Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study
Identifieur interne : 002456 ( Istex/Corpus ); précédent : 002455; suivant : 002457Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study
Auteurs : Serge Pinto ; Ste Phane Thobois ; Nicolas Costes ; Didier Le Bars ; Alim-Louis Benabid ; Emmanuel Broussolle ; Pierre Pollak ; Miche Le GentilSource :
- Brain [ 0006-8950 ] ; 2004-03.
English descriptors
- KwdEn :
- BA = Brodmann area; DLPFC = dorsolateral prefrontal cortex; MT = movement time; R = rest; rCBF = regional cerebral blood flow; RI = relative intensity; RT = reaction time; SA = silent articulation; SMA = supplementary motor area; SP = speech production; STN = subthalamic nucleus, Parkinson’s disease; subthalamic nucleus stimulation; speech production; [15O]H2O; PET.
Abstract
In Parkinson’s disease, functional imaging studies during limb motor tasks reveal cerebral activation abnormalities that can be reversed by subthalamic nucleus (STN) stimulation. The effect of STN stimulation on parkinsonian dysarthria has not, however, been investigated using PET. The aim of the present study was to evaluate the effect of STN stimulation on regional cerebral blood flow (rCBF) during speech production and silent articulation in patients with Parkinson’s disease. Ten Parkinson’s disease patients surgically implanted bilaterally in the STN and with significant improvement of their dysarthria induced by STN stimulation were included. Ten healthy control subjects also participated in this study. Control subjects performed six sessions of [15O]H2O–PET scanning corresponding to three duplicated conditions externally cued by an auditory signal. The conditions were: (i) rest; (ii) production of a short, simple sentence; and (iii) silent articulation of the same sentence. Parkinson’s disease patients carried out the six PET sessions twice, i.e., in the ON and OFF STN stimulation states. PET data analysis was performed using statistical parametric mapping (SPM99). In control subjects, speech production (SP) compared with rest was associated with increased rCBF bilaterally in the primary motor cortex (M1) corresponding to the orofacial somatotopy, the supplementary motor area (SMA), the associative auditory cortex and the cerebellar hemispheres. Silent articulation (SA) compared with rest induced a bilateral rCBF increase restricted to the orofacial M1 and cerebellar hemispheres. In Parkinson’s disease patients in the OFF stimulation condition, during both SP and SA there was a lack of activation in the right orofacial M1 and in the cerebellum, abnormal increased rCBF in the right superior premotor cortex, and overactivation of the SMA. There was also an abnormal, increased rCBF in the dorsolateral prefrontal cortex (DLPFC) only during SP and increased rCBF in the left insula only during SA. In Parkinson’s disease patients ON stimulation, for both SP and SA the activation pattern appeared similar to that in control subjects. In conclusion, our results suggest that parkinsonian dysarthria is associated with altered recruitment of the main motor cerebral regions (orofacial M1, cerebellum), and increased involvement of the premotor and prefrontal cortices (DLPFC, SMA, superior premotor cortex). These abnormal activations are different from those reported during hand motor tasks. They could be a compensatory mechanism, but might also arise directly as part of the pathophysiology of Parkinson’s disease. STN stimulation tends to reverse these abnormal activations, which is consistent with the observed improvement of Parkinson’s disease dysarthria.
