Increased basal‐ganglia activation performing a non‐dystonia‐related task in focal dystonia
Identifieur interne : 000B03 ( Istex/Corpus ); précédent : 000B02; suivant : 000B04Increased basal‐ganglia activation performing a non‐dystonia‐related task in focal dystonia
Auteurs : M. Obermann ; O. Yaldizli ; A. De Greiff ; J. Konczak ; M. L. Lachenmayer ; F. Tumczak ; A. R. Buhl ; N. Putzki ; J. Vollmer-Haase ; E. R. Gizewski ; H. Diener ; M. MaschkeSource :
- European Journal of Neurology [ 1351-5101 ] ; 2008-08.
English descriptors
Abstract
Background and purpose: We tried to determine whether altered sensorimotor cortex and basal‐ganglia activation in blepharospasm (BSP) and cervical dystonia (CD) are restricted to areas directly responsible for the innervation of dystonic muscles, or whether impairment in focal dystonia reaches beyond these direct associations supporting a more global disturbance of sensory and motor control in focal dystonia.
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DOI: 10.1111/j.1468-1331.2008.02196.x
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De Greiff</name><affiliation><mods:affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Konczak, J" sort="Konczak, J" uniqKey="Konczak J" first="J." last="Konczak">J. Konczak</name><affiliation><mods:affiliation>Human Sensorimotor Control Laboratory, University of Minnesota, Minneapolis, MN, USA</mods:affiliation></affiliation></author><author><name sortKey="Lachenmayer, M L" sort="Lachenmayer, M L" uniqKey="Lachenmayer M" first="M. L." last="Lachenmayer">M. L. Lachenmayer</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Tumczak, F" sort="Tumczak, F" uniqKey="Tumczak F" first="F." last="Tumczak">F. Tumczak</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Buhl, A R" sort="Buhl, A R" uniqKey="Buhl A" first="A. R." last="Buhl">A. R. Buhl</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Putzki, N" sort="Putzki, N" uniqKey="Putzki N" first="N." last="Putzki">N. Putzki</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Vollmer Aase, J" sort="Vollmer Aase, J" uniqKey="Vollmer Aase J" first="J." last="Vollmer-Haase">J. 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Obermann</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Yaldizli, O" sort="Yaldizli, O" uniqKey="Yaldizli O" first="O." last="Yaldizli">O. Yaldizli</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="De Greiff, A" sort="De Greiff, A" uniqKey="De Greiff A" first="A." last="De Greiff">A. De Greiff</name><affiliation><mods:affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Konczak, J" sort="Konczak, J" uniqKey="Konczak J" first="J." last="Konczak">J. Konczak</name><affiliation><mods:affiliation>Human Sensorimotor Control Laboratory, University of Minnesota, Minneapolis, MN, USA</mods:affiliation></affiliation></author><author><name sortKey="Lachenmayer, M L" sort="Lachenmayer, M L" uniqKey="Lachenmayer M" first="M. L." last="Lachenmayer">M. L. Lachenmayer</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Tumczak, F" sort="Tumczak, F" uniqKey="Tumczak F" first="F." last="Tumczak">F. Tumczak</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Buhl, A R" sort="Buhl, A R" uniqKey="Buhl A" first="A. R." last="Buhl">A. R. Buhl</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Putzki, N" sort="Putzki, N" uniqKey="Putzki N" first="N." last="Putzki">N. Putzki</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Vollmer Aase, J" sort="Vollmer Aase, J" uniqKey="Vollmer Aase J" first="J." last="Vollmer-Haase">J. Vollmer-Haase</name><affiliation><mods:affiliation>Department of Neurology, Knappschafts‐Krankenhaus Recklinghausen, Recklinghausen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Gizewski, E R" sort="Gizewski, E R" uniqKey="Gizewski E" first="E. R." last="Gizewski">E. R. Gizewski</name><affiliation><mods:affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Diener, H" sort="Diener, H" uniqKey="Diener H" first="H." last="Diener">H. Diener</name><affiliation><mods:affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Maschke, M" sort="Maschke, M" uniqKey="Maschke M" first="M." last="Maschke">M. Maschke</name><affiliation><mods:affiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Trier, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neurology</title><idno type="ISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2008-08">2008-08</date><biblScope unit="volume">15</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="831">831</biblScope><biblScope unit="page" to="838">838</biblScope></imprint><idno type="ISSN">1351-5101</idno></series><idno type="istex">D18A6ED3F85D9000A26590B55D34006BB2E969AE</idno><idno type="DOI">10.1111/j.1468-1331.2008.02196.x</idno><idno type="ArticleID">ENE2196</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1351-5101</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>blepharospasm</term><term>cervical dystonia</term><term>fMRI</term><term>focal dystonia</term><term>sensorimotor integration</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background and purpose: We tried to determine whether altered sensorimotor cortex and basal‐ganglia activation in blepharospasm (BSP) and cervical dystonia (CD) are restricted to areas directly responsible for the innervation of dystonic muscles, or whether impairment in focal dystonia reaches beyond these direct associations supporting a more global disturbance of sensory and motor control in focal dystonia.