐matched controls. High‐resolution MRI was employed to evaluate healthy controls and individuals with BEB and CD. Eleven BEB, 9 CD, and 14 healthy control subjects were imaged. VBM revealed alterations of gray matter structures involved in sensorimotor processing in the individuals with focal dystonia. In CD subjects there was increased gray matter in the thalamus, caudate head bilaterally, superior temporal lobe, and left cerebellum, while gray matter was decreased in the putamen bilaterally. BEB subjects had increased gray matter in the caudate head and cerebellum bilaterally as well as decrease in the putamen and thalamus bilaterally. These findings strongly underline the recent notion that idiopathic focal dystonias might have a detectable structural correlate. They also demonstrate structural similarities of the investigated focal dystonias, possibly reflecting a shared common pathophysiological origin. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Mark Obermann MD</name><affiliations><json:string>Department of Neurology, University of Duisburg—Essen, Essen, Germany</json:string><json:string>Department of Neurology, University of Duisburg—Essen, Hufelandstr. 55, 45122 Essen, Germany</json:string></affiliations></json:item><json:item><name>Ozguer Yaldizli MD</name><affiliations><json:string>Department of Neurology, University of Duisburg—Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>Armin De Greiff</name><affiliations><json:string>Department of Neuroradiology, University of Duisburg—Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>Martin Lenard Lachenmayer MD</name><affiliations><json:string>Department of Neurology, University of Duisburg—Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>Anna Rebecca Buhl</name><affiliations><json:string>Department of Neurology, University of Duisburg—Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>Felicitus Tumczak</name><affiliations><json:string>Department of Neurology, University of Duisburg—Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>Elke Ruth Gizewski MD</name><affiliations><json:string>Department of Neuroradiology, University of Duisburg—Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>Hans‐Christoph Diener MD</name><affiliations><json:string>Department of Neurology, University of Duisburg—Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>Matthias Maschke MD</name><affiliations><json:string>Department of Neurology, University of Duisburg—Essen, Essen, Germany</json:string><json:string>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>focal dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>voxel‐based morphometry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>blepharospasm</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cervical dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>torticollis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sensorimotor integration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>basal ganglia.</value></json:item></subject><articleId><json:string>MDS21495</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Idiopathic cervical dystonia (CD) and benign essential blepharospasm (BEB) are the most common forms of focal dystonia. Previous autopsy and imaging studies suggested that these disorders are not accompanied by structural brain abnormalities. However, recent brain voxel‐based morphometry (VBM) studies of these conditions suggest that there actually may be changes in gray matter. The objective of this stdy was to detect possible gray matter abnormalities in patients with CD and BEB using VBM and to compare the results between the two conditions and with age‐ and gender‐matched controls. High‐resolution MRI was employed to evaluate healthy controls and individuals with BEB and CD. Eleven BEB, 9 CD, and 14 healthy control subjects were imaged. VBM revealed alterations of gray matter structures involved in sensorimotor processing in the individuals with focal dystonia. In CD subjects there was increased gray matter in the thalamus, caudate head bilaterally, superior temporal lobe, and left cerebellum, while gray matter was decreased in the putamen bilaterally. BEB subjects had increased gray matter in the caudate head and cerebellum bilaterally as well as decrease in the putamen and thalamus bilaterally. These findings strongly underline the recent notion that idiopathic focal dystonias might have a detectable structural correlate. They also demonstrate structural similarities of the investigated focal dystonias, possibly reflecting a shared common pathophysiological origin. © 2007 Movement Disorder Society</abstract><qualityIndicators><score>6.472</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1528</abstractCharCount><pdfWordCount>3820</pdfWordCount><pdfCharCount>24044</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>221</abstractWordCount></qualityIndicators><title>Morphometric changes of sensorimotor structures in focal dystonia</title><refBibs><json:item><author><json:item><name>A Beradelli</name></json:item><json:item><name>JC Rothwell</name></json:item><json:item><name>M Hallet</name></json:item><json:item><name>PD Thompson</name></json:item><json:item><name>M Manfredi</name></json:item><json:item><name>CD 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BEB subjects had increased gray matter in the caudate head and cerebellum bilaterally as well as decrease in the putamen and thalamus bilaterally. These findings strongly underline the recent notion that idiopathic focal dystonias might have a detectable structural correlate. 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Previous autopsy and imaging studies suggested that these disorders are not accompanied by structural brain abnormalities. However, recent brain voxel‐based morphometry (VBM) studies of these conditions suggest that there actually may be changes in gray matter. The objective of this stdy was to detect possible gray matter abnormalities in patients with CD and BEB using VBM and to compare the results between the two conditions and with age‐ and gender‐matched controls. High‐resolution MRI was employed to evaluate healthy controls and individuals with BEB and CD. Eleven BEB, 9 CD, and 14 healthy control subjects were imaged. VBM revealed alterations of gray matter structures involved in sensorimotor processing in the individuals with focal dystonia. In CD subjects there was increased gray matter in the thalamus, caudate head bilaterally, superior temporal lobe, and left cerebellum, while gray matter was decreased in the putamen bilaterally. BEB subjects had increased gray matter in the caudate head and cerebellum bilaterally as well as decrease in the putamen and thalamus bilaterally. These findings strongly underline the recent notion that idiopathic focal dystonias might have a detectable structural correlate. They also demonstrate structural similarities of the investigated focal dystonias, possibly reflecting a shared common pathophysiological origin. © 2007 Movement Disorder Society</abstract><subject lang="en"><genre>keywords</genre><topic>focal dystonia</topic><topic>voxel‐based morphometry</topic><topic>blepharospasm</topic><topic>cervical dystonia</topic><topic>torticollis</topic><topic>sensorimotor integration</topic><topic>basal ganglia.</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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