In vivo evidence for GABAA receptor changes in the sensorimotor system in primary dystonia
Identifieur interne : 002A19 ( Istex/Corpus ); précédent : 002A18; suivant : 002A20In vivo evidence for GABAA receptor changes in the sensorimotor system in primary dystonia
Auteurs : Valentina Garibotto ; Luigi M. Romito ; Antonio E. Elia ; Paola Soliveri ; Andrea Panzacchi ; Assunta Carpinelli ; Michele Tinazzi ; Alberto Albanese ; Daniela PeraniSource :
- Movement Disorders [ 0885-3185 ] ; 2011-04.
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Abstract
Background:: Preclinical and clinical evidence suggests that impaired gamma‐aminobutyric (GABA) control, leading to disinhibition within the sensorimotor system, might play a role in dystonia. Aim of this study is the in vivo assessment of the GABAergic system in dystonia using positron emission tomography (PET) and 11C‐flumazenil, a selective GABAA receptor ligand. Methods:: Fourteen subjects with primary dystonia (9 carriers of the DYT1 mutation and 5 sporadic cases) were compared to 11 controls, using a simplified reference tissue model to measure binding potential. Results:: Voxel‐based analyses showed a reduction in GABAA receptor expression/affinity both in DYT1 carriers and sporadic patients in primary motor and premotor cortex, primary and secondary somatosensory cortex, and in the motor component of the cingulate gyrus. Conclusions:: Dysfunction of GABAA receptors in sensorimotor systems in primary (genetic and sporadic) dystonia supports the view that lack of GABAergic control may be associated with the generation of dystonic movements. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23553
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ISTEX:967970D0720C6C7DBA0845355D7C453F3DFA429DLe document en format XML
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Romito</name><affiliation><mods:affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Elia, Antonio E" sort="Elia, Antonio E" uniqKey="Elia A" first="Antonio E." last="Elia">Antonio E. Elia</name><affiliation><mods:affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Soliveri, Paola" sort="Soliveri, Paola" uniqKey="Soliveri P" first="Paola" last="Soliveri">Paola Soliveri</name><affiliation><mods:affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Panzacchi, Andrea" sort="Panzacchi, Andrea" uniqKey="Panzacchi A" first="Andrea" last="Panzacchi">Andrea Panzacchi</name><affiliation><mods:affiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Carpinelli, Assunta" sort="Carpinelli, Assunta" uniqKey="Carpinelli A" first="Assunta" last="Carpinelli">Assunta Carpinelli</name><affiliation><mods:affiliation>IBFM‐CNR, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Tinazzi, Michele" sort="Tinazzi, Michele" uniqKey="Tinazzi M" first="Michele" last="Tinazzi">Michele Tinazzi</name><affiliation><mods:affiliation>Department of Neurological and Visual Sciences, University of Verona, Verona, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Borgo Trento Hospital, Verona, Italy</mods:affiliation></affiliation></author><author><name sortKey="Albanese, Alberto" sort="Albanese, Alberto" uniqKey="Albanese A" first="Alberto" last="Albanese">Alberto Albanese</name><affiliation><mods:affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</mods:affiliation></affiliation></author><author><name sortKey="Perani, Daniela" sort="Perani, Daniela" uniqKey="Perani D" first="Daniela" last="Perani">Daniela Perani</name><affiliation><mods:affiliation>Division of Neuroscience, Vita‐Salute San Raffaele University, Milan, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</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="2011-04">2011-04</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="852">852</biblScope><biblScope unit="page" to="857">857</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">967970D0720C6C7DBA0845355D7C453F3DFA429D</idno><idno type="DOI">10.1002/mds.23553</idno><idno type="ArticleID">MDS23553</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>GABA</term><term>GABAA receptors</term><term>PET</term><term>dystonia</term><term>sensorimotor cortex</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background:: Preclinical and clinical evidence suggests that impaired gamma‐aminobutyric (GABA) control, leading to disinhibition within the sensorimotor system, might play a role in dystonia. Aim of this study is the in vivo assessment of the GABAergic system in dystonia using positron emission tomography (PET) and 11C‐flumazenil, a selective GABAA receptor ligand. Methods:: Fourteen subjects with primary dystonia (9 carriers of the DYT1 mutation and 5 sporadic cases) were compared to 11 controls, using a simplified reference tissue model to measure binding potential. Results:: Voxel‐based analyses showed a reduction in GABAA receptor expression/affinity both in DYT1 carriers and sporadic patients in primary motor and premotor cortex, primary and secondary somatosensory cortex, and in the motor component of the cingulate gyrus. Conclusions:: Dysfunction of GABAA receptors in sensorimotor systems in primary (genetic and sporadic) dystonia supports the view that lack of GABAergic control may be associated with the generation of dystonic movements. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Valentina Garibotto MD</name><affiliations><json:string>Division of Neuroscience, Vita‐Salute San Raffaele University, Milan, Italy</json:string><json:string>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</json:string><json:string>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</json:string></affiliations></json:item><json:item><name>Luigi M. Romito MD</name><affiliations><json:string>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</json:string><json:string>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</json:string></affiliations></json:item><json:item><name>Antonio E. Elia MD</name><affiliations><json:string>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</json:string><json:string>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</json:string></affiliations></json:item><json:item><name>Paola Soliveri MD</name><affiliations><json:string>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</json:string></affiliations></json:item><json:item><name>Andrea Panzacchi MD</name><affiliations><json:string>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</json:string><json:string>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</json:string></affiliations></json:item><json:item><name>Assunta Carpinelli MSc</name><affiliations><json:string>IBFM‐CNR, Milan, Italy</json:string></affiliations></json:item><json:item><name>Michele Tinazzi MD</name><affiliations><json:string>Department of Neurological and Visual Sciences, University of Verona, Verona, Italy</json:string><json:string>Department of Neurology, Borgo Trento Hospital, Verona, Italy</json:string></affiliations></json:item><json:item><name>Alberto Albanese MD</name><affiliations><json:string>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</json:string><json:string>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</json:string></affiliations></json:item><json:item><name>Daniela Perani MD</name><affiliations><json:string>Division of Neuroscience, Vita‐Salute San Raffaele University, Milan, Italy</json:string><json:string>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</json:string><json:string>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>GABA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GABAA receptors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dystonia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sensorimotor cortex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Background:: Preclinical and clinical evidence suggests that impaired gamma‐aminobutyric (GABA) control, leading to disinhibition within the sensorimotor system, might play a role in dystonia. Aim of this study is the in vivo assessment of the GABAergic system in dystonia using positron emission tomography (PET) and 11C‐flumazenil, a selective GABAA receptor ligand. Methods:: Fourteen subjects with primary dystonia (9 carriers of the DYT1 mutation and 5 sporadic cases) were compared to 11 controls, using a simplified reference tissue model to measure binding potential. Results:: Voxel‐based analyses showed a reduction in GABAA receptor expression/affinity both in DYT1 carriers and sporadic patients in primary motor and premotor cortex, primary and secondary somatosensory cortex, and in the motor component of the cingulate gyrus. Conclusions:: Dysfunction of GABAA receptors in sensorimotor systems in primary (genetic and sporadic) dystonia supports the view that lack of GABAergic control may be associated with the generation of dystonic movements. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>4.849</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1095</abstractCharCount><pdfWordCount>2989</pdfWordCount><pdfCharCount>19950</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>155</abstractWordCount></qualityIndicators><title>In vivo evidence for GABAA receptor changes in the sensorimotor system in primary dystonia</title><genre><json:string>Serial article</json:string></genre><host><volume>26</volume><pages><total>6</total><last>857</last><first>852</first></pages><issn><json:string>0885-3185</json:string></issn><issue>5</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23553</json:string></doi><id>967970D0720C6C7DBA0845355D7C453F3DFA429D</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/967970D0720C6C7DBA0845355D7C453F3DFA429D/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/967970D0720C6C7DBA0845355D7C453F3DFA429D/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/967970D0720C6C7DBA0845355D7C453F3DFA429D/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">In vivo evidence for GABAA receptor changes in the sensorimotor system in primary dystonia</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Relevant conflict of interest: Nothing to report. This study was financially supported by Diagnostic Molecular Imaging (DIMI), Sixth European Program, project No: LSHB‐CT‐2005‐512146 and the ItalianMinistry of Health, COFIN project (N. 2004062394_002 and N. 2006068233_003).