Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception
Identifieur interne : 001388 ( Istex/Corpus ); précédent : 001387; suivant : 001389Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception
Auteurs : Aparna Wagle Shukla ; Elena Moro ; Carolyn Gunraj ; Andres Lozano ; Mojgan Hodaie ; Anthony Lang ; Robert ChenSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2013-09.
Abstract
Objective Sensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used to measure sensorimotor integration. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been found to restore these abnormalities, but the time course of these changes is not known. We prospectively evaluated the short-term and long-term effects of STN DBS on SAI, LAI and proprioception. We hypothesised plasticity changes induced by chronic stimulation are necessary to normalise sensorimotor integration and proprioception. Methods Patients with PD were studied preoperatively, at 1 month and more than 6 months postoperatively. SAI was tested with median nerve stimulation to the wrist preceding TMS pulse to motor cortex by ∼20 ms and LAI by 200 ms. Proprioception (distance and spatial errors) in the arm was quantitatively assessed. For postoperative assessments, patients were studied in the medication-off/stimulator-off, medication-off/stimulator-on, medication-on/stimulator-off and medication-on/stimulator-on conditions. Results 11 patients with PD and 10 controls were enrolled. Preoperatively, SAI and proprioception was abnormal during the medication-on conditions and LAI was reduced regardless of the medication status. STN DBS had no significant effect on SAI, LAI and proprioception at 1 month. However, at 6 months SAI, LAI and distance errors were normalised in the medication-on/stimulator-on condition. Spatial error was normalised with DBS on and off. Conclusions Chronic STN DBS in PD normalises sensorimotor integration and proprioception, likely through long-term plastic changes in the basal ganglia thalamocortical circuit.
Url:
DOI: 10.1136/jnnp-2012-304102
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Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gunraj, Carolyn" sort="Gunraj, Carolyn" uniqKey="Gunraj C" first="Carolyn" last="Gunraj">Carolyn Gunraj</name><affiliation><mods:affiliation>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name><affiliation><mods:affiliation>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Hodaie, Mojgan" sort="Hodaie, Mojgan" uniqKey="Hodaie M" first="Mojgan" last="Hodaie">Mojgan Hodaie</name><affiliation><mods:affiliation>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lang, Anthony" sort="Lang, Anthony" uniqKey="Lang A" first="Anthony" last="Lang">Anthony Lang</name><affiliation><mods:affiliation>Edmond J. 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Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gunraj, Carolyn" sort="Gunraj, Carolyn" uniqKey="Gunraj C" first="Carolyn" last="Gunraj">Carolyn Gunraj</name><affiliation><mods:affiliation>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name><affiliation><mods:affiliation>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Hodaie, Mojgan" sort="Hodaie, Mojgan" uniqKey="Hodaie M" first="Mojgan" last="Hodaie">Mojgan Hodaie</name><affiliation><mods:affiliation>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lang, Anthony" sort="Lang, Anthony" uniqKey="Lang A" first="Anthony" last="Lang">Anthony Lang</name><affiliation><mods:affiliation>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name><affiliation><mods:affiliation>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</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="2013-09">2013-09</date><biblScope unit="volume">84</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1020">1020</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30</idno><idno type="DOI">10.1136/jnnp-2012-304102</idno><idno type="href">jnnp-84-1020.pdf</idno><idno type="ArticleID">jnnp-2012-304102</idno><idno type="PMID">23616568</idno><idno type="local">jnnp;84/9/1020</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">Objective Sensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used to measure sensorimotor integration. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been found to restore these abnormalities, but the time course of these changes is not known. We prospectively evaluated the short-term and long-term effects of STN DBS on SAI, LAI and proprioception. We hypothesised plasticity changes induced by chronic stimulation are necessary to normalise sensorimotor integration and proprioception. Methods Patients with PD were studied preoperatively, at 1 month and more than 6 months postoperatively. SAI was tested with median nerve stimulation to the wrist preceding TMS pulse to motor cortex by ∼20 ms and LAI by 200 ms. Proprioception (distance and spatial errors) in the arm was quantitatively assessed. For postoperative assessments, patients were studied in the medication-off/stimulator-off, medication-off/stimulator-on, medication-on/stimulator-off and medication-on/stimulator-on conditions. Results 11 patients with PD and 10 controls were enrolled. Preoperatively, SAI and proprioception was abnormal during the medication-on conditions and LAI was reduced regardless of the medication status. STN DBS had no significant effect on SAI, LAI and proprioception at 1 month. However, at 6 months SAI, LAI and distance errors were normalised in the medication-on/stimulator-on condition. Spatial error was normalised with DBS on and off. Conclusions Chronic STN DBS in PD normalises sensorimotor integration and proprioception, likely through long-term plastic changes in the basal ganglia thalamocortical circuit.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>Aparna Wagle Shukla</name><affiliations><json:string>Center for Movement Disorders and Neurorestoration, University of Florida, Gainesville, Florida, USA</json:string></affiliations></json:item><json:item><name>Elena Moro</name><affiliations><json:string>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</json:string><json:string>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Carolyn Gunraj</name><affiliations><json:string>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Andres Lozano</name><affiliations><json:string>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Mojgan Hodaie</name><affiliations><json:string>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Anthony Lang</name><affiliations><json:string>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</json:string><json:string>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Robert Chen</name><affiliations><json:string>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</json:string><json:string>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</json:string><json:string>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</json:string></affiliations></json:item></author><subject><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>NEUROPHYSIOLOGY</value></json:item></subject><articleId><json:string>jnnp-2012-304102</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Objective Sensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used to measure sensorimotor integration. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been found to restore these abnormalities, but the time course of these changes is not known. We prospectively evaluated the short-term and long-term effects of STN DBS on SAI, LAI and proprioception. We hypothesised plasticity changes induced by chronic stimulation are necessary to normalise sensorimotor integration and proprioception. Methods Patients with PD were studied preoperatively, at 1 month and more than 6 months postoperatively. SAI was tested with median nerve stimulation to the wrist preceding TMS pulse to motor cortex by ∼20 ms and LAI by 200 ms. Proprioception (distance and spatial errors) in the arm was quantitatively assessed. For postoperative assessments, patients were studied in the medication-off/stimulator-off, medication-off/stimulator-on, medication-on/stimulator-off and medication-on/stimulator-on conditions. Results 11 patients with PD and 10 controls were enrolled. Preoperatively, SAI and proprioception was abnormal during the medication-on conditions and LAI was reduced regardless of the medication status. STN DBS had no significant effect on SAI, LAI and proprioception at 1 month. However, at 6 months SAI, LAI and distance errors were normalised in the medication-on/stimulator-on condition. Spatial error was normalised with DBS on and off. Conclusions Chronic STN DBS in PD normalises sensorimotor integration and proprioception, likely through long-term plastic changes in the basal ganglia thalamocortical circuit.</abstract><qualityIndicators><score>7.868</score><pdfWordCount>5700</pdfWordCount><pdfCharCount>38424</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>239</abstractWordCount><abstractCharCount>1800</abstractCharCount><keywordCount>2</keywordCount></qualityIndicators><title>Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception</title><pmid><json:string>23616568</json:string></pmid><genre><json:string>research-article</json:string></genre><host><title>Journal of Neurology, Neurosurgery & Psychiatry</title><language><json:string>unknown</json:string></language><issn><json:string>0022-3050</json:string></issn><eissn><json:string>1468-330X</json:string></eissn><publisherId><json:string>jnnp</json:string></publisherId><volume>84</volume><issue>9</issue><pages><first>1020</first></pages><genre><json:string>journal</json:string></genre></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><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string></inist></categories><publicationDate>2013</publicationDate><copyrightDate>2013</copyrightDate><doi><json:string>10.1136/jnnp-2012-304102</json:string></doi><id>506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>BMJ Publishing Group Ltd</publisher><availability><p>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</p></availability><date>2013-04-24</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception</title><author xml:id="author-1"><persName><forename type="first">Aparna</forename><surname>Wagle Shukla</surname></persName><affiliation>Center for Movement Disorders and Neurorestoration, University of Florida, Gainesville, Florida, USA</affiliation></author><author xml:id="author-2"><persName><forename type="first">Elena</forename><surname>Moro</surname></persName><affiliation>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</affiliation><affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation></author><author xml:id="author-3"><persName><forename type="first">Carolyn</forename><surname>Gunraj</surname></persName><affiliation>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</affiliation></author><author xml:id="author-4"><persName><forename type="first">Andres</forename><surname>Lozano</surname></persName><affiliation>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation></author><author xml:id="author-5"><persName><forename type="first">Mojgan</forename><surname>Hodaie</surname></persName><affiliation>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation></author><author xml:id="author-6"><persName><forename type="first">Anthony</forename><surname>Lang</surname></persName><affiliation>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</affiliation><affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation></author><author xml:id="author-7"><persName><forename type="first">Robert</forename><surname>Chen</surname></persName><affiliation>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</affiliation><affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation><affiliation>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</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="2013-09"></date><biblScope unit="volume">84</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1020">1020</biblScope></imprint></monogr><idno type="istex">506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30</idno><idno type="DOI">10.1136/jnnp-2012-304102</idno><idno type="href">jnnp-84-1020.pdf</idno><idno type="ArticleID">jnnp-2012-304102</idno><idno type="PMID">23616568</idno><idno type="local">jnnp;84/9/1020</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2013-04-24</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Objective Sensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used to measure sensorimotor integration. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been found to restore these abnormalities, but the time course of these changes is not known. We prospectively evaluated the short-term and long-term effects of STN DBS on SAI, LAI and proprioception. We hypothesised plasticity changes induced by chronic stimulation are necessary to normalise sensorimotor integration and proprioception. Methods Patients with PD were studied preoperatively, at 1 month and more than 6 months postoperatively. SAI was tested with median nerve stimulation to the wrist preceding TMS pulse to motor cortex by ∼20 ms and LAI by 200 ms. Proprioception (distance and spatial errors) in the arm was quantitatively assessed. For postoperative assessments, patients were studied in the medication-off/stimulator-off, medication-off/stimulator-on, medication-on/stimulator-off and medication-on/stimulator-on conditions. Results 11 patients with PD and 10 controls were enrolled. Preoperatively, SAI and proprioception was abnormal during the medication-on conditions and LAI was reduced regardless of the medication status. STN DBS had no significant effect on SAI, LAI and proprioception at 1 month. However, at 6 months SAI, LAI and distance errors were normalised in the medication-on/stimulator-on condition. Spatial error was normalised with DBS on and off. Conclusions Chronic STN DBS in PD normalises sensorimotor integration and proprioception, likely through long-term plastic changes in the basal ganglia thalamocortical circuit.