Subthalamic nucleus stimulation and dysarthria in Parkinson's disease: a PET study
Identifieur interne : 000D67 ( PascalFrancis/Corpus ); précédent : 000D66; suivant : 000D68Subthalamic nucleus stimulation and dysarthria in Parkinson's disease: a PET study
Auteurs : Serge Pinto ; Stéphane Thobois ; Nicolas Costes ; Didier Le Bars ; Alim-Louis Benabid ; Emmanuel Broussolle ; Pierre Pollak ; Michèle GentilSource :
- Brain [ 0006-8950 ] ; 2004.
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- Pascal (Inist)
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- KwdEn :
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 Ml, 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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Format Inist (serveur)
| NO : | PASCAL 04-0503323 INIST |
|---|---|
| ET : | Subthalamic nucleus stimulation and dysarthria in Parkinson's disease: a PET study |
| AU : | PINTO (Serge); THOBOIS (Stéphane); COSTES (Nicolas); LE BARS (Didier); BENABID (Alim-Louis); BROUSSOLLE (Emmanuel); POLLAK (Pierre); GENTIL (Michèle) |
| AF : | INSERM U318/Grenoble/France (1 aut., 5 aut., 7 aut., 8 aut.); Hôpital Neurologique Pierre Wertheimer/Lyon/France (2 aut., 6 aut.); Centre d'Exploration et de Recherche Médicales par Emission de Positrons (CERMEP)/Lyon/France (2 aut., 3 aut., 4 aut., 6 aut.); Département de Neurologie, CHU de Grenoble/France (7 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Brain; ISSN 0006-8950; Royaume-Uni; Da. 2004; Vol. 127; No. p.3; Pp. 602-615; Bibl. 1 p.3/4 |
| LA : | Anglais |
| EA : | 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 Ml, 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. |
| CC : | 002B17 |
| FD : | Dysarthrie; Noyau sousthalamique; Tomoscintigraphie; Parkinson maladie; Positon; Parole; Système nerveux pathologie |
| FG : | Encéphale pathologie; Système nerveux central; Trouble langage; Trouble neurologique; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Exploration radioisotopique; Trouble communication |
| ED : | Dysarthria; Subthalamic nucleus; Emission tomography; Parkinson disease; Positron; Speech; Nervous system diseases |
| EG : | Cerebral disorder; Central nervous system; Language disorder; Neurological disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Radionuclide study; Communication disorder |
| SD : | Disartria; Núcleo subtalámico; Tomocentelleografía; Parkinson enfermedad; Positrón; Habla; Sistema nervioso patología |
| LO : | INIST-998.354000116596540130 |
| ID : | 04-0503323 |
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Pascal:04-0503323Le document en format XML
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sort="Pinto, Serge" uniqKey="Pinto S" first="Serge" last="Pinto">Serge Pinto</name><affiliation><inist:fA14 i1="01"><s1>INSERM U318</s1><s2>Grenoble</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Thobois, Stephane" sort="Thobois, Stephane" uniqKey="Thobois S" first="Stéphane" last="Thobois">Stéphane Thobois</name><affiliation><inist:fA14 i1="02"><s1>Hôpital Neurologique Pierre Wertheimer</s1><s2>Lyon</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Centre d'Exploration et de Recherche Médicales par Emission de Positrons (CERMEP)</s1><s2>Lyon</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Costes, Nicolas" sort="Costes, Nicolas" uniqKey="Costes N" first="Nicolas" last="Costes">Nicolas Costes</name><affiliation><inist:fA14 i1="03"><s1>Centre d'Exploration et de Recherche Médicales par Emission de Positrons (CERMEP)</s1><s2>Lyon</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></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><inist:fA14 i1="03"><s1>Centre d'Exploration et de Recherche Médicales par Emission de Positrons (CERMEP)</s1><s2>Lyon</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Benabid, Alim Louis" sort="Benabid, Alim Louis" uniqKey="Benabid A" first="Alim-Louis" last="Benabid">Alim-Louis Benabid</name><affiliation><inist:fA14 i1="01"><s1>INSERM U318</s1><s2>Grenoble</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Broussolle, Emmanuel" sort="Broussolle, Emmanuel" uniqKey="Broussolle E" first="Emmanuel" last="Broussolle">Emmanuel Broussolle</name><affiliation><inist:fA14 i1="02"><s1>Hôpital Neurologique Pierre Wertheimer</s1><s2>Lyon</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Centre d'Exploration et de Recherche Médicales par Emission de Positrons (CERMEP)</s1><s2>Lyon</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name><affiliation><inist:fA14 i1="01"><s1>INSERM U318</s1><s2>Grenoble</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Département de Neurologie, CHU de Grenoble</s1><s3>FRA</s3><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Gentil, Michele" sort="Gentil, Michele" uniqKey="Gentil M" first="Michèle" last="Gentil">Michèle Gentil</name><affiliation><inist:fA14 i1="01"><s1>INSERM U318</s1><s2>Grenoble</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno><imprint><date when="2004">2004</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dysarthria</term><term>Emission tomography</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Positron</term><term>Speech</term><term>Subthalamic nucleus</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dysarthrie</term><term>Noyau sousthalamique</term><term>Tomoscintigraphie</term><term>Parkinson maladie</term><term>Positon</term><term>Parole</term><term>Système nerveux pathologie</term></keywords></textClass></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 [<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 Ml, 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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-8950</s0></fA01><fA03 i2="1"><s0>Brain</s0></fA03><fA05><s2>127</s2></fA05><fA06><s3>p.3</s3></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Subthalamic