</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">In vivo evidence for GABAA receptor changes in the sensorimotor system in primary dystonia</title><author><persName><forename type="first">Valentina</forename><surname>Garibotto</surname><roleName type="degree">MD</roleName></persName><affiliation>Division of Neuroscience, Vita‐Salute San Raffaele University, Milan, Italy</affiliation><affiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</affiliation><affiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</affiliation></author><author><persName><forename type="first">Luigi M.</forename><surname>Romito</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</affiliation><affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</affiliation></author><author><persName><forename type="first">Antonio E.</forename><surname>Elia</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</affiliation><affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</affiliation></author><author><persName><forename type="first">Paola</forename><surname>Soliveri</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</affiliation></author><author><persName><forename type="first">Andrea</forename><surname>Panzacchi</surname><roleName type="degree">MD</roleName></persName><affiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</affiliation><affiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</affiliation></author><author><persName><forename type="first">Assunta</forename><surname>Carpinelli</surname><roleName type="degree">MSc</roleName></persName><affiliation>IBFM‐CNR, Milan, Italy</affiliation></author><author><persName><forename type="first">Michele</forename><surname>Tinazzi</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurological and Visual Sciences, University of Verona, Verona, Italy</affiliation><affiliation>Department of Neurology, Borgo Trento Hospital, Verona, Italy</affiliation></author><author><persName><forename type="first">Alberto</forename><surname>Albanese</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</affiliation><affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</affiliation></author><author><persName><forename type="first">Daniela</forename><surname>Perani</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Nuclear Medicine Unit and Division of Neuroscience, San Raffaele Scientific Institute, 60 – 20132 via Olgettina, Milano, Italy</p></note><affiliation>Division of Neuroscience, Vita‐Salute San Raffaele University, Milan, Italy</affiliation><affiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</affiliation><affiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-04"></date><biblScope unit="vol">26</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="852">852</biblScope><biblScope unit="page" to="857">857</biblScope></imprint></monogr><idno type="istex">967970D0720C6C7DBA0845355D7C453F3DFA429D</idno><idno type="DOI">10.1002/mds.23553</idno><idno type="ArticleID">MDS23553</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background:: Preclinical and clinical evidence suggests that impaired gamma‐aminobutyric (GABA) control, leading to disinhibition within the sensorimotor system, might play a role in dystonia. Aim of this study is the in vivo assessment of the GABAergic system in dystonia using positron emission tomography (PET) and 11C‐flumazenil, a selective GABAA receptor ligand. Methods:: Fourteen subjects with primary dystonia (9 carriers of the DYT1 mutation and 5 sporadic cases) were compared to 11 controls, using a simplified reference tissue model to measure binding potential. Results:: Voxel‐based analyses showed a reduction in GABAA receptor expression/affinity both in DYT1 carriers and sporadic patients in primary motor and premotor cortex, primary and secondary somatosensory cortex, and in the motor component of the cingulate gyrus. Conclusions:: Dysfunction of GABAA receptors in sensorimotor systems in primary (genetic and sporadic) dystonia supports the view that lack of GABAergic control may be associated with the generation of dystonic movements. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>GABA</term></item><item><term>GABAA receptors</term></item><item><term>dystonia</term></item><item><term>sensorimotor cortex</term></item><item><term>PET</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-05-19">Received</change><change when="2010-11-01">Registration</change><change when="2011-04">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/967970D0720C6C7DBA0845355D7C453F3DFA429D/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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date="2010-11-01"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.5.2 mode:FullText" date="2011-07-19"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-03-02"></event><event type="publishedOnlineFinalForm" date="2011-04-21"></event><event type="firstOnline" date="2011-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">852</numbering><numbering type="pageLast">857</numbering></numberingGroup><correspondenceTo>Nuclear Medicine Unit and Division of Neuroscience, San Raffaele Scientific Institute, 60 – 20132 via Olgettina, Milano, Italy</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23553.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="38"></count><count type="wordTotal" number="3733"></count></countGroup><titleGroup><title type="main" xml:lang="en">In vivo evidence for GABA<sub>A</sub> receptor changes in the sensorimotor system in primary dystonia<link href="#fn1"></link></title><title type="short" xml:lang="en">GABA<sub>A</sub> Receptor Changes in Primary Dystonia</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2 #af3"><personName><givenNames>Valentina</givenNames><familyName>Garibotto</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af4 #af5"><personName><givenNames>Luigi M.</givenNames><familyName>Romito</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af4 #af5"><personName><givenNames>Antonio E.</givenNames><familyName>Elia</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Paola</givenNames><familyName>Soliveri</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2 #af3"><personName><givenNames>Andrea</givenNames><familyName>Panzacchi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Assunta</givenNames><familyName>Carpinelli</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af7 #af8"><personName><givenNames>Michele</givenNames><familyName>Tinazzi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af4 #af5"><personName><givenNames>Alberto</givenNames><familyName>Albanese</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1 #af2 #af3" corresponding="yes"><personName><givenNames>Daniela</givenNames><familyName>Perani</familyName><degrees>MD</degrees></personName><contactDetails><email>daniela.perani@hsr.it</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IT" type="organization"><unparsedAffiliation>Division of Neuroscience, Vita‐Salute San Raffaele University, Milan, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IT" type="organization"><unparsedAffiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="IT" type="organization"><unparsedAffiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="IT" type="organization"><unparsedAffiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="IT" type="organization"><unparsedAffiliation>IBFM‐CNR, Milan, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurological and Visual Sciences, University of Verona, Verona, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurology, Borgo Trento Hospital, Verona, Italy</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">GABA</keyword><keyword xml:id="kwd2">GABA<sub>A</sub> receptors</keyword><keyword xml:id="kwd3">dystonia</keyword><keyword xml:id="kwd4">sensorimotor cortex</keyword><keyword xml:id="kwd5">PET</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Background:</title><p>Preclinical and clinical evidence suggests that impaired gamma‐aminobutyric (GABA) control, leading to disinhibition within the sensorimotor system, might play a role in dystonia. Aim of this study is the in vivo assessment of the GABAergic system in dystonia using positron emission tomography (PET) and <sup>11</sup>C‐flumazenil, a selective GABA<sub>A</sub> receptor ligand.</p></section><section xml:id="abs1-2"><title type="main">Methods:</title><p>Fourteen subjects with primary dystonia (9 carriers of the DYT1 mutation and 5 sporadic cases) were compared to 11 controls, using a simplified reference tissue model to measure binding potential.</p></section><section xml:id="abs1-3"><title type="main">Results:</title><p>Voxel‐based analyses showed a reduction in GABA<sub>A</sub> receptor expression/affinity both in DYT1 carriers and sporadic patients in primary motor and premotor cortex, primary and secondary somatosensory cortex, and in the motor component of the cingulate gyrus.</p></section><section xml:id="abs1-4"><title type="main">Conclusions:</title><p>Dysfunction of GABA<sub>A</sub> receptors in sensorimotor systems in primary (genetic and sporadic) dystonia supports the view that lack of GABAergic control may be associated with the generation of dystonic movements. © 2011 Movement Disorder Society</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflict of interest</b>: Nothing to report. This study was financially supported by Diagnostic Molecular Imaging (DIMI), Sixth European Program, project No: LSHB‐CT‐2005‐512146 and the ItalianMinistry of Health, COFIN project (N. 2004062394_002 and N. 2006068233_003).