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DOI: 10.1093/brain/awh074
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Positrons (CERMEP), Lyon and</mods:affiliation></affiliation></author><author><name sortKey="Costes, Nicolas" sort="Costes, Nicolas" uniqKey="Costes N" first="Nicolas" last="Costes">Nicolas Costes</name><affiliation><mods:affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</mods:affiliation></affiliation></author><author><name sortKey="Le Bars, Didier" sort="Le Bars, Didier" uniqKey="Le Bars D" first="Didier" last="Le Bars">Didier Le Bars</name><affiliation><mods:affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</mods:affiliation></affiliation></author><author><name sortKey="Benabid, Alim Ouis" sort="Benabid, Alim Ouis" uniqKey="Benabid A" first="Alim-Louis" last="Benabid">Alim-Louis Benabid</name><affiliation><mods:affiliation>INSERM U318, Grenoble,</mods:affiliation></affiliation></author><author><name sortKey="Broussolle, Emmanuel" sort="Broussolle, Emmanuel" uniqKey="Broussolle E" first="Emmanuel" last="Broussolle">Emmanuel Broussolle</name><affiliation><mods:affiliation>Hôpital Neurologique Pierre Wertheimer,</mods:affiliation></affiliation><affiliation><mods:affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</mods:affiliation></affiliation></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name><affiliation><mods:affiliation>INSERM U318, Grenoble,</mods:affiliation></affiliation><affiliation><mods:affiliation>Département de Neurologie, CHU de Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Gentil, Miche Le" sort="Gentil, Miche Le" uniqKey="Gentil M" first="Miche Le" last="Gentil">Miche Le Gentil</name><affiliation><mods:affiliation>INSERM U318, Grenoble,</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2004-03">2004-03</date><biblScope unit="volume">127</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="602">602</biblScope><biblScope unit="page" to="615">615</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA</idno><idno type="DOI">10.1093/brain/awh074</idno><idno type="local">awh074</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>BA = Brodmann area; DLPFC = dorsolateral prefrontal cortex; MT = movement time; R = rest; rCBF = regional cerebral blood flow; RI = relative intensity; RT = reaction time; SA = silent articulation; SMA = supplementary motor area; SP = speech production; STN = subthalamic nucleus</term><term>Parkinson’s disease; subthalamic nucleus stimulation; speech production; [15O]H2O; PET</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In Parkinson’s disease, functional imaging studies during limb motor tasks reveal cerebral activation abnormalities that can be reversed by subthalamic nucleus (STN) stimulation. The effect of STN stimulation on parkinsonian dysarthria has not, however, been investigated using PET. The aim of the present study was to evaluate the effect of STN stimulation on regional cerebral blood flow (rCBF) during speech production and silent articulation in patients with Parkinson’s disease. Ten Parkinson’s disease patients surgically implanted bilaterally in the STN and with significant improvement of their dysarthria induced by STN stimulation were included. Ten healthy control subjects also participated in this study. Control subjects performed six sessions of [15O]H2O–PET scanning corresponding to three duplicated conditions externally cued by an auditory signal. The conditions were: (i) rest; (ii) production of a short, simple sentence; and (iii) silent articulation of the same sentence. Parkinson’s disease patients carried out the six PET sessions twice, i.e., in the ON and OFF STN stimulation states. PET data analysis was performed using statistical parametric mapping (SPM99). In control subjects, speech production (SP) compared with rest was associated with increased rCBF bilaterally in the primary motor cortex (M1) corresponding to the orofacial somatotopy, the supplementary motor area (SMA), the associative auditory cortex and the cerebellar hemispheres. Silent articulation (SA) compared with rest induced a bilateral rCBF increase restricted to the orofacial M1 and cerebellar hemispheres. In Parkinson’s disease patients in the OFF stimulation condition, during both SP and SA there was a lack of activation in the right orofacial M1 and in the cerebellum, abnormal increased rCBF in the right superior premotor cortex, and overactivation of the SMA. There was also an abnormal, increased rCBF in the dorsolateral prefrontal cortex (DLPFC) only during SP and increased rCBF in the left insula only during SA. In Parkinson’s disease patients ON stimulation, for both SP and SA the activation pattern appeared similar to that in control subjects. In conclusion, our results suggest that parkinsonian dysarthria is associated with altered recruitment of the main motor cerebral regions (orofacial M1, cerebellum), and increased involvement of the premotor and prefrontal cortices (DLPFC, SMA, superior premotor cortex). These abnormal activations are different from those reported during hand motor tasks. They could be a compensatory mechanism, but might also arise directly as part of the pathophysiology of Parkinson’s disease. STN stimulation tends to reverse these abnormal activations, which is consistent with the observed improvement of Parkinson’s disease dysarthria.