Subthalamic nucleus stimulation and dysarthria in Parkinson’s disease: a PET study
Identifieur interne : 002E70 ( Main/Corpus ); précédent : 002E69; suivant : 002E71Subthalamic 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.
Url:
DOI: 10.1093/brain/awh074
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ISTEX:D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEALe document en format XML
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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. 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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>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>611 x 791 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>3</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><genre><json:string>research-article</json:string></genre><host><volume>127</volume><pages><last>615</last><first>602</first></pages><issn><json:string>0006-8950</json:string></issn><issue>3</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2156</json:string></eissn><title>Brain</title></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>2004</publicationDate><copyrightDate>2004</copyrightDate><doi><json:string>10.1093/brain/awh074</json:string></doi><id>D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><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 xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</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><persName><forename type="first">Serge</forename><surname>Pinto</surname></persName><affiliation>8, Grenoble,</affiliation></author><author><persName><forename type="first">Stéphane</forename><surname>Thobois</surname></persName><affiliation></affiliation><affiliation></affiliation></author><author><persName><forename type="first">Nicolas</forename><surname>Costes</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">Didier</forename><surname>Le Bars</surname></persName><affiliation></affiliation></author><author><persName><forename type="first">Alim‐Louis</forename><surname>Benabid</surname></persName><affiliation>8, Grenoble,</affiliation></author><author><persName><forename type="first">Emmanuel</forename><surname>Broussolle</surname></persName><affiliation></affiliation><affiliation></affiliation></author><author><persName><forename type="first">Pierre</forename><surname>Pollak</surname></persName><affiliation>8, Grenoble,</affiliation><affiliation></affiliation></author><author><persName><forename type="first">Michèle</forename><surname>Gentil</surname></persName><affiliation>8, 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="2016-3-14">References 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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>8, Grenoble,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stéphane</namePart><namePart type="family">Thobois</namePart><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nicolas</namePart><namePart type="family">Costes</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Didier</namePart><namePart type="family">Le Bars</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alim‐Louis</namePart><namePart type="family">Benabid</namePart><affiliation>8, Grenoble,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Emmanuel</namePart><namePart type="family">Broussolle</namePart><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Pollak</namePart><affiliation>8, Grenoble,</affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michèle</namePart><namePart type="family">Gentil</namePart><affiliation>8, 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><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/annexes/gif</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/D3E9286B4E1EBE12E67A77AE56C3E346CB84FEEA/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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