</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>In vivo evidence for GABAA receptor changes in the sensorimotor system in primary dystonia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>GABAA Receptor Changes in Primary Dystonia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>In vivo evidence for GABA</title></titleInfo><name type="personal"><namePart type="given">Valentina</namePart><namePart type="family">Garibotto</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Division of Neuroscience, Vita‐Salute San Raffaele University, Milan, Italy</affiliation><affiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</affiliation><affiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Luigi M.</namePart><namePart type="family">Romito</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</affiliation><affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Antonio E.</namePart><namePart type="family">Elia</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</affiliation><affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Soliveri</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrea</namePart><namePart type="family">Panzacchi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</affiliation><affiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Assunta</namePart><namePart type="family">Carpinelli</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>IBFM‐CNR, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michele</namePart><namePart type="family">Tinazzi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological and Visual Sciences, University of Verona, Verona, Italy</affiliation><affiliation>Department of Neurology, Borgo Trento Hospital, Verona, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alberto</namePart><namePart type="family">Albanese</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology I, I.R.C.C.S. Istituto Neurologico “Carlo Besta”, Milan, Italy</affiliation><affiliation>Neurology Institute, Università Cattolica del Sacro Cuore, Milan, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniela</namePart><namePart type="family">Perani</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Division of Neuroscience, Vita‐Salute San Raffaele University, Milan, Italy</affiliation><affiliation>Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy</affiliation><affiliation>Nuclear Medicine Unit, San Raffaele Scientific Institute, Milan, Italy</affiliation><description>Correspondence: Nuclear Medicine Unit and Division of Neuroscience, San Raffaele Scientific Institute, 60 – 20132 via Olgettina, Milano, Italy</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-04</dateIssued><dateCaptured encoding="w3cdtf">2010-05-19</dateCaptured><dateValid encoding="w3cdtf">2010-11-01</dateValid><copyrightDate encoding="w3cdtf">2011</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">1</extent><extent unit="tables">1</extent><extent unit="references">38</extent><extent unit="words">3733</extent></physicalDescription><abstract lang="en">Background:: Preclinical and clinical evidence suggests that impaired gamma‐aminobutyric (GABA) control, leading to disinhibition within the sensorimotor system, might play a role in dystonia. Aim of this study is the in vivo assessment of the GABAergic system in dystonia using positron emission tomography (PET) and 11C‐flumazenil, a selective GABAA receptor ligand. Methods:: Fourteen subjects with primary dystonia (9 carriers of the DYT1 mutation and 5 sporadic cases) were compared to 11 controls, using a simplified reference tissue model to measure binding potential. Results:: Voxel‐based analyses showed a reduction in GABAA receptor expression/affinity both in DYT1 carriers and sporadic patients in primary motor and premotor cortex, primary and secondary somatosensory cortex, and in the motor component of the cingulate gyrus. Conclusions:: Dysfunction of GABAA receptors in sensorimotor systems in primary (genetic and sporadic) dystonia supports the view that lack of GABAergic control may be associated with the generation of dystonic movements. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflict of interest: Nothing to report. This study was financially supported by Diagnostic Molecular Imaging (DIMI), Sixth European Program, project No: LSHB‐CT‐2005‐512146 and the ItalianMinistry of Health, COFIN project (N. 2004062394_002 and N. 2006068233_003).</note><subject lang="en"><genre>Keywords</genre><topic>GABA</topic><topic>GABAA receptors</topic><topic>dystonia</topic><topic>sensorimotor cortex</topic><topic>PET</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>852</start><end>857</end><total>6</total></extent></part></relatedItem><identifier type="istex">967970D0720C6C7DBA0845355D7C453F3DFA429D</identifier><identifier type="DOI">10.1002/mds.23553</identifier><identifier type="ArticleID">MDS23553</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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