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Serge Pinto</name><affiliations><json:string>INSERM U318, Grenoble,</json:string></affiliations></json:item><json:item><name>Stéphane Thobois</name><affiliations><json:string>Hôpital Neurologique Pierre Wertheimer,</json:string><json:string>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</json:string></affiliations></json:item><json:item><name>Nicolas Costes</name><affiliations><json:string>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</json:string></affiliations></json:item><json:item><name>Didier Le Bars</name><affiliations><json:string>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</json:string></affiliations></json:item><json:item><name>Alim‐Louis Benabid</name><affiliations><json:string>INSERM U318, Grenoble,</json:string></affiliations></json:item><json:item><name>Emmanuel Broussolle</name><affiliations><json:string>Hôpital Neurologique Pierre Wertheimer,</json:string><json:string>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</json:string></affiliations></json:item><json:item><name>Pierre Pollak</name><affiliations><json:string>INSERM U318, Grenoble,</json:string><json:string>Département de Neurologie, CHU de Grenoble, France</json:string></affiliations></json:item><json:item><name>Michèle Gentil</name><affiliations><json:string>INSERM U318, Grenoble,</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson’s disease; subthalamic nucleus stimulation; speech production; [15O]H2O; PET</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>BA = Brodmann area; DLPFC = dorsolateral prefrontal cortex; MT = movement time; R = rest; rCBF = regional cerebral blood flow; RI = relative intensity; RT = reaction time; SA = silent articulation; SMA = supplementary motor area; SP = speech production; STN = subthalamic nucleus</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>In Parkinson’s disease, functional imaging studies during limb motor tasks reveal cerebral activation abnormalities that can be reversed by subthalamic nucleus (STN) stimulation. The effect of STN stimulation on parkinsonian dysarthria has not, however, been investigated using PET. The aim of the present study was to evaluate the effect of STN stimulation on regional cerebral blood flow (rCBF) during speech production and silent articulation in patients with Parkinson’s disease. Ten Parkinson’s disease patients surgically implanted bilaterally in the STN and with significant improvement of their dysarthria induced by STN stimulation were included. Ten healthy control subjects also participated in this study. Control subjects performed six sessions of [15O]H2O–PET scanning corresponding to three duplicated conditions externally cued by an auditory signal. The conditions were: (i) rest; (ii) production of a short, simple sentence; and (iii) silent articulation of the same sentence. Parkinson’s disease patients carried out the six PET sessions twice, i.e., in the ON and OFF STN stimulation states. PET data analysis was performed using statistical parametric mapping (SPM99). In control subjects, speech production (SP) compared with rest was associated with increased rCBF bilaterally in the primary motor cortex (M1) corresponding to the orofacial somatotopy, the supplementary motor area (SMA), the associative auditory cortex and the cerebellar hemispheres. Silent articulation (SA) compared with rest induced a bilateral rCBF increase restricted to the orofacial M1 and cerebellar hemispheres. In Parkinson’s disease patients in the OFF stimulation condition, during both SP and SA there was a lack of activation in the right orofacial M1 and in the cerebellum, abnormal increased rCBF in the right superior premotor cortex, and overactivation of the SMA. There was also an abnormal, increased rCBF in the dorsolateral prefrontal cortex (DLPFC) only during SP and increased rCBF in the left insula only during SA. In Parkinson’s disease patients ON stimulation, for both SP and SA the activation pattern appeared similar to that in control subjects. In conclusion, our results suggest that parkinsonian dysarthria is associated with altered recruitment of the main motor cerebral regions (orofacial M1, cerebellum), and increased involvement of the premotor and prefrontal cortices (DLPFC, SMA, superior premotor cortex). These abnormal activations are different from those reported during hand motor tasks. They could be a compensatory mechanism, but might also arise directly as part of the pathophysiology of Parkinson’s disease. STN stimulation tends to reverse these abnormal activations, which is consistent with the observed improvement of Parkinson’s disease dysarthria.