Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease
Identifieur interne : 001146 ( Istex/Corpus ); précédent : 001145; suivant : 001147Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease
Auteurs : D. Devos ; E. Labyt ; F. Cassim ; J. L. Bourriez ; N. Reyns ; G. Touzet ; S. Blond ; J. D. Guieu ; P. Derambure ; A. Destée ; L. DefebvreSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2003-10.
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Abstract
In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement‐related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l‐dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self‐paced wrist flexion in four conditions according to the presence or not of stimulation and l‐dopa. Compared to without treatment, the motor score improved by ≈ 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l‐dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l‐dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement‐related somatosensory processing at the end of the movement through the basal ganglia into the cortex.
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DOI: 10.1046/j.1460-9568.2003.02925.x
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Devos</name><affiliation><mods:affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</mods:affiliation></affiliation></author><author><name sortKey="Labyt, E" sort="Labyt, E" uniqKey="Labyt E" first="E." last="Labyt">E. Labyt</name><affiliation><mods:affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</mods:affiliation></affiliation></author><author><name sortKey="Cassim, F" sort="Cassim, F" uniqKey="Cassim F" first="F." last="Cassim">F. Cassim</name><affiliation><mods:affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</mods:affiliation></affiliation></author><author><name sortKey="Bourriez, J L" sort="Bourriez, J L" uniqKey="Bourriez J" first="J. L." last="Bourriez">J. L. 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Defebvre</name><affiliation><mods:affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neuroscience</title><idno type="ISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><imprint><publisher>Blackwell Science, Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-10">2003-10</date><biblScope unit="volume">18</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1884">1884</biblScope><biblScope unit="page" to="1888">1888</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">FC5D8CA50AAB4EFF904A1ACC8E4490C219FBE3B2</idno><idno type="DOI">10.1046/j.1460-9568.2003.02925.x</idno><idno type="ArticleID">EJN2925</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>EEG</term><term>advanced Parkinsonian</term><term>event‐related synchronization</term><term>human</term><term>l‐dopa</term><term>movement</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement‐related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l‐dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self‐paced wrist flexion in four conditions according to the presence or not of stimulation and l‐dopa. Compared to without treatment, the motor score improved by ≈ 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l‐dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l‐dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement‐related somatosensory processing at the end of the movement through the basal ganglia into the cortex.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>D. Devos</name><affiliations><json:string>Department of Neurology, EA2683, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>E. Labyt</name><affiliations><json:string>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>F. Cassim</name><affiliations><json:string>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>J. L. Bourriez</name><affiliations><json:string>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>N. Reyns</name><affiliations><json:string>Department of Neurosurgery, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>G. Touzet</name><affiliations><json:string>Department of Neurosurgery, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>S. Blond</name><affiliations><json:string>Department of Neurosurgery, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>J. D. Guieu</name><affiliations><json:string>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>P. Derambure</name><affiliations><json:string>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>A. Destée</name><affiliations><json:string>Department of Neurology, EA2683, Lille University Medical Centre, France</json:string></affiliations></json:item><json:item><name>L. Defebvre</name><affiliations><json:string>Department of Neurology, EA2683, Lille University Medical Centre, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>advanced Parkinsonian</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>EEG</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>event‐related synchronization</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>human</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>l‐dopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>movement</value></json:item></subject><articleId><json:string>EJN2925</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement‐related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l‐dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self‐paced wrist flexion in four conditions according to the presence or not of stimulation and l‐dopa. Compared to without treatment, the motor score improved by ≈ 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l‐dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l‐dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement‐related somatosensory processing at the end of the movement through the basal ganglia into the cortex.</abstract><qualityIndicators><score>6.517</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1639</abstractCharCount><pdfWordCount>3925</pdfWordCount><pdfCharCount>26362</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>216</abstractWordCount></qualityIndicators><title>Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease</title><refBibs><json:item><author><json:item><name>P. Ashby</name></json:item><json:item><name>Y.J. Kim</name></json:item><json:item><name>R. Kumar</name></json:item><json:item><name>A.E. Lang</name></json:item><json:item><name>A.M. Lozano</name></json:item></author><host><volume>122</volume><pages><last>1931</last><first>1919</first></pages><author></author><title>Brain</title></host><title>Neurophysiological effects of stimulation through electrodes in the human subthalamic nucleus</title></json:item><json:item><author><json:item><name>C. Beurrier</name></json:item><json:item><name>B. Bioulac</name></json:item><json:item><name>J. Audin</name></json:item><json:item><name>C. Hammond</name></json:item></author><host><volume>85</volume><pages><last>1356</last><first>1351</first></pages><author></author><title>J. Neurophysiol.</title></host><title>High‐frequency stimulation produces a transient blockade of voltage‐gated currents in subthalamic neurons</title></json:item><json:item><author><json:item><name>P. Brown</name></json:item><json:item><name>C.D. Marsden</name></json:item></author><host><volume>351</volume><pages><last>1804</last><first>1801</first></pages><author></author><title>Lancet</title></host><title>What do the basal ganglia do? [Review]</title></json:item><json:item><author><json:item><name>M. Cassidy</name></json:item><json:item><name>P. Mazzone</name></json:item><json:item><name>A. Oliviero</name></json:item><json:item><name>A. Insola</name></json:item><json:item><name>P. Tonali</name></json:item><json:item><name>V. Di Lazzaro</name></json:item><json:item><name>P. Brown</name></json:item></author><host><volume>125</volume><pages><last>1246</last><first>1235</first></pages><author></author><title>Brain</title></host><title>Movement‐related changes in synchronization in the human basal ganglia</title></json:item><json:item><author><json:item><name>F. Cassim</name></json:item><json:item><name>C. Monaca</name></json:item><json:item><name>W. Szurhaj</name></json:item><json:item><name>J.L. Bourriez</name></json:item><json:item><name>L. Defebvre</name></json:item><json:item><name>P. Derambure</name></json:item><json:item><name>J.D. Guieu</name></json:item></author><host><volume>12</volume><pages><last>3863</last><first>3859</first></pages><author></author><title>Neuroreport</title></host><title>Does post movement beta synchronization reflect an ‘idling’ motor cortex?</title></json:item><json:item><author><json:item><name>F.C. Cassim</name></json:item><json:item><name>W. Szurhaj</name></json:item><json:item><name>H. Sediri</name></json:item><json:item><name>D. Devos</name></json:item><json:item><name>J.L. Bourriez</name></json:item><json:item><name>I. Poirot</name></json:item><json:item><name>Ph Derambure</name></json:item><json:item><name>L. Defebvre</name></json:item><json:item><name>J.D. Guieu</name></json:item></author><host><volume>111</volume><pages><last>2039</last><first>2032</first></pages><author></author><title>Clin. Neurophysiol.</title></host><title>Brief and sustained movements: differences in event‐related (de) synchronization (ERD/ERS) patterns</title></json:item><json:item><author><json:item><name>R. Chen</name></json:item><json:item><name>Z. Yassen</name></json:item><json:item><name>L.G. Cohen</name></json:item><json:item><name>M. Hallett</name></json:item></author><host><volume>44</volume><pages><last>325</last><first>317</first></pages><author></author><title>Ann. Neurol.</title></host><title>The time course of corticospinal excitability in reaction time and self‐paced movements</title></json:item><json:item><author><json:item><name>W.J. Conover</name></json:item><json:item><name>R.L. Iman</name></json:item></author><host><volume>35</volume><pages><last>129</last><first>124</first></pages><author></author><title>Am. Statistician Assoc</title></host><title>Rank transformation as a bridge between parametric and nonparametric statistics</title></json:item><json:item><author><json:item><name>J.L. Contreras‐Vidal</name></json:item><json:item><name>C.E. Stelmach</name></json:item></author><host><volume>73</volume><pages><last>476</last><first>467</first></pages><author></author><title>Biol. Cybern.</title></host><title>A neural model of basal ganglia–thalamocortical relations in normal and parkinsonian movement</title></json:item><json:item><author><json:item><name>D. Cunic</name></json:item><json:item><name>L. Roshan</name></json:item><json:item><name>F.I. Khan</name></json:item><json:item><name>A.M. Lozano</name></json:item><json:item><name>A.E. Lang</name></json:item><json:item><name>R. Chen</name></json:item></author><host><volume>58</volume><pages><last>1672</last><first>1665</first></pages><author></author><title>Neurology</title></host><title>Effects of subthalamic nucleus stimulation on motor cortex excitability in Parkinson's disease</title></json:item><json:item><author><json:item><name>R. Cunnington</name></json:item><json:item><name>R. Iansek</name></json:item><json:item><name>K. Johnson</name></json:item><json:item><name>J.L. Bradshaw</name></json:item></author><host><volume>120</volume><pages><last>1353</last><first>1339</first></pages><author></author><title>Brain</title></host><title>Movement‐related potentials in Parkinson's disease. Motor imagery and movement preparation</title></json:item><json:item><author><json:item><name>D. Devos</name></json:item><json:item><name>P. Derambure</name></json:item><json:item><name>J.L. Bourriez</name></json:item><json:item><name>D.F. Cassim</name></json:item><json:item><name>S. Blond</name></json:item><json:item><name>J.D. Guieu</name></json:item><json:item><name>A. Destee</name></json:item><json:item><name>L. Defebvre</name></json:item></author><host><volume>113</volume><pages><last>1120</last><first>1110</first></pages><author></author><title>Clin. Neurophysiol.</title></host><title>Influence of internal globus pallidus stimulation on motor cortex activation pattern in Parkinson's disease</title></json:item><json:item><host><author></author><title>Devos, D., Labyt, E., Derambure, P., Bourriez, J.L., Cassim, D.F., Blond, S., Guieu, J.D., Destee, A. & Defebvre, L. (2002a) Cortical activation improvement obtained by subthalamic nucleus stimulation in Parkinson's disease and its relation to bradykinesia. In Neurology 2002 Proceedings of the 54th Meeting of the American Academy of Neurology Congress, Denver, 2002, 58 (Suppl. 3), p. A56.</title></host></json:item><json:item><author><json:item><name>W. Gerschlager</name></json:item><json:item><name>F. Alesch</name></json:item><json:item><name>R. Cunnington</name></json:item><json:item><name>L. Deecke</name></json:item><json:item><name>G. Dirnberger</name></json:item><json:item><name>W. Endl</name></json:item><json:item><name>G. Lindinger</name></json:item><json:item><name>W. Lang</name></json:item></author><host><volume>122</volume><pages><last>2373</last><first>2365</first></pages><author></author><title>Brain</title></host><title>Bilateral subthalamic nucleus stimulation improves frontal cortex function in Parkinson's disease. An electrophysiological study of the contingent negative variation</title></json:item><json:item><author><json:item><name>J.D. Guieu</name></json:item><json:item><name>J.L. Bourriez</name></json:item><json:item><name>Ph Derambure</name></json:item><json:item><name>L. Defebvre</name></json:item><json:item><name>F. Cassim</name></json:item></author><host><pages><last>290</last><first>279</first></pages><author></author><title>Event‐Related Desynchronization. Handbook of Electroencephalography and Clinical Neurophysiology. Revised Series</title></host><title>Temporal and spatial aspects of event‐related desynchronization and movement‐related cortical potential</title></json:item><json:item><author><json:item><name>T. Hashimoto</name></json:item><json:item><name>C.M. Elder</name></json:item><json:item><name>M.S. Okun</name></json:item><json:item><name>S.K. Patrick</name></json:item><json:item><name>J.L. Vitek</name></json:item></author><host><volume>23</volume><pages><last>1923</last><first>1916</first></pages><author></author><title>J. Neurosci.</title></host><title>Stimulation of the subthalamic nucleus changes the firing pattern of pallidal neurons</title></json:item><json:item><author><json:item><name>P. Limousin</name></json:item><json:item><name>J. Greene</name></json:item><json:item><name>P. Pollak</name></json:item><json:item><name>J. Rothwell</name></json:item><json:item><name>A.L. Benabid</name></json:item><json:item><name>R. Frackowiak</name></json:item></author><host><volume>42</volume><pages><last>291</last><first>283</first></pages><author></author><title>Ann. Neurol.</title></host><title>Changes in cerebral activity pattern due to subthalamic nucleus or internal pallidum stimulation in Parkinson's disease</title></json:item><json:item><author><json:item><name>J.A. Obeso</name></json:item><json:item><name>M.C. Rodriguez‐Oroz</name></json:item><json:item><name>M. Rodriguez</name></json:item><json:item><name>R. Macias</name></json:item><json:item><name>L. Alvarez</name></json:item><json:item><name>J. Guridi</name></json:item><json:item><name>J. Vitek</name></json:item><json:item><name>M.R. DeLong</name></json:item></author><host><volume>55</volume><pages><last>12</last><first>7</first></pages><issue>Suppl. 6</issue><author></author><title>Neurology</title></host><title>Pathophysiologic basis of surgery for Parkinson's disease</title></json:item><json:item><host><author></author><title>Event‐related synchronization of beta rhythms in idiopathic Parkinson's diseaseEvent‐Related Desynchronization.</title></host></json:item><json:item><author><json:item><name>G. Pfürtscheller</name></json:item><json:item><name>K. Pichler‐Zalaudek</name></json:item><json:item><name>B. Ortmayr</name></json:item><json:item><name>J. Diez</name></json:item><json:item><name>F. Reisecker</name></json:item></author><host><volume>15</volume><pages><last>250</last><first>243</first></pages><author></author><title>J. Clin. Neurophysiol.</title></host><title>Post‐movement beta synchronization in patients with Parkinson's disease</title></json:item><json:item><author><json:item><name>A. Stancak Jr</name></json:item><json:item><name>G. Pfürtscheller</name></json:item></author><host><volume>4</volume><pages><last>183</last><first>171</first></pages><author></author><title>Cognitive Brain Res.</title></host><title>Event‐related desynchronisation of central beta‐rhythms during brisk and slow self‐paced finger movements</title></json:item><json:item><author><json:item><name> </name></json:item></author><host><volume>345</volume><pages><last>963</last><first>956</first></pages><author></author><title>N. Engl. J. Med.</title></host><title>Deep‐brain stimulation of the subthalamic nucleus or the pars interna of the globus pallidus in Parkinson's disease</title></json:item><json:item><author><json:item><name>R.L. Watts</name></json:item><json:item><name>A.S. Mandir</name></json:item></author><host><volume>10</volume><pages><last>469</last><first>451</first></pages><author></author><title>Neurol. Clin.</title></host><title>The role of motor cortex in the pathophysiology of voluntary movement deficits associated with parkinsonism</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>18</volume><publisherId><json:string>EJN</json:string></publisherId><pages><last>1888</last><first>1884</first></pages><issn><json:string>0953-816X</json:string></issn><issue>7</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-9568</json:string></eissn><title>European Journal of Neuroscience</title><doi><json:string>10.1111/(ISSN)1460-9568</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>neurosciences</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>2003</publicationDate><copyrightDate>2003</copyrightDate><doi><json:string>10.1046/j.1460-9568.2003.02925.x</json:string></doi><id>FC5D8CA50AAB4EFF904A1ACC8E4490C219FBE3B2</id><score>0.20432676</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/FC5D8CA50AAB4EFF904A1ACC8E4490C219FBE3B2/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/FC5D8CA50AAB4EFF904A1ACC8E4490C219FBE3B2/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/FC5D8CA50AAB4EFF904A1ACC8E4490C219FBE3B2/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Science, Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2003</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease</title><author xml:id="author-1"><persName><forename type="first">D.</forename><surname>Devos</surname></persName><affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">E.</forename><surname>Labyt</surname></persName><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">F.</forename><surname>Cassim</surname></persName><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">J. L.</forename><surname>Bourriez</surname></persName><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation></author><author xml:id="author-5"><persName><forename type="first">N.</forename><surname>Reyns</surname></persName><affiliation>Department of Neurosurgery, Lille University Medical Centre, France</affiliation></author><author xml:id="author-6"><persName><forename type="first">G.</forename><surname>Touzet</surname></persName><affiliation>Department of Neurosurgery, Lille University Medical Centre, France</affiliation></author><author xml:id="author-7"><persName><forename type="first">S.</forename><surname>Blond</surname></persName><affiliation>Department of Neurosurgery, Lille University Medical Centre, France</affiliation></author><author xml:id="author-8"><persName><forename type="first">J. D.</forename><surname>Guieu</surname></persName><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation></author><author xml:id="author-9"><persName><forename type="first">P.</forename><surname>Derambure</surname></persName><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation></author><author xml:id="author-10"><persName><forename type="first">A.</forename><surname>Destée</surname></persName><affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</affiliation></author><author xml:id="author-11"><persName><forename type="first">L.</forename><surname>Defebvre</surname></persName><affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</affiliation></author></analytic><monogr><title level="j">European Journal of Neuroscience</title><idno type="pISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><idno type="DOI">10.1111/(ISSN)1460-9568</idno><imprint><publisher>Blackwell Science, Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-10"></date><biblScope unit="volume">18</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1884">1884</biblScope><biblScope unit="page" to="1888">1888</biblScope></imprint></monogr><idno type="istex">FC5D8CA50AAB4EFF904A1ACC8E4490C219FBE3B2</idno><idno type="DOI">10.1046/j.1460-9568.2003.02925.x</idno><idno type="ArticleID">EJN2925</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement‐related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l‐dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self‐paced wrist flexion in four conditions according to the presence or not of stimulation and l‐dopa. Compared to without treatment, the motor score improved by ≈ 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l‐dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l‐dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement‐related somatosensory processing at the end of the movement through the basal ganglia into the cortex.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>advanced Parkinsonian</term></item><item><term>EEG</term></item><item><term>event‐related synchronization</term></item><item><term>human</term></item><item><term>l‐dopa</term></item><item><term>movement</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/FC5D8CA50AAB4EFF904A1ACC8E4490C219FBE3B2/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science, Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="10007"><doi origin="wiley">10.1111/ejn.2003.18.issue-7</doi><numberingGroup><numbering type="journalVolume" number="18">18</numbering><numbering type="journalIssue" number="7">7</numbering></numberingGroup><coverDate startDate="2003-10">October 2003</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0188400" status="forIssue"><doi origin="wiley">10.1046/j.1460-9568.2003.02925.x</doi><idGroup><id type="unit" value="EJN2925"></id></idGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2003-10-21"></event><event type="publishedOnlineFinalForm" date="2003-10-21"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1884">1884</numbering><numbering type="pageLast" number="1888">1888</numbering></numberingGroup><correspondenceTo> : Dr David Devos, Hôpital R. Salengro, Clinique Neurologique, CHRU, F‐59037 Lille cedex, France.
E‐mail: <email normalForm="d-devos@chru-lille.fr">d‐devos@chru‐lille.fr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN2925.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 20 May 2003, revised 21 July 2003, accepted 25 July 2003</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="23"></count><count type="wordTotal" number="4632"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease</title><title type="shortAuthors">D. Devos <i>et al.</i></title><title type="short">Subthalamic stimulation and Parkinson's disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>D.</givenNames><familyName>Devos</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>E.</givenNames><familyName>Labyt</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>F.</givenNames><familyName>Cassim</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>J. L.</givenNames><familyName>Bourriez</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a3"><personName><givenNames>N.</givenNames><familyName>Reyns</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a3"><personName><givenNames>G.</givenNames><familyName>Touzet</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a3"><personName><givenNames>S.</givenNames><familyName>Blond</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a2"><personName><givenNames>J. D.</givenNames><familyName>Guieu</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a2"><personName><givenNames>P.</givenNames><familyName>Derambure</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a1"><personName><givenNames>A.</givenNames><familyName>Destée</familyName></personName></creator><creator creatorRole="author" xml:id="cr11" affiliationRef="#a1"><personName><givenNames>L.</givenNames><familyName>Defebvre</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="FR"><unparsedAffiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="FR"><unparsedAffiliation>Department of Neurosurgery, Lille University Medical Centre, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">advanced Parkinsonian</keyword><keyword xml:id="k2">EEG</keyword><keyword xml:id="k3">event‐related synchronization</keyword><keyword xml:id="k4">human</keyword><keyword xml:id="k5"><sc>l</sc>‐dopa</keyword><keyword xml:id="k6">movement</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement‐related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and <sc>l</sc>‐dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self‐paced wrist flexion in four conditions according to the presence or not of stimulation and <sc>l</sc>‐dopa. Compared to without treatment, the motor score improved by ≈ 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under <sc>l</sc>‐dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and <sc>l</sc>‐dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement‐related somatosensory processing at the end of the movement through the basal ganglia into the cortex.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Subthalamic stimulation and Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Devos</namePart><affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Labyt</namePart><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Cassim</namePart><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. L.</namePart><namePart type="family">Bourriez</namePart><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Reyns</namePart><affiliation>Department of Neurosurgery, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Touzet</namePart><affiliation>Department of Neurosurgery, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Blond</namePart><affiliation>Department of Neurosurgery, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. D.</namePart><namePart type="family">Guieu</namePart><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Derambure</namePart><affiliation>Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Destée</namePart><affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Defebvre</namePart><affiliation>Department of Neurology, EA2683, Lille University Medical Centre, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science, Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2003-10</dateIssued><edition>Received 20 May 2003, revised 21 July 2003, accepted 25 July 2003</edition><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">2</extent><extent unit="references">23</extent><extent unit="words">4632</extent></physicalDescription><abstract lang="en">In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement‐related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l‐dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self‐paced wrist flexion in four conditions according to the presence or not of stimulation and l‐dopa. Compared to without treatment, the motor score improved by ≈ 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l‐dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l‐dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement‐related somatosensory processing at the end of the movement through the basal ganglia into the cortex.</abstract><subject lang="en"><genre>keywords</genre><topic>advanced Parkinsonian</topic><topic>EEG</topic><topic>event‐related synchronization</topic><topic>human</topic><topic>l‐dopa</topic><topic>movement</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>1884</start><end>1888</end></extent></part></relatedItem><identifier type="istex">FC5D8CA50AAB4EFF904A1ACC8E4490C219FBE3B2</identifier><identifier type="DOI">10.1046/j.1460-9568.2003.02925.x</identifier><identifier type="ArticleID">EJN2925</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science, Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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