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>M. Obermann</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>O. Yaldizli</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>A. De Greiff</name><affiliations><json:string>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>J. Konczak</name><affiliations><json:string>Human Sensorimotor Control Laboratory, University of Minnesota, Minneapolis, MN, USA</json:string></affiliations></json:item><json:item><name>M. L. Lachenmayer</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>F. Tumczak</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>A. R. Buhl</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>N. Putzki</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>J. Vollmer‐Haase</name><affiliations><json:string>Department of Neurology, Knappschafts‐Krankenhaus Recklinghausen, Recklinghausen, Germany</json:string></affiliations></json:item><json:item><name>E. R. Gizewski</name><affiliations><json:string>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>H.‐C. Diener</name><affiliations><json:string>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</json:string></affiliations></json:item><json:item><name>M. Maschke</name><affiliations><json:string>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Trier, Germany</json:string></affiliations></json:item></author><subject><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>fMRI</value></json:item><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>sensorimotor integration</value></json:item></subject><articleId><json:string>ENE2196</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><qualityIndicators><score>4.428</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>413</abstractCharCount><pdfWordCount>3744</pdfWordCount><pdfCharCount>25825</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>57</abstractWordCount></qualityIndicators><title>Increased basal‐ganglia activation performing a non‐dystonia‐related task in focal dystonia</title><refBibs><json:item><author><json:item><name>AO Ceballos‐Baumann</name></json:item><json:item><name>RE Passingham</name></json:item><json:item><name>T Warner</name></json:item><json:item><name>ED Playford</name></json:item><json:item><name>CD Marsden</name></json:item><json:item><name>DJ Brooks</name></json:item></author><host><volume>37</volume><pages><last>757</last><first>746</first></pages><author></author><title>Annals of Neurology</title></host><title>Overactive prefrontal and underactive motor cortical areas in idiopathic dystonia</title></json:item><json:item><author><json:item><name>AO Ceballos‐Baumann</name></json:item><json:item><name>G Sheean</name></json:item><json:item><name>RE Passingham</name></json:item><json:item><name>CD Marsden</name></json:item><json:item><name>DJ Brooks</name></json:item></author><host><volume>120</volume><pages><last>582</last><first>571</first></pages><author></author><title>Brain</title></host><title>Botulinum toxin does not reverse the cortical dysfunction associated with writer’s cramp. 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Journal compilation © 2008 EFNS</p></availability><date>2008</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Increased basal‐ganglia activation performing a non‐dystonia‐related task in focal dystonia</title><author xml:id="author-1"><persName><forename type="first">M.</forename><surname>Obermann</surname></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-2"><persName><forename type="first">O.</forename><surname>Yaldizli</surname></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-3"><persName><forename type="first">A.</forename><surname>De Greiff</surname></persName><affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-4"><persName><forename type="first">J.</forename><surname>Konczak</surname></persName><affiliation>Human Sensorimotor Control Laboratory, University of Minnesota, Minneapolis, MN, USA</affiliation></author><author xml:id="author-5"><persName><forename type="first">M. L.</forename><surname>Lachenmayer</surname></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-6"><persName><forename type="first">F.</forename><surname>Tumczak</surname></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-7"><persName><forename type="first">A. R.</forename><surname>Buhl</surname></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-8"><persName><forename type="first">N.</forename><surname>Putzki</surname></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-9"><persName><forename type="first">J.</forename><surname>Vollmer‐Haase</surname></persName><affiliation>Department of Neurology, Knappschafts‐Krankenhaus Recklinghausen, Recklinghausen, Germany</affiliation></author><author xml:id="author-10"><persName><forename type="first">E. R.</forename><surname>Gizewski</surname></persName><affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-11"><persName><forename type="first">H.‐C.</forename><surname>Diener</surname></persName><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation></author><author xml:id="author-12"><persName><forename type="first">M.</forename><surname>Maschke</surname></persName><affiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Trier, Germany</affiliation></author></analytic><monogr><title level="j">European Journal of Neurology</title><idno type="pISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><idno type="DOI">10.1111/(ISSN)1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2008-08"></date><biblScope unit="volume">15</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="831">831</biblScope><biblScope unit="page" to="838">838</biblScope></imprint></monogr><idno type="istex">D18A6ED3F85D9000A26590B55D34006BB2E969AE</idno><idno type="DOI">10.1111/j.1468-1331.2008.02196.x</idno><idno type="ArticleID">ENE2196</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Background and purpose: We tried to determine whether altered sensorimotor cortex and basal‐ganglia activation in blepharospasm (BSP) and cervical dystonia (CD) are restricted to areas directly responsible for the innervation of dystonic muscles, or whether impairment in focal dystonia reaches beyond these direct associations supporting a more global disturbance of sensory and motor control in focal dystonia.</p></abstract><abstract><p>Methods: Twenty patients with focal dystonia (11 BSP, 9 CD) and 14 healthy controls were investigated with functional magnetic resonance imaging (fMRI) performing a simple grip force forearm contraction task.</p></abstract><abstract><p>Results: BSP and CD patients and healthy controls showed similar activation in the pre‐motor, primary motor and primary sensory cortex, whilst basal‐ganglia activation was increased in BSP and CD with related activation patterns compared with controls. BSP patients had increased activation in the thalamus, caudate nucleus, putamen and lateral globus pallidus, whilst CD patients showed increased activation in the caudate nucleus, putamen and thalamus. No differences in applied grip force were detected between groups.</p></abstract><abstract><p>Conclusions: In both, BSP and CD, increased basal‐ganglia activation could be demonstrated in a task not primarily involving the dystonic musculature affected by these disorders. Comparable activation changes may also indicate a common pathway in the pathophysiology in BSP and CD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>blepharospasm</term></item><item><term>cervical dystonia</term></item><item><term>fMRI</term></item><item><term>focal dystonia</term></item><item><term>sensorimotor integration</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/D18A6ED3F85D9000A26590B55D34006BB2E969AE/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1468-1331</doi><issn type="print">1351-5101</issn><issn type="electronic">1468-1331</issn><idGroup><id type="product" value="ENE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROLOGY">European Journal of Neurology</title></titleGroup></publicationMeta><publicationMeta level="part" position="08008"><doi origin="wiley">10.1111/ene.2008.15.issue-8</doi><numberingGroup><numbering type="journalVolume" number="15">15</numbering><numbering type="journalIssue" number="8">8</numbering></numberingGroup><coverDate startDate="2008-08">August 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="15" status="forIssue"><doi origin="wiley">10.1111/j.1468-1331.2008.02196.x</doi><idGroup><id type="unit" value="ENE2196"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><copyright>© 2008 The Author(s). Journal compilation © 2008 EFNS</copyright><eventGroup><event type="firstOnline" date="2008-06-28"></event><event type="publishedOnlineFinalForm" date="2008-07-09"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="831">831</numbering><numbering type="pageLast" number="838">838</numbering></numberingGroup><correspondenceTo>Mark Obermann, MD, Department of Neurology, University of Duisburg‐Essen, Hufelandstr. 55, 45122 Essen, Germany (tel.: +49 201 723 84385; fax: +49 201 723 5953; e‐mail: <email normalForm="mark.obermann@uni-due.de">mark.obermann@uni‐due.de</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE2196.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 9 November 2007 Accepted 30 April 2008</unparsedEditorialHistory><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="4"></count></countGroup><titleGroup><title type="main">Increased basal‐ganglia activation performing a non‐dystonia‐related task in focal dystonia</title><title type="shortAuthors">M. Obermann <i>et al.</i></title><title type="short">Basal‐ganglia activation in focal dystonia</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>M.</givenNames><familyName>Obermann</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>O.</givenNames><familyName>Yaldizli</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>A.</givenNames><familyName>De Greiff</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>J.</givenNames><familyName>Konczak</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>M. L.</givenNames><familyName>Lachenmayer</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>F.</givenNames><familyName>Tumczak</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>A. R.</givenNames><familyName>Buhl</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>N.</givenNames><familyName>Putzki</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a4"><personName><givenNames>J.</givenNames><familyName>Vollmer‐Haase</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a2"><personName><givenNames>E. R.</givenNames><familyName>Gizewski</familyName></personName></creator><creator creatorRole="author" xml:id="cr11" affiliationRef="#a1"><personName><givenNames>H.‐C.</givenNames><familyName>Diener</familyName></personName></creator><creator creatorRole="author" xml:id="cr12" affiliationRef="#a5"><personName><givenNames>M.</givenNames><familyName>Maschke</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="DE"><unparsedAffiliation>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="US"><unparsedAffiliation>Human Sensorimotor Control Laboratory, University of Minnesota, Minneapolis, MN, USA</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="DE"><unparsedAffiliation>Department of Neurology, Knappschafts‐Krankenhaus Recklinghausen, Recklinghausen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="DE"><unparsedAffiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Trier, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">blepharospasm</keyword><keyword xml:id="k2">cervical dystonia</keyword><keyword xml:id="k3">fMRI</keyword><keyword xml:id="k4">focal dystonia</keyword><keyword xml:id="k5">sensorimotor integration</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Background and purpose: </b> We tried to determine whether altered sensorimotor cortex and basal‐ganglia activation in blepharospasm (BSP) and cervical dystonia (CD) are restricted to areas directly responsible for the innervation of dystonic muscles, or whether impairment in focal dystonia reaches beyond these direct associations supporting a more global disturbance of sensory and motor control in focal dystonia.</p><p><b>Methods: </b> Twenty patients with focal dystonia (11 BSP, 9 CD) and 14 healthy controls were investigated with functional magnetic resonance imaging (fMRI) performing a simple grip force forearm contraction task.</p><p><b>Results: </b> BSP and CD patients and healthy controls showed similar activation in the pre‐motor, primary motor and primary sensory cortex, whilst basal‐ganglia activation was increased in BSP and CD with related activation patterns compared with controls. BSP patients had increased activation in the thalamus, caudate nucleus, putamen and lateral globus pallidus, whilst CD patients showed increased activation in the caudate nucleus, putamen and thalamus. No differences in applied grip force were detected between groups.</p><p><b>Conclusions: </b> In both, BSP and CD, increased basal‐ganglia activation could be demonstrated in a task not primarily involving the dystonic musculature affected by these disorders. Comparable activation changes may also indicate a common pathway in the pathophysiology in BSP and CD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Increased basal‐ganglia activation performing a non‐dystonia‐related task in focal dystonia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Basal‐ganglia activation in focal dystonia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Increased basal‐ganglia activation performing a non‐dystonia‐related task in focal dystonia</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Obermann</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O.</namePart><namePart type="family">Yaldizli</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">De Greiff</namePart><affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Konczak</namePart><affiliation>Human Sensorimotor Control Laboratory, University of Minnesota, Minneapolis, MN, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. L.</namePart><namePart type="family">Lachenmayer</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Tumczak</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. R.</namePart><namePart type="family">Buhl</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Putzki</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Vollmer‐Haase</namePart><affiliation>Department of Neurology, Knappschafts‐Krankenhaus Recklinghausen, Recklinghausen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E. R.</namePart><namePart type="family">Gizewski</namePart><affiliation>Department of Neuroradiology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.‐C.</namePart><namePart type="family">Diener</namePart><affiliation>Department of Neurology, University of Duisburg‐Essen, Essen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Maschke</namePart><affiliation>Department of Neurology and Neurophysiology, Bruederkrankenhaus Trier, Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2008-08</dateIssued><edition>Received 9 November 2007 Accepted 30 April 2008</edition><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">4</extent></physicalDescription><abstract>Background and purpose: We tried to determine whether altered sensorimotor cortex and basal‐ganglia activation in blepharospasm (BSP) and cervical dystonia (CD) are restricted to areas directly responsible for the innervation of dystonic muscles, or whether impairment in focal dystonia reaches beyond these direct associations supporting a more global disturbance of sensory and motor control in focal dystonia.</abstract><abstract>Methods: Twenty patients with focal dystonia (11 BSP, 9 CD) and 14 healthy controls were investigated with functional magnetic resonance imaging (fMRI) performing a simple grip force forearm contraction task.</abstract><abstract>Results: BSP and CD patients and healthy controls showed similar activation in the pre‐motor, primary motor and primary sensory cortex, whilst basal‐ganglia activation was increased in BSP and CD with related activation patterns compared with controls. BSP patients had increased activation in the thalamus, caudate nucleus, putamen and lateral globus pallidus, whilst CD patients showed increased activation in the caudate nucleus, putamen and thalamus. No differences in applied grip force were detected between groups.</abstract><abstract>Conclusions: In both, BSP and CD, increased basal‐ganglia activation could be demonstrated in a task not primarily involving the dystonic musculature affected by these disorders. Comparable activation changes may also indicate a common pathway in the pathophysiology in BSP and CD.</abstract><subject lang="en"><genre>keywords</genre><topic>blepharospasm</topic><topic>cervical dystonia</topic><topic>fMRI</topic><topic>focal dystonia</topic><topic>sensorimotor integration</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>831</start><end>838</end><total>8</total></extent></part></relatedItem><identifier type="istex">D18A6ED3F85D9000A26590B55D34006BB2E969AE</identifier><identifier type="DOI">10.1111/j.1468-1331.2008.02196.x</identifier><identifier type="ArticleID">ENE2196</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2008 The Author(s). 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