nucleus stimulation and dysarthria in Parkinson's disease: a PET study</s1></fA08><fA11 i1="01" i2="1"><s1>PINTO (Serge)</s1></fA11><fA11 i1="02" i2="1"><s1>THOBOIS (Stéphane)</s1></fA11><fA11 i1="03" i2="1"><s1>COSTES (Nicolas)</s1></fA11><fA11 i1="04" i2="1"><s1>LE BARS (Didier)</s1></fA11><fA11 i1="05" i2="1"><s1>BENABID (Alim-Louis)</s1></fA11><fA11 i1="06" i2="1"><s1>BROUSSOLLE (Emmanuel)</s1></fA11><fA11 i1="07" i2="1"><s1>POLLAK (Pierre)</s1></fA11><fA11 i1="08" i2="1"><s1>GENTIL (Michèle)</s1></fA11><fA14 i1="01"><s1>INSERM U318</s1><s2>Grenoble</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></fA14><fA14 i1="02"><s1>Hôpital Neurologique Pierre Wertheimer</s1><s2>Lyon</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="03"><s1>Centre d'Exploration et de Recherche Médicales par Emission de Positrons (CERMEP)</s1><s2>Lyon</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="04"><s1>Département de Neurologie, CHU de Grenoble</s1><s3>FRA</s3><sZ>7 aut.</sZ></fA14><fA20><s1>602-615</s1></fA20><fA21><s1>2004</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>998</s2><s5>354000116596540130</s5></fA43><fA44><s0>0000</s0><s1>© 2004 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.3/4</s0></fA45><fA47 i1="01" i2="1"><s0>04-0503323</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Brain</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>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 Ml, 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.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Dysarthrie</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Dysarthria</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Disartria</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Noyau sousthalamique</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Subthalamic nucleus</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Núcleo subtalámico</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Tomoscintigraphie</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Emission tomography</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Tomocentelleografía</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Parkinson disease</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Positon</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Positron</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Positrón</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Parole</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Speech</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Habla</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>07</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Trouble langage</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Language disorder</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Trastorno lenguaje</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Trouble neurologique</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Neurological disorder</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Trastorno neurológico</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>42</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>43</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>43</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>43</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Exploration radioisotopique</s0><s5>45</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Radionuclide study</s0><s5>45</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Exploración radioisotópica</s0><s5>45</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Trouble communication</s0><s5>46</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Communication disorder</s0><s5>46</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Trastorno comunicación</s0><s5>46</s5></fC07><fN21><s1>285</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 04-0503323 INIST</NO><ET>Subthalamic nucleus stimulation and dysarthria in Parkinson's disease: a PET study</ET><AU>PINTO (Serge); THOBOIS (Stéphane); COSTES (Nicolas); LE BARS (Didier); BENABID (Alim-Louis); BROUSSOLLE (Emmanuel); POLLAK (Pierre); GENTIL (Michèle)</AU><AF>INSERM U318/Grenoble/France (1 aut., 5 aut., 7 aut., 8 aut.); Hôpital Neurologique Pierre Wertheimer/Lyon/France (2 aut., 6 aut.); Centre d'Exploration et de Recherche Médicales par Emission de Positrons (CERMEP)/Lyon/France (2 aut., 3 aut., 4 aut., 6 aut.); Département de Neurologie, CHU de Grenoble/France (7 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Brain; ISSN 0006-8950; Royaume-Uni; Da. 2004; Vol. 127; No. p.3; Pp. 602-615; Bibl. 1 p.3/4</SO><LA>Anglais</LA><EA>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 Ml, 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.</EA><CC>002B17</CC><FD>Dysarthrie; Noyau sousthalamique; Tomoscintigraphie; Parkinson maladie; Positon; Parole; Système nerveux pathologie</FD><FG>Encéphale pathologie; Système nerveux central; Trouble langage; Trouble neurologique; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Exploration radioisotopique; Trouble communication</FG><ED>Dysarthria; Subthalamic nucleus; Emission tomography; Parkinson disease; Positron; Speech; Nervous system diseases</ED><EG>Cerebral disorder; Central nervous system; Language disorder; Neurological disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Radionuclide study; Communication disorder</EG><SD>Disartria; Núcleo subtalámico; Tomocentelleografía; Parkinson enfermedad; Positrón; Habla; Sistema nervioso patología</SD><LO>INIST-998.354000116596540130</LO><ID>04-0503323</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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