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.
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DOI: 10.1136/jnnp.2010.217489
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<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>
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<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>
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<notesStmt><note>P Brown holds a consultancy with Medtronic Inc.</note>
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<surname>Eusebio</surname>
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<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>
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<surname>Thevathasan</surname>
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<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>
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<author xml:id="author-3"><persName><forename type="first">L</forename>
<surname>Doyle Gaynor</surname>
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<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation>
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<surname>Pogosyan</surname>
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<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation>
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<author xml:id="author-5"><persName><forename type="first">E</forename>
<surname>Bye</surname>
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<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation>
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<author xml:id="author-6"><persName><forename type="first">T</forename>
<surname>Foltynie</surname>
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<affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, UK</affiliation>
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<affiliation>Neurosurgery, King's College Hospital, Denmark Hill, London, UK</affiliation>
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<surname>Aziz</surname>
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<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>
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<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>
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<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>
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<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>
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<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>
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<affiliation>Department of Clinical Neurology, John Radcliffe Hospital, Oxford, UK</affiliation>
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<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>
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