</abstract><qualityIndicators><score>10</score><pdfVersion>1.3</pdfVersion><pdfPageSize>611 x 791 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>2</keywordCount><abstractCharCount>2797</abstractCharCount><pdfWordCount>8476</pdfWordCount><pdfCharCount>53825</pdfCharCount><pdfPageCount>14</pdfPageCount><abstractWordCount>403</abstractWordCount></qualityIndicators><title>Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study</title><refBibs><json:item><author><json:item><name>H Ackermann</name></json:item><json:item><name>I Hertrich</name></json:item><json:item><name>I Daum</name></json:item><json:item><name>G Scharf</name></json:item><json:item><name>S Spieker</name></json:item></author><host><volume>12</volume><pages><last>27</last><first>1019</first></pages><author></author><title>Mov Disord</title><publicationDate>1997</publicationDate></host><title>Kinematic analysis of articulatory movements in central motor disorders</title><publicationDate>1997</publicationDate></json:item><json:item><author><json:item><name>H Ackermann</name></json:item><json:item><name>D Wildgruber</name></json:item><json:item><name>I Daum</name></json:item><json:item><name>W Grodd</name></json:item><json:item><name> 187±90</name></json:item><json:item><name>Sm Barlow</name></json:item><json:item><name>Jh Abbs</name></json:item></author><host><volume>247</volume><pages><last>21</last><first>616</first></pages><issue>336</issue><author></author><title>Neurosci Lett J Speech Hear Res Bates JF J Comp Neurol</title><publicationDate>1983</publicationDate></host><title>Does the cerebellum contribute to cognitive aspects of speech production? 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stimulation on actual and imagined movement in Parkinson's disease: a PET study Brain regions involved in articulation</title><publicationDate>1999</publicationDate></json:item></refBibs><genre><json:string>research-article</json:string></genre><host><volume>127</volume><publisherId><json:string>brainj</json:string></publisherId><pages><last>615</last><first>602</first></pages><issn><json:string>0006-8950</json:string></issn><issue>3</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2156</json:string></eissn><title>Brain</title></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string><json:string>clinical neurology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>2004</publicationDate><copyrightDate>2004</copyrightDate><doi><json:string>10.1093/brain/awh074</json:string></doi><id>D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA</id><score>0.107543156</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study</title><respStmt><resp>Références bibliographiques récupérées via GROBID</resp><name resp="ISTEX-API">ISTEX-API (INIST-CNRS)</name></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>The Guarantors of Brain 2004</p></availability><date>2004</date></publicationStmt><notesStmt><note>Correspondence to: Serge Pinto, PhD, Département de Neurologie, CHU de Grenoble, BP 217, 38043 Grenoble cedex 09, France E‐mail: serge_pinto@yahoo.fr</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study</title><author xml:id="author-1"><persName><forename type="first">Serge</forename><surname>Pinto</surname></persName><affiliation>INSERM U318, Grenoble,</affiliation></author><author xml:id="author-2"><persName><forename type="first">Stéphane</forename><surname>Thobois</surname></persName><affiliation>Hôpital Neurologique Pierre Wertheimer,</affiliation><affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</affiliation></author><author xml:id="author-3"><persName><forename type="first">Nicolas</forename><surname>Costes</surname></persName><affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</affiliation></author><author xml:id="author-4"><persName><forename type="first">Didier</forename><surname>Le Bars</surname></persName><affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</affiliation></author><author xml:id="author-5"><persName><forename type="first">Alim‐Louis</forename><surname>Benabid</surname></persName><affiliation>INSERM U318, Grenoble,</affiliation></author><author xml:id="author-6"><persName><forename type="first">Emmanuel</forename><surname>Broussolle</surname></persName><affiliation>Hôpital Neurologique Pierre Wertheimer,</affiliation><affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</affiliation></author><author xml:id="author-7"><persName><forename type="first">Pierre</forename><surname>Pollak</surname></persName><affiliation>INSERM U318, Grenoble,</affiliation><affiliation>Département de Neurologie, CHU de Grenoble, France</affiliation></author><author xml:id="author-8"><persName><forename type="first">Michèle</forename><surname>Gentil</surname></persName><affiliation>INSERM U318, Grenoble,</affiliation></author></analytic><monogr><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="pISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2004-03"></date><biblScope unit="volume">127</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="602">602</biblScope><biblScope unit="page" to="615">615</biblScope></imprint></monogr><idno type="istex">D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA</idno><idno type="DOI">10.1093/brain/awh074</idno><idno type="local">awh074</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In Parkinson’s disease, functional imaging studies during limb motor tasks reveal cerebral activation abnormalities