</p></abstract><textClass><keywords scheme="keyword"><list><head>keywords</head><item><term>PARKINSON'S DISEASE</term></item><item><term>NEUROPHYSIOLOGY</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2013-04-24">Created</change><change when="2013-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30/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">jnnp-2012-304102</article-id><article-id pub-id-type="doi">10.1136/jnnp-2012-304102</article-id><article-id pub-id-type="other">jnnp;84/9/1020</article-id><article-id pub-id-type="other">jnnp;jnnp-2012-304102</article-id><article-id pub-id-type="pmid">23616568</article-id><article-id pub-id-type="other">1020</article-id><article-id pub-id-type="other">jnnp-2012-304102</article-id><article-categories><subj-group subj-group-type="heading"><subject>Movement disorders</subject></subj-group><series-title>Research paper</series-title></article-categories><title-group><article-title>Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Wagle Shukla</surname><given-names>Aparna</given-names></name><xref ref-type="aff" rid="af1">1</xref></contrib><contrib contrib-type="author"><name><surname>Moro</surname><given-names>Elena</given-names></name><xref ref-type="aff" rid="af2">2</xref><xref ref-type="aff" rid="af3">3</xref></contrib><contrib contrib-type="author"><name><surname>Gunraj</surname><given-names>Carolyn</given-names></name><xref ref-type="aff" rid="af4">4</xref></contrib><contrib contrib-type="author"><name><surname>Lozano</surname><given-names>Andres</given-names></name><xref ref-type="aff" rid="af5">5</xref></contrib><contrib contrib-type="author"><name><surname>Hodaie</surname><given-names>Mojgan</given-names></name><xref ref-type="aff" rid="af5">5</xref></contrib><contrib contrib-type="author"><name><surname>Lang</surname><given-names>Anthony</given-names></name><xref ref-type="aff" rid="af2">2</xref><xref ref-type="aff" rid="af3">3</xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>Robert</given-names></name><xref ref-type="aff" rid="af2">2</xref><xref ref-type="aff" rid="af3">3</xref><xref ref-type="aff" rid="af4">4</xref></contrib></contrib-group><aff id="af1"><label>1</label><institution>Center for Movement Disorders and Neurorestoration</institution>, <institution>University of Florida</institution>, <addr-line>Gainesville, Florida</addr-line>, <country>USA</country></aff><aff id="af2"><label>2</label><addr-line>Edmond J. Safra Program</addr-line>, <institution>Parkinson's Disease and National Parkinson's Disease Centre of Excellence</institution>, <addr-line>Toronto, Ontario</addr-line>, <country>Canada</country></aff><aff id="af3"><label>3</label><addr-line>Division of Neurology, Department of Medicine</addr-line>, <institution>University Health Network</institution>, <institution>University of Toronto</institution>, <addr-line>Toronto, Ontario</addr-line>, <country>Canada</country></aff><aff id="af4"><label>4</label><addr-line>Division of Brain Imaging and Behavior Systems—Neuroscience</addr-line>, <institution>Toronto Western Research Institute, University Health Network</institution>, <addr-line>Toronto, Ontario</addr-line>, <country>Canada</country></aff><aff id="af5"><label>5</label><addr-line>Division of Neurosurgery, Department of Surgery</addr-line>, <institution>University Health Network</institution>, <institution>University of Toronto</institution>, <addr-line>Toronto, Ontario</addr-line>, <country>Canada</country></aff><author-notes><corresp><label>Correspondence to</label> Dr Robert Chen, Toronto Western Hospital, 7MC411, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8; <email>robert.chen@uhn.ca</email></corresp></author-notes><pub-date pub-type="ppub"><month>9</month><year>2013</year></pub-date><pub-date pub-type="epub-original"><day>24</day><month>4</month><year>2013</year></pub-date><pub-date pub-type="epub"><day>24</day><month>4</month><year>2013</year></pub-date><volume>84</volume><volume-id pub-id-type="other">84</volume-id><volume-id pub-id-type="other">84</volume-id><issue>9</issue><issue-id pub-id-type="other">jnnp;84/9</issue-id><issue-id pub-id-type="other">9</issue-id><issue-id pub-id-type="other">84/9</issue-id><fpage>1020</fpage><history><date date-type="received"><day>5</day><month>9</month><year>2012</year></date><date date-type="rev-recd"><day>14</day><month>3</month><year>2013</year></date><date date-type="accepted"><day>25</day><month>3</month><year>2013</year></date></history><permissions><copyright-statement>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>2013</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-84-1020.pdf"></self-uri><abstract><sec><title>Objective</title><p>Sensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used to measure sensorimotor integration. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been found to restore these abnormalities, but the time course of these changes is not known. We prospectively evaluated the short-term and long-term effects of STN DBS on SAI, LAI and proprioception. We hypothesised plasticity changes induced by chronic stimulation are necessary to normalise sensorimotor integration and proprioception.</p></sