Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients
Identifieur interne : 002241 ( Istex/Corpus ); précédent : 002240; suivant : 002242Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients
Auteurs : A. Eusebio ; W. Thevathasan ; L. Doyle Gaynor ; A. Pogosyan ; E. Bye ; T. Foltynie ; L. Zrinzo ; K. Ashkan ; T. Aziz ; P. BrownSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2011-05.
Abstract
Background Although deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a highly effective therapeutic intervention in severe Parkinson's disease, its mechanism of action remains unclear. One possibility is that DBS suppresses local pathologically synchronised oscillatory activity. Methods To explore this, the authors recorded from DBS electrodes implanted in the STN of 16 patients with Parkinson's disease during simultaneous stimulation (pulse width 60 μs; frequency 130 Hz) of the same target using a specially designed amplifier. The authors analysed data from 25 sides. Results The authors found that DBS progressively suppressed peaks in local field potential activity at frequencies between 11 and 30 Hz as voltage was increased beyond a stimulation threshold of 1.5 V. Median peak power had fallen to 54% of baseline values by a stimulation intensity of 3.0 V. Conclusion The findings suggest that DBS can suppress pathological 11–30 Hz activity in the vicinity of stimulation in patients with Parkinson's disease. This suppression occurs at stimulation voltages that are clinically effective.
Url:
DOI: 10.1136/jnnp.2010.217489
Links to Exploration step
ISTEX:293DA10CF672BED0E6B8B1BEFB56FB3229B2D373Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients</title><author><name sortKey="Eusebio, A" sort="Eusebio, A" uniqKey="Eusebio A" first="A" last="Eusebio">A. Eusebio</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology and Movement Disorders, Timone University Hospital, Marseille, France</mods:affiliation></affiliation></author><author><name sortKey="Thevathasan, W" sort="Thevathasan, W" uniqKey="Thevathasan W" first="W" last="Thevathasan">W. Thevathasan</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</mods:affiliation></affiliation></author><author><name sortKey="Doyle Gaynor, L" sort="Doyle Gaynor, L" uniqKey="Doyle Gaynor L" first="L" last="Doyle Gaynor">L. Doyle Gaynor</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Pogosyan, A" sort="Pogosyan, A" uniqKey="Pogosyan A" first="A" last="Pogosyan">A. Pogosyan</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Bye, E" sort="Bye, E" uniqKey="Bye E" first="E" last="Bye">E. Bye</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Foltynie, T" sort="Foltynie, T" uniqKey="Foltynie T" first="T" last="Foltynie">T. Foltynie</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Zrinzo, L" sort="Zrinzo, L" uniqKey="Zrinzo L" first="L" last="Zrinzo">L. Zrinzo</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Ashkan, K" sort="Ashkan, K" uniqKey="Ashkan K" first="K" last="Ashkan">K. Ashkan</name><affiliation><mods:affiliation>Neurosurgery, King's College Hospital, Denmark Hill, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Aziz, T" sort="Aziz, T" uniqKey="Aziz T" first="T" last="Aziz">T. Aziz</name><affiliation><mods:affiliation>Department of Neurological Surgery, John Radcliffe Hospital, Oxford, UK</mods:affiliation></affiliation></author><author><name sortKey="Brown, P" sort="Brown, P" uniqKey="Brown P" first="P" last="Brown">P. Brown</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: peter.brown@clneuro.ox.ac.uk</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:293DA10CF672BED0E6B8B1BEFB56FB3229B2D373</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1136/jnnp.2010.217489</idno><idno type="url">https://api.istex.fr/document/293DA10CF672BED0E6B8B1BEFB56FB3229B2D373/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002241</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002241</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients</title><author><name sortKey="Eusebio, A" sort="Eusebio, A" uniqKey="Eusebio A" first="A" last="Eusebio">A. Eusebio</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology and Movement Disorders, Timone University Hospital, Marseille, France</mods:affiliation></affiliation></author><author><name sortKey="Thevathasan, W" sort="Thevathasan, W" uniqKey="Thevathasan W" first="W" last="Thevathasan">W. Thevathasan</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</mods:affiliation></affiliation></author><author><name sortKey="Doyle Gaynor, L" sort="Doyle Gaynor, L" uniqKey="Doyle Gaynor L" first="L" last="Doyle Gaynor">L. Doyle Gaynor</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Pogosyan, A" sort="Pogosyan, A" uniqKey="Pogosyan A" first="A" last="Pogosyan">A. Pogosyan</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Bye, E" sort="Bye, E" uniqKey="Bye E" first="E" last="Bye">E. Bye</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Foltynie, T" sort="Foltynie, T" uniqKey="Foltynie T" first="T" last="Foltynie">T. Foltynie</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Zrinzo, L" sort="Zrinzo, L" uniqKey="Zrinzo L" first="L" last="Zrinzo">L. Zrinzo</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Ashkan, K" sort="Ashkan, K" uniqKey="Ashkan K" first="K" last="Ashkan">K. Ashkan</name><affiliation><mods:affiliation>Neurosurgery, King's College Hospital, Denmark Hill, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Aziz, T" sort="Aziz, T" uniqKey="Aziz T" first="T" last="Aziz">T. Aziz</name><affiliation><mods:affiliation>Department of Neurological Surgery, John Radcliffe Hospital, Oxford, UK</mods:affiliation></affiliation></author><author><name