that can be reversed by subthalamic nucleus (STN) stimulation. The effect of STN stimulation on parkinsonian dysarthria has not, however, been investigated using PET. The aim of the present study was to evaluate the effect of STN stimulation on regional cerebral blood flow (rCBF) during speech production and silent articulation in patients with Parkinson’s disease. Ten Parkinson’s disease patients surgically implanted bilaterally in the STN and with significant improvement of their dysarthria induced by STN stimulation were included. Ten healthy control subjects also participated in this study. Control subjects performed six sessions of [15O]H2O–PET scanning corresponding to three duplicated conditions externally cued by an auditory signal. The conditions were: (i) rest; (ii) production of a short, simple sentence; and (iii) silent articulation of the same sentence. Parkinson’s disease patients carried out the six PET sessions twice, i.e., in the ON and OFF STN stimulation states. PET data analysis was performed using statistical parametric mapping (SPM99). In control subjects, speech production (SP) compared with rest was associated with increased rCBF bilaterally in the primary motor cortex (M1) corresponding to the orofacial somatotopy, the supplementary motor area (SMA), the associative auditory cortex and the cerebellar hemispheres. Silent articulation (SA) compared with rest induced a bilateral rCBF increase restricted to the orofacial M1 and cerebellar hemispheres. In Parkinson’s disease patients in the OFF stimulation condition, during both SP and SA there was a lack of activation in the right orofacial M1 and in the cerebellum, abnormal increased rCBF in the right superior premotor cortex, and overactivation of the SMA. There was also an abnormal, increased rCBF in the dorsolateral prefrontal cortex (DLPFC) only during SP and increased rCBF in the left insula only during SA. In Parkinson’s disease patients ON stimulation, for both SP and SA the activation pattern appeared similar to that in control subjects. In conclusion, our results suggest that parkinsonian dysarthria is associated with altered recruitment of the main motor cerebral regions (orofacial M1, cerebellum), and increased involvement of the premotor and prefrontal cortices (DLPFC, SMA, superior premotor cortex). These abnormal activations are different from those reported during hand motor tasks. They could be a compensatory mechanism, but might also arise directly as part of the pathophysiology of Parkinson’s disease. STN stimulation tends to reverse these abnormal activations, which is consistent with the observed improvement of Parkinson’s disease dysarthria.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>Parkinson’s disease; subthalamic nucleus stimulation; speech production; [15O]H2O; PET</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>BA = Brodmann area; DLPFC = dorsolateral prefrontal cortex; MT = movement time; R = rest; rCBF = regional cerebral blood flow; RI = relative intensity; RT = reaction time; SA = silent articulation; SMA = supplementary motor area; SP = speech production; STN = subthalamic nucleus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2004-03">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-12-22">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="nlm-ta">Brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><abbrev-journal-title abbrev-type="publisher">Brain</abbrev-journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">awh074</article-id><article-id pub-id-type="doi">10.1093/brain/awh074</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Pinto</surname><given-names>Serge</given-names></name><xref rid="AWH074A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Thobois</surname><given-names>Stéphane</given-names></name><xref rid="AWH074A2">2</xref><xref rid="AWH074A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Costes</surname><given-names>Nicolas</given-names></name><xref rid="AWH074A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Le Bars</surname><given-names>Didier</given-names></name><xref rid="AWH074A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Benabid</surname><given-names>Alim‐Louis</given-names></name><xref rid="AWH074A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Broussolle</surname><given-names>Emmanuel</given-names></name><xref rid="AWH074A2">2</xref><xref rid="AWH074A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Pollak</surname><given-names>Pierre</given-names></name><xref rid="AWH074A1">1</xref><xref rid="AWH074A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Gentil</surname><given-names>Michèle</given-names></name><xref rid="AWH074A1">1</xref></contrib><aff id="AWH074A1"><label>1</label>INSERM U318, Grenoble,</aff><aff id="AWH074A2"><label>2</label>Hôpital Neurologique Pierre Wertheimer,</aff><aff id="AWH074A3"><label>3</label>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</aff><aff id="AWH074A4"><label>4</label>Département de Neurologie, CHU de Grenoble, France</aff></contrib-group><author-notes><corresp id="COR1"><label></label>Correspondence to: Serge Pinto, PhD, Département de