sortKey="Brown, P" sort="Brown, P" uniqKey="Brown P" first="P" last="Brown">P. Brown</name><affiliation><mods:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: peter.brown@clneuro.ox.ac.uk</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2011-05">2011-05</date><biblScope unit="volume">82</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="569">569</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">293DA10CF672BED0E6B8B1BEFB56FB3229B2D373</idno><idno type="DOI">10.1136/jnnp.2010.217489</idno><idno type="href">jnnp-82-569.pdf</idno><idno type="ArticleID">jnnp217489</idno><idno type="PMID">20935326</idno><idno type="local">jnnp;82/5/569</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background Although deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a highly effective therapeutic intervention in severe Parkinson's disease, its mechanism of action remains unclear. One possibility is that DBS suppresses local pathologically synchronised oscillatory activity. Methods To explore this, the authors recorded from DBS electrodes implanted in the STN of 16 patients with Parkinson's disease during simultaneous stimulation (pulse width 60 μs; frequency 130 Hz) of the same target using a specially designed amplifier. The authors analysed data from 25 sides. Results The authors found that DBS progressively suppressed peaks in local field potential activity at frequencies between 11 and 30 Hz as voltage was increased beyond a stimulation threshold of 1.5 V. Median peak power had fallen to 54% of baseline values by a stimulation intensity of 3.0 V. Conclusion The findings suggest that DBS can suppress pathological 11–30 Hz activity in the vicinity of stimulation in patients with Parkinson's disease. This suppression occurs at stimulation voltages that are clinically effective.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>A Eusebio</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</json:string><json:string>Department of Neurology and Movement Disorders, Timone University Hospital, Marseille, France</json:string></affiliations></json:item><json:item><name>W Thevathasan</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</json:string><json:string>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</json:string></affiliations></json:item><json:item><name>L Doyle Gaynor</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>A Pogosyan</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>E Bye</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>T Foltynie</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>L Zrinzo</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>K Ashkan</name><affiliations><json:string>Neurosurgery, King's College Hospital, Denmark Hill, London, UK</json:string></affiliations></json:item><json:item><name>T Aziz</name><affiliations><json:string>Department of Neurological Surgery, John Radcliffe Hospital, Oxford, UK</json:string></affiliations></json:item><json:item><name>P Brown</name><affiliations><json:string>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</json:string><json:string>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</json:string><json:string>E-mail: peter.brown@clneuro.ox.ac.uk</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Unlocked</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>basal ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>deep brain stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>oscillations</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neurophysiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>electrical stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor physiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>movement disorders</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor</value></json:item></subject><articleId><json:string>jnnp217489</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Background Although deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a highly effective therapeutic intervention in severe Parkinson's disease, its mechanism of action remains unclear. One possibility is that DBS suppresses local pathologically synchronised oscillatory activity. Methods To explore this, the authors recorded from DBS electrodes implanted in the STN of 16 patients with Parkinson's disease during simultaneous stimulation (pulse width 60 μs; frequency 130 Hz) of the same target using a specially designed amplifier. The authors analysed data from 25 sides. Results The authors found that DBS progressively suppressed peaks in local field potential activity at frequencies between 11 and 30 Hz as voltage was increased beyond a stimulation threshold of 1.5 V. Median peak power had fallen to 54% of baseline values by a stimulation intensity of 3.0 V. Conclusion The findings suggest that DBS can suppress pathological 11–30 Hz activity in the vicinity of stimulation in patients with Parkinson's disease. This suppression occurs at stimulation voltages that are clinically effective.</abstract><qualityIndicators><score>8.724</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>10</keywordCount><abstractCharCount>1117</abstractCharCount><pdfWordCount>4816</pdfWordCount><pdfCharCount>30756</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>159</abstractWordCount></qualityIndicators><title>Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients</title><pmid><json:string>20935326</json:string></pmid><refBibs><json:item><author><json:item><name>C Hammond</name></json:item><json:item><name>R Ammari</name></json:item><json:item><name>B Bioulac</name></json:item></author><host><volume>23</volume><author></author><title>Mov Disord</title></host><title>Latest view on the mechanism of action of deep brain stimulation</title></json:item><json:item><author><json:item><name>P Brown</name></json:item><json:item><name>A Eusebio</name></json:item></author><host><volume>23</volume><pages><last>20</last><first>12</first></pages><author></author><title>Mov Disord</title></host><title>Paradoxes of functional neurosurgery: clues from basal ganglia recordings</title></json:item><json:item><author><json:item><name>P Gatev</name></json:item><json:item><name>O Darbin</name></json:item><json:item><name>T Wichmann</name></json:item></author><host><volume>21</volume><author></author><title>Mov Disord</title></host><title>Oscillations in the basal ganglia under normal conditions and in movement disorders</title></json:item><json:item><author><json:item><name>C Hammond</name></json:item><json:item><name>H Bergman</name></json:item><json:item><name>P Brown</name></json:item></author><host><volume>30</volume><author></author><title>Trends Neurosci</title></host><title>Pathological synchronization in Parkinson's disease: networks, models and treatments</title></json:item><json:item><author><json:item><name>PJ Uhlhaas</name></json:item><json:item><name>W Singer</name></json:item></author><host><volume>52</volume><author></author><title>Neuron</title></host><title>Neural synchrony in brain disorders: relevance for cognitive dysfunctions and pathophysiology</title></json:item><json:item><author><json:item><name>M Weinberger</name></json:item><json:item><name>WD Hutchison</name></json:item><json:item><name>J Dostrovsky</name></json:item></author><host><volume>219</volume><pages><last>61</last><first>58</first></pages><author></author><title>Exp Neurol</title></host><title>Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?</title></json:item><json:item><author><json:item><name>L Rossi</name></json:item><json:item><name>G Foffani</name></json:item><json:item><name>S Marceglia</name></json:item></author><host><volume>4</volume><pages><last>106</last><first>96</first></pages><author></author><title>J Neural Eng</title></host><title>An electronic device for artefact suppression in human local field potential recordings during deep brain stimulation</title></json:item><json:item><author><json:item><name>H Bronte-Stewart</name></json:item><json:item><name>C Barberini</name></json:item><json:item><name>MM Koop</name></json:item></author><host><volume>215</volume><author></author><title>Exp Neurol</title></host><title>The STN beta-band profile in Parkinson's disease is stationary and shows prolonged attenuation after deep brain stimulation</title></json:item><json:item><author><json:item><name>P Brown</name></json:item><json:item><name>P Mazzone</name></json:item><json:item><name>A Oliviero</name></json:item></author><host><volume>188</volume><author></author><title>Exp Neurol</title></host><title>Effects of stimulation of the subthalamic area on oscillatory pallidal activity in Parkinson's disease</title></json:item><json:item><author><json:item><name>AA Kuhn</name></json:item><json:item><name>F Kempf</name></json:item><json:item><name>C Brucke</name></json:item></author><host><volume>28</volume><author></author><title>J Neurosci</title></host><title>High-frequency stimulation of the subthalamic nucleus suppresses oscillatory beta activity in patients with Parkinson's disease in parallel with improvement in motor performance</title></json:item><json:item><author><json:item><name>P Silberstein</name></json:item><json:item><name>AA Kuhn</name></json:item><json:item><name>A Kupsch</name></json:item></author><host><volume>126</volume><author></author><title>Brain</title></host><title>Patterning of globus pallidus local field potentials differs between Parkinson's disease and dystonia</title></json:item><json:item><author><json:item><name>B Wingeier</name></json:item><json:item><name>T Tcheng</name></json:item><json:item><name>MM Koop</name></json:item></author><host><volume>197</volume><author></author><title>Exp Neurol</title></host><title>Intra-operative STN DBS attenuates the prominent beta rhythm in the STN in Parkinson's disease</title></json:item><json:item><author><json:item><name>G Foffani</name></json:item><json:item><name>G Ardolino</name></json:item><json:item><name>M Egidi</name></json:item></author><host><volume>69</volume><author></author><title>Brain Res Bull</title></host><title>Subthalamic oscillatory activities at beta or higher frequency do not change after high-frequency DBS in Parkinson's disease</title></json:item><json:item><author><json:item><name>L Rossi</name></json:item><json:item><name>S Marceglia</name></json:item><json:item><name>G Foffani</name></json:item></author><host><volume>76</volume><author></author><title>Brain Res Bull</title></host><title>Subthalamic local field potential oscillations during ongoing deep brain stimulation in Parkinson's disease</title></json:item><json:item><author><json:item><name>CC Chen</name></json:item><json:item><name>A Pogosyan</name></json:item><json:item><name>LU Zrinzo</name></json:item></author><host><volume>198</volume><author></author><title>Exp Neurol</title></host><title>Intra-operative recordings of local field potentials can help localize the subthalamic nucleus in Parkinson's disease surgery</title></json:item><json:item><author><json:item><name>F Alonso-Frech</name></json:item><json:item><name>I Zamarbide</name></json:item><json:item><name>M Alegre</name></json:item></author><host><volume>129</volume><author></author><title>Brain</title></host><title>Slow oscillatory activity and levodopa-induced dyskinesias in Parkinson's disease</title></json:item><json:item><author><json:item><name>D Devos</name></json:item><json:item><name>W Szurhaj</name></json:item><json:item><name>N Reyns</name></json:item></author><host><volume>117</volume><author></author><title>Clin Neurophysiol</title></host><title>Predominance of the contralateral movement-related activity in the subthalamo-cortical loop</title></json:item><json:item><author><json:item><name>Y Miyagi</name></json:item><json:item><name>T Okamoto</name></json:item><json:item><name>T Morioka</name></json:item></author><host><volume>87</volume><author></author><title>Stereotact Funct Neurosurg</title></host><title>Spectral analysis of field potential recordings by deep brain stimulation electrode for localization of subthalamic nucleus in patients with Parkinson's disease</title></json:item><json:item><author><json:item><name>F Yoshida</name></json:item><json:item><name>I Martinez-Torres</name></json:item><json:item><name>A Pogosyan</name></json:item></author><host><volume>81</volume><author></author><title>J Neurol Neuropsych Neurosurg</title></host><title>Value of subthalamic nucleus local field potentials recordings in prediciting stimulation parameters for deep brain stimulation in Parkinson's Disease</title></json:item><json:item><author><json:item><name>A Priori</name></json:item><json:item><name>G Foffani</name></json:item><json:item><name>A Pesenti</name></json:item></author><host><volume>23</volume><pages><last>2</last><first>101</first></pages><issue>Suppl 2</issue><author></author><title>Neurol Sci</title></host><title>Movement-related modulation of neural activity in human basal ganglia and its l-DOPA dependency: recordings from deep brain stimulation electrodes in patients with Parkinson's disease</title></json:item><json:item><author><json:item><name>A Priori</name></json:item><json:item><name>G Foffani</name></json:item><json:item><name>A Pesenti</name></json:item></author><host><volume>189</volume><author></author><title>Exp Neurol</title></host><title>Rhythm-specific pharmacological modulation of subthalamic activity in Parkinson's disease</title></json:item><json:item><author><json:item><name>D Williams</name></json:item><json:item><name>M Tijssen</name></json:item><json:item><name>G Van Bruggen</name></json:item></author><host><volume>125</volume><author></author><title>Brain</title></host><title>Dopamine-dependent changes in the functional connectivity between basal ganglia and cerebral cortex in humans</title></json:item><json:item><author><json:item><name>G Foffani</name></json:item><json:item><name>AM Bianchi</name></json:item><json:item><name>G Baselli</name></json:item></author><host><volume>568</volume><pages><last>711</last><first>699</first></pages><author></author><title>J Physiol</title></host><title>Movement-related frequency modulation of beta oscillatory activity in the human subthalamic nucleus</title></json:item><json:item><author><json:item><name>D Curran-Everett</name></json:item></author><host><volume>279</volume><pages><last>8</last><first>1</first></pages><author></author><title>Am J Physiol Regul Integr Comp Physiol</title></host><title>Multiple comparisons: philosophies and illustrations</title></json:item><json:item><author><json:item><name>AA Kühn</name></json:item><json:item><name>C Brücke</name></json:item><json:item><name>G-H Schneider</name></json:item></author><host><volume>214</volume><author></author><title>Exp Neurol</title></host><title>Beta activity in dystonia patients after drug-induced dopamine deficiency</title></json:item><json:item><author><json:item><name>JC Ecceles</name></json:item></author><host><volume>3</volume><author></author><title>Electroencephalogr Clin Neurophysiol</title></host><title>Interpretation of action potentials evoked in the cerebral cortex</title></json:item><json:item><author><json:item><name>NK Logothetis</name></json:item></author><host><volume>357</volume><author></author><title>Philos Trans R Soc Lond B Biol Sci</title></host><title>The neural basis of the blood-oxygen-level-dependent functional magnetic resonance imaging signal</title></json:item><json:item><author><json:item><name>N Fogelson</name></json:item><json:item><name>D Williams</name></json:item><json:item><name>M Tijssen</name></json:item></author><host><volume>16</volume><pages><last>75</last><first>64</first></pages><author></author><title>Cereb Cortex</title></host><title>Different functional loops between cerebral cortex and the subthalmic area in Parkinson's disease</title></json:item><json:item><author><json:item><name>E Lalo</name></json:item><json:item><name>S Thobois</name></json:item><json:item><name>A Sharott</name></json:item></author><host><volume>28</volume><author></author><title>J Neurosci</title></host><title>Patterns of bidirectional communication between cortex and basal ganglia during movement in patients with Parkinson disease</title></json:item><json:item><author><json:item><name>V Gradinaru</name></json:item><json:item><name>M Mogri</name></json:item><json:item><name>KR Thompson</name></json:item></author><host><volume>324</volume><author></author><title>Science</title></host><title>Optical deconstruction of parkinsonian neural circuitry</title></json:item><json:item><author><json:item><name>AD Dorval</name></json:item><json:item><name>GS Russo</name></json:item><json:item><name>T Hashimoto</name></json:item></author><host><volume>100</volume><author></author><title>J Neurophysiol</title></host><title>Deep brain stimulation reduces neuronal entropy in the MPTP-primate model of Parkinson's disease</title></json:item><json:item><author><json:item><name>EBJ Montgomery</name></json:item><json:item><name>JT Gale</name></json:item></author><host><volume>32</volume><pages><last>407</last><first>388</first></pages><author></author><title>Neurosci Biobehav Rev</title></host><title>Mechanisms of action of deep brain stimulation</title></json:item><json:item><author><json:item><name>L Garcia</name></json:item><json:item><name>G D'Alessandro</name></json:item><json:item><name>B Bioulac</name></json:item></author><host><volume>28</volume><author></author><title>Trends Neurosci</title></host><title>High-frequency stimulation in Parkinson's disease: more or less?</title></json:item><json:item><author><json:item><name>T Hashimoto</name></json:item><json:item><name>CM Elder</name></json:item><json:item><name>MS Okun</name></json:item></author><host><volume>23</volume><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>N Maurice</name></json:item><json:item><name>AM Thierry</name></json:item><json:item><name>J Glowinski</name></json:item></author><host><volume>23</volume><author></author><title>J Neurosci</title></host><title>Spontaneous and evoked activity of substantia nigra pars reticulata neurons during high-frequency stimulation of the subthalamic nucleus</title></json:item><json:item><author><json:item><name>R Hilker</name></json:item><json:item><name>J Voges</name></json:item><json:item><name>T Weber</name></json:item></author><host><volume>71</volume><author></author><title>Neurology</title></host><title>STN-DBS activates the target area in Parkinson disease: an FDG-PET study</title></json:item><json:item><author><json:item><name>MM Koop</name></json:item><json:item><name>A Andrzejewski</name></json:item><json:item><name>BC Hill</name></json:item></author><host><volume>21</volume><author></author><title>Mov Disord</title></host><title>Improvement in a quantitative measure of bradykinesia after microelectrode recording in patients with Parkinson's disease during deep brain stimulation surgery</title></json:item><json:item><author><json:item><name>M Rosa</name></json:item><json:item><name>S Marceglia</name></json:item><json:item><name>D Servello</name></json:item></author><host><volume>222</volume><author></author><title>Exp Neurol</title></host><title>Time dependent subthalamic local field potential changes after DBS surgery in Parkinson's disease</title></json:item><json:item><author><json:item><name>AA Kuhn</name></json:item><json:item><name>A Kupsch</name></json:item><json:item><name>GH Schneider</name></json:item></author><host><volume>23</volume><author></author><title>Eur J Neurosci</title></host><title>Reduction in subthalamic 8–35 Hz oscillatory activity correlates with clinical improvement in Parkinson's disease</title></json:item><json:item><author><json:item><name>AA Kuhn</name></json:item><json:item><name>A Tsui</name></json:item><json:item><name>T Aziz</name></json:item></author><host><volume>215</volume><author></author><title>Exp Neurol</title></host><title>Pathological synchronisation in the subthalamic nucleus of patients with Parkinson's disease relates to both bradykinesia and rigidity</title></json:item><json:item><author><json:item><name>NJ Ray</name></json:item><json:item><name>N Jenkinson</name></json:item><json:item><name>S Wang</name></json:item></author><host><volume>213</volume><author></author><title>Exp Neurol</title></host><title>Local field potential beta activity in the subthalamic nucleus of patients with Parkinson's disease is associated with improvements in bradykinesia after dopamine and deep brain stimulation</title></json:item><json:item><author><json:item><name>AA Kühn</name></json:item><json:item><name>T Trottenberg</name></json:item><json:item><name>A Kivi</name></json:item></author><host><volume>194</volume><author></author><title>Exp Neurol</title></host><title>The relationship between local field potential and neuronal discharge in the subthalamic nucleus of patients with Parkinson's disease</title></json:item><json:item><author><json:item><name>A Zaidel</name></json:item><json:item><name>A Spivak</name></json:item><json:item><name>B Grieb</name></json:item></author><host><volume>133</volume><author></author><title>Brain</title></host><title>Subthalamic span of beta oscillations predicts deep brain stimulation efficacy for patients with Parkinson's disease</title></json:item><json:item><author><json:item><name>JA Saint-Cyr</name></json:item><json:item><name>T Hoque</name></json:item><json:item><name>LC Pereira</name></json:item></author><host><volume>97</volume><author></author><title>J Neurosurg</title></host><title>Localization of clinically effective stimulating electrodes in the human subthalamic nucleus on magnetic resonance imaging</title></json:item><json:item><author><json:item><name>J Voges</name></json:item><json:item><name>J Volkmann</name></json:item><json:item><name>N Allert</name></json:item></author><host><volume>96</volume><author></author><title>J Neurosurg</title></host><title>Bilateral high-frequency stimulation in the subthalamic nucleus for the treatment of Parkinson disease: correlation of therapeutic effect with anatomical electrode position</title></json:item><json:item><author><json:item><name>P Plaha</name></json:item><json:item><name>Y Ben-Shlomo</name></json:item><json:item><name>NK Patel</name></json:item></author><host><volume>129</volume><author></author><title>Brain</title></host><title>Stimulation of the caudal zona incerta is superior to stimulation of the subthalamic nucleus in improving contralateral parkinsonism</title></json:item><json:item><author><json:item><name>E Moro</name></json:item><json:item><name>RJ Esselink</name></json:item><json:item><name>J Xie</name></json:item></author><host><volume>59</volume><author></author><title>Neurology</title></host><title>The impact on Parkinson's disease of electrical parameter settings in STN stimulation</title></json:item><json:item><author><json:item><name>R Levy</name></json:item><json:item><name>P Ashby</name></json:item><json:item><name>WD Hutchison</name></json:item></author><host><volume>125</volume><author></author><title>Brain</title></host><title>Dependence of subthalamic nucleus oscillations on movement and dopamine in Parkinson's disease</title></json:item><json:item><author><json:item><name>M Weinberger</name></json:item><json:item><name>N Mahant</name></json:item><json:item><name>WD Hutchison</name></json:item></author><host><volume>96</volume><author></author><title>J Neurophysiol</title></host><title>Beta oscillatory activity in the subthalamic nucleus and its relation to dopaminergic response in Parkinson's disease</title></json:item><json:item><author><json:item><name>S Stanslaski</name></json:item><json:item><name>P Cong</name></json:item><json:item><name>D Carlson</name></json:item></author><host><volume>2009</volume><author></author><title>Conf Proc IEEE Eng Med Biol Soc</title></host><title>An implantable bi-directional brain–machine interface system for chronic neuroprosthesis research</title></json:item><json:item><author><json:item><name>CC Chen</name></json:item><json:item><name>YT Hsu</name></json:item><json:item><name>HL Chan</name></json:item></author><host><volume>224</volume><author></author><title>Exp Neurol</title></host><title>Complexity of subthalamic 13–35 Hz oscillatory activity directly correlates with clinical impairment in patients with Parkinson's disease</title></json:item></refBibs><genre><json:string>research-article</json:string></genre><host><volume>82</volume><publisherId><json:string>jnnp</json:string></publisherId><pages><first>569</first></pages><issn><json:string>0022-3050</json:string></issn><issue>5</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-330X</json:string></eissn><title>Journal of Neurology, Neurosurgery & Psychiatry</title></host><categories><wos><json:string>social science</json:string><json:string>psychiatry</json:string><json:string>science</json:string><json:string>surgery</json:string><json:string>clinical neurology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>2011</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1136/jnnp.2010.217489</json:string></doi><id>293DA10CF672BED0E6B8B1BEFB56FB3229B2D373</id><score>0.11409356</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/293DA10CF672BED0E6B8B1BEFB56FB3229B2D373/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/293DA10CF672BED0E6B8B1BEFB56FB3229B2D373/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/293DA10CF672BED0E6B8B1BEFB56FB3229B2D373/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>BMJ Publishing Group Ltd</publisher><availability status="free"><p>Open Access</p></availability><date>2010-10-09</date></publicationStmt><notesStmt><note>P Brown holds a consultancy with Medtronic Inc.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients</title><author xml:id="author-1"><persName><forename type="first">A</forename><surname>Eusebio</surname></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><affiliation>Department of Neurology and Movement Disorders, Timone University Hospital, Marseille, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">W</forename><surname>Thevathasan</surname></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</affiliation></author><author xml:id="author-3"><persName><forename type="first">L</forename><surname>Doyle Gaynor</surname></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation></author><author xml:id="author-4"><persName><forename type="first">A</forename><surname>Pogosyan</surname></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation></author><author xml:id="author-5"><persName><forename type="first">E</forename><surname>Bye</surname></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation></author><author xml:id="author-6"><persName><forename type="first">T</forename><surname>Foltynie</surname></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation></author><author xml:id="author-7"><persName><forename type="first">L</forename><surname>Zrinzo</surname></persName><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation></author><author xml:id="author-8"><persName><forename type="first">K</forename><surname>Ashkan</surname></persName><affiliation>Neurosurgery, King's College Hospital, Denmark Hill, London, UK</affiliation></author><author xml:id="author-9"><persName><forename type="first">T</forename><surname>Aziz</surname></persName><affiliation>Department of Neurological Surgery, John Radcliffe Hospital, Oxford, UK</affiliation></author><author xml:id="author-10" corresp="yes"><persName><forename type="first">P</forename><surname>Brown</surname></persName><email>peter.brown@clneuro.ox.ac.uk</email><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</affiliation></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2011-05"></date><biblScope unit="volume">82</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="569">569</biblScope></imprint></monogr><idno type="istex">293DA10CF672BED0E6B8B1BEFB56FB3229B2D373</idno><idno type="DOI">10.1136/jnnp.2010.217489</idno><idno type="href">jnnp-82-569.pdf</idno><idno type="ArticleID">jnnp217489</idno><idno type="PMID">20935326</idno><idno type="local">jnnp;82/5/569</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010-10-09</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Background Although deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a highly effective therapeutic intervention in severe Parkinson's disease, its mechanism of action remains unclear. One possibility is that DBS suppresses local pathologically synchronised oscillatory activity. Methods To explore this, the authors recorded from DBS electrodes implanted in the STN of 16 patients with Parkinson's disease during simultaneous stimulation (pulse width 60 μs; frequency 130 Hz) of the same target using a specially designed amplifier. The authors analysed data from 25 sides. Results The authors found that DBS progressively suppressed peaks in local field potential activity at frequencies between 11 and 30 Hz as voltage was increased beyond a stimulation threshold of 1.5 V. Median peak power had fallen to 54% of baseline values by a stimulation intensity of 3.0 V. Conclusion The findings suggest that DBS can suppress pathological 11–30 Hz activity in the vicinity of stimulation in patients with Parkinson's disease. This suppression occurs at stimulation voltages that are clinically effective.</p></abstract><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Unlocked</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>keywords</head><item><term>Parkinson's disease</term></item><item><term>basal ganglia</term></item><item><term>deep brain stimulation</term></item><item><term>oscillations</term></item><item><term>neurophysiology</term></item><item><term>electrical stimulation</term></item><item><term>motor physiology</term></item><item><term>movement disorders</term></item><item><term>motor</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-10-09">Created</change><change when="2011-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/293DA10CF672BED0E6B8B1BEFB56FB3229B2D373/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-id journal-id-type="publisher-id">jnnp</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><abbrev-journal-title>J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">jnnp217489</article-id><article-id pub-id-type="doi">10.1136/jnnp.2010.217489</article-id><article-id pub-id-type="other">jnnp;82/5/569</article-id><article-id pub-id-type="other">jnnp;jnnp.2010.217489</article-id><article-id pub-id-type="pmid">20935326</article-id><article-id pub-id-type="other">569</article-id><article-id pub-id-type="other">jnnp.2010.217489</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research paper</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Unlocked</subject></subj-group></article-categories><title-group><article-title>Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Eusebio</surname><given-names>A</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Thevathasan</surname><given-names>W</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff3">3</xref></contrib><contrib contrib-type="author"><name><surname>Doyle Gaynor</surname><given-names>L</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Pogosyan</surname><given-names>A</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Bye</surname><given-names>E</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Foltynie</surname><given-names>T</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Zrinzo</surname><given-names>L</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Ashkan</surname><given-names>K</given-names></name><xref ref-type="aff" rid="aff4">4</xref></contrib><contrib contrib-type="author"><name><surname>Aziz</surname><given-names>T</given-names></name><xref ref-type="aff" rid="aff5">5</xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Brown</surname><given-names>P</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff3">3</xref></contrib></contrib-group><aff id="aff1"><label>1</label>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</aff><aff id="aff2"><label>2</label>Department of Neurology and Movement Disorders, Timone University Hospital, Marseille, France</aff><aff id="aff3"><label>3</label>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</aff><aff id="aff4"><label>4</label>Neurosurgery, King's College Hospital, Denmark Hill, London, UK</aff><aff id="aff5"><label>5</label>Department of Neurological Surgery, John Radcliffe Hospital, Oxford, UK</aff><author-notes><corresp><label>Correspondence to</label> Professor P Brown, Department of Clinical Neurology, John Radcliffe Hospital, Oxford OX3 9DU, UK; <email>peter.brown@clneuro.ox.ac.uk</email></corresp><fn fn-type="other"><p>P Brown holds a consultancy with Medtronic Inc.</p></fn></author-notes><pub-date pub-type="epub-original"><day>9</day><month>10</month><year>2010</year></pub-date><pub-date pub-type="ppub"><month>5</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>9</day><month>10</month><year>2010</year></pub-date><volume>82</volume><volume-id pub-id-type="other">82</volume-id><volume-id pub-id-type="other">82</volume-id><issue>5</issue><issue-id pub-id-type="other">jnnp;82/5</issue-id><issue-id pub-id-type="other">5</issue-id><issue-id pub-id-type="other">82/5</issue-id><fpage>569</fpage><history><date date-type="received"><day>19</day><month>5</month><year>2010</year></date><date date-type="rev-recd"><day>27</day><month>8</month><year>2010</year></date><date date-type="accepted"><day>2</day><month>9</month><year>2010</year></date></history><permissions><copyright-statement>© 2011, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</copyright-statement><copyright-year>2011</copyright-year><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/"><p>This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/2.0/">http://creativecommons.org/licenses/by-nc/2.0/</ext-link> and <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/2.0/legalcode">http://creativecommons.org/licenses/by-nc/2.0/legalcode</ext-link>.</p></license></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-82-569.pdf"></self-uri><abstract><sec><title>Background</title><p>Although deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a highly effective therapeutic intervention in severe Parkinson's disease, its mechanism of action remains unclear. One possibility is that DBS suppresses local pathologically synchronised oscillatory activity.</p></sec><sec><title>Methods</title><p>To explore this, the authors recorded from DBS electrodes implanted in the STN of 16 patients with Parkinson's disease during simultaneous stimulation (pulse width 60 μs; frequency 130 Hz) of the same target using a specially designed amplifier. The authors analysed data from 25 sides.</p></sec><sec><title>Results</title><p>The authors found that DBS progressively suppressed peaks in local field potential activity at frequencies between 11 and 30 Hz as voltage was increased beyond a stimulation threshold of 1.5 V. Median peak power had fallen to 54% of baseline values by a stimulation intensity of 3.0 V.</p></sec><sec><title>Conclusion</title><p>The findings suggest that DBS can suppress pathological 11–30 Hz activity in the vicinity of stimulation in patients with Parkinson's disease. This suppression occurs at stimulation voltages that are clinically effective.</p></sec></abstract><kwd-group><kwd>Parkinson's disease</kwd><kwd>basal ganglia</kwd><kwd>deep brain stimulation</kwd><kwd>oscillations</kwd><kwd>neurophysiology</kwd><kwd>electrical stimulation</kwd><kwd>motor physiology</kwd><kwd>movement disorders</kwd><kwd>motor</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Eusebio</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><affiliation>Department of Neurology and Movement Disorders, Timone University Hospital, Marseille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Thevathasan</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Doyle Gaynor</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Pogosyan</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Bye</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Foltynie</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Zrinzo</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Ashkan</namePart><affiliation>Neurosurgery, King's College Hospital, Denmark Hill, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Aziz</namePart><affiliation>Department of Neurological Surgery, John Radcliffe Hospital, Oxford, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">P</namePart><namePart type="family">Brown</namePart><affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation><affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</affiliation><affiliation>E-mail: peter.brown@clneuro.ox.ac.uk</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><genre>hwp-journal-coll</genre><topic>Unlocked</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2011-05</dateIssued><dateCreated encoding="w3cdtf">2010-10-09</dateCreated><copyrightDate encoding="w3cdtf">2010</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>Background Although deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a highly effective therapeutic intervention in severe Parkinson's disease, its mechanism of action remains unclear. One possibility is that DBS suppresses local pathologically synchronised oscillatory activity. Methods To explore this, the authors recorded from DBS electrodes implanted in the STN of 16 patients with Parkinson's disease during simultaneous stimulation (pulse width 60 μs; frequency 130 Hz) of the same target using a specially designed amplifier. The authors analysed data from 25 sides. Results The authors found that DBS progressively suppressed peaks in local field potential activity at frequencies between 11 and 30 Hz as voltage was increased beyond a stimulation threshold of 1.5 V. Median peak power had fallen to 54% of baseline values by a stimulation intensity of 3.0 V. Conclusion The findings suggest that DBS can suppress pathological 11–30 Hz activity in the vicinity of stimulation in patients with Parkinson's disease. This suppression occurs at stimulation voltages that are clinically effective.</abstract><note type="footnotes">P Brown holds a consultancy with Medtronic Inc.</note><subject><genre>keywords</genre><topic>Parkinson's disease</topic><topic>basal ganglia</topic><topic>deep brain stimulation</topic><topic>oscillations</topic><topic>neurophysiology</topic><topic>electrical stimulation</topic><topic>motor physiology</topic><topic>movement disorders</topic><topic>motor</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID">jnnp</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>82</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>569</start></extent></part></relatedItem><identifier type="istex">293DA10CF672BED0E6B8B1BEFB56FB3229B2D373</identifier><identifier type="DOI">10.1136/jnnp.2010.217489</identifier><identifier type="href">jnnp-82-569.pdf</identifier><identifier type="ArticleID">jnnp217489</identifier><identifier type="PMID">20935326</identifier><identifier type="local">jnnp;82/5/569</identifier><accessCondition type="use and reproduction" contentType="open-access">This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: http://creativecommons.org/licenses/by-nc/2.0/ and http://creativecommons.org/licenses/by-nc/2.0/legalcode.</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><extension>jpeg</extension><original>true</original><mimetype>image/jpeg</mimetype><uri>https://api.istex.fr/document/293DA10CF672BED0E6B8B1BEFB56FB3229B2D373/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002241 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 002241 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:293DA10CF672BED0E6B8B1BEFB56FB3229B2D373
|texte= Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients
}}
| This area was generated with Dilib version V0.6.29. |  |