Neurologie, CHU de Grenoble, BP 217, 38043 Grenoble cedex 09, France E‐mail: <ext-link xlink:href="serge_pinto@yahoo.fr" ext-link-type="email">serge_pinto@yahoo.fr</ext-link></corresp></author-notes><pub-date pub-type="ppub"><month>03</month><year>2004</year></pub-date><volume>127</volume><issue>3</issue><fpage>602</fpage><lpage>615</lpage><history><date date-type="accepted"><day>30</day><month>10</month><year>2003</year></date><date date-type="received"><day>02</day><month>06</month><year>2003</year></date><date date-type="rev-recd"><day>15</day><month>10</month><year>2003</year></date></history><copyright-statement>The Guarantors of Brain 2004</copyright-statement><copyright-year>2004</copyright-year><abstract xml:lang="en"><p>In Parkinson’s disease, functional imaging studies during limb motor tasks reveal cerebral activation abnormalities that can be reversed by subthalamic nucleus (STN) stimulation. The effect of STN stimulation on parkinsonian dysarthria has not, however, been investigated using PET. The aim of the present study was to evaluate the effect of STN stimulation on regional cerebral blood flow (rCBF) during speech production and silent articulation in patients with Parkinson’s disease. Ten Parkinson’s disease patients surgically implanted bilaterally in the STN and with significant improvement of their dysarthria induced by STN stimulation were included. Ten healthy control subjects also participated in this study. Control subjects performed six sessions of [<sup>15</sup>O]H<sub>2</sub>O–PET scanning corresponding to three duplicated conditions externally cued by an auditory signal. The conditions were: (i) rest; (ii) production of a short, simple sentence; and (iii) silent articulation of the same sentence. Parkinson’s disease patients carried out the six PET sessions twice, i.e., in the ON and OFF STN stimulation states. PET data analysis was performed using statistical parametric mapping (SPM99). In control subjects, speech production (SP) compared with rest was associated with increased rCBF bilaterally in the primary motor cortex (M1) corresponding to the orofacial somatotopy, the supplementary motor area (SMA), the associative auditory cortex and the cerebellar hemispheres. Silent articulation (SA) compared with rest induced a bilateral rCBF increase restricted to the orofacial M1 and cerebellar hemispheres. In Parkinson’s disease patients in the OFF stimulation condition, during both SP and SA there was a lack of activation in the right orofacial M1 and in the cerebellum, abnormal increased rCBF in the right superior premotor cortex, and overactivation of the SMA. There was also an abnormal, increased rCBF in the dorsolateral prefrontal cortex (DLPFC) only during SP and increased rCBF in the left insula only during SA. In Parkinson’s disease patients ON stimulation, for both SP and SA the activation pattern appeared similar to that in control subjects. In conclusion, our results suggest that parkinsonian dysarthria is associated with altered recruitment of the main motor cerebral regions (orofacial M1, cerebellum), and increased involvement of the premotor and prefrontal cortices (DLPFC, SMA, superior premotor cortex). These abnormal activations are different from those reported during hand motor tasks. They could be a compensatory mechanism, but might also arise directly as part of the pathophysiology of Parkinson’s disease. STN stimulation tends to reverse these abnormal activations, which is consistent with the observed improvement of Parkinson’s disease dysarthria. </p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>Parkinson’s disease; subthalamic nucleus stimulation; speech production; [<sup>15</sup>O]H<sub>2</sub>O; PET</kwd></kwd-group><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd>BA = Brodmann area; DLPFC = dorsolateral prefrontal cortex; MT = movement time; R = rest; rCBF = regional cerebral blood flow; RI = relative intensity; RT = reaction time; SA = silent articulation; SMA = supplementary motor area; SP = speech production; STN = subthalamic nucleus</kwd></kwd-group><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>602</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>Article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study</title></titleInfo><name type="personal"><namePart type="given">Serge</namePart><namePart type="family">Pinto</namePart><affiliation>INSERM U318, Grenoble,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stéphane</namePart><namePart type="family">Thobois</namePart><affiliation>Hôpital Neurologique Pierre Wertheimer,</affiliation><affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nicolas</namePart><namePart type="family">Costes</namePart><affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Didier</namePart><namePart type="family">Le Bars</namePart><affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alim‐Louis</namePart><namePart type="family">Benabid</namePart><affiliation>INSERM U318, Grenoble,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Emmanuel</namePart><namePart type="family">Broussolle</namePart><affiliation>Hôpital Neurologique Pierre Wertheimer,</affiliation><affiliation>Centre d’Exploration et de Recherche Médicales par Emission de Positrons (CERMEP), Lyon and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Pollak</namePart><affiliation>INSERM U318, Grenoble,</affiliation><affiliation>Département de Neurologie, CHU de Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michèle</namePart><namePart type="family">Gentil</namePart><affiliation>INSERM U318, Grenoble,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2004-03</dateIssued><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">In Parkinson’s disease, functional imaging studies during limb motor tasks reveal cerebral activation abnormalities that can be reversed by subthalamic nucleus (STN) stimulation. The effect of STN stimulation on parkinsonian dysarthria has not, however, been investigated using PET. The aim of the present study was to evaluate the effect of STN stimulation on regional cerebral blood flow (rCBF) during speech production and silent articulation in patients with Parkinson’s disease. Ten Parkinson’s disease patients surgically implanted bilaterally in the STN and with significant improvement of their dysarthria induced by STN stimulation were included. Ten healthy control subjects also participated in this study. Control subjects performed six sessions of [15O]H2O–PET scanning corresponding to three duplicated conditions externally cued by an auditory signal. The conditions were: (i) rest; (ii) production of a short, simple sentence; and (iii) silent articulation of the same sentence. Parkinson’s disease patients carried out the six PET sessions twice, i.e., in the ON and OFF STN stimulation states. PET data analysis was performed using statistical parametric mapping (SPM99). In control subjects, speech production (SP) compared with rest was associated with increased rCBF bilaterally in the primary motor cortex (M1) corresponding to the orofacial somatotopy, the supplementary motor area (SMA), the associative auditory cortex and the cerebellar hemispheres. Silent articulation (SA) compared with rest induced a bilateral rCBF increase restricted to the orofacial M1 and cerebellar hemispheres. In Parkinson’s disease patients in the OFF stimulation condition, during both SP and SA there was a lack of activation in the right orofacial M1 and in the cerebellum, abnormal increased rCBF in the right superior premotor cortex, and overactivation of the SMA. There was also an abnormal, increased rCBF in the dorsolateral prefrontal cortex (DLPFC) only during SP and increased rCBF in the left insula only during SA. In Parkinson’s disease patients ON stimulation, for both SP and SA the activation pattern appeared similar to that in control subjects. In conclusion, our results suggest that parkinsonian dysarthria is associated with altered recruitment of the main motor cerebral regions (orofacial M1, cerebellum), and increased involvement of the premotor and prefrontal cortices (DLPFC, SMA, superior premotor cortex). These abnormal activations are different from those reported during hand motor tasks. They could be a compensatory mechanism, but might also arise directly as part of the pathophysiology of Parkinson’s disease. STN stimulation tends to reverse these abnormal activations, which is consistent with the observed improvement of Parkinson’s disease dysarthria.</abstract><note type="author-notes">Correspondence to: Serge Pinto, PhD, Département de Neurologie, CHU de Grenoble, BP 217, 38043 Grenoble cedex 09, France E‐mail: serge_pinto@yahoo.fr</note><subject lang="en"><genre>KWD</genre><topic>Parkinson’s disease; subthalamic nucleus stimulation; speech production; [15O]H2O; PET</topic></subject><subject lang="en"><genre>ABR</genre><topic>BA = Brodmann area; DLPFC = dorsolateral prefrontal cortex; MT = movement time; R = rest; rCBF = regional cerebral blood flow; RI = relative intensity; RT = reaction time; SA = silent articulation; SMA = supplementary motor area; SP = speech production; STN = subthalamic nucleus</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><titleInfo type="abbreviated"><title>Brain</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><identifier type="PublisherID-nlm-ta">Brain</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>127</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>602</start><end>615</end></extent></part></relatedItem><identifier type="istex">D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA</identifier><identifier type="DOI">10.1093/brain/awh074</identifier><identifier type="local">awh074</identifier><accessCondition type="use and reproduction" contentType="copyright">The Guarantors of Brain 2004</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><extension>jpeg</extension><original>true</original><mimetype>image/jpeg</mimetype><uri>https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/annexes/jpeg</uri></json:item><json:item><extension>gif</extension><original>true</original><mimetype>image/gif</mimetype><uri>https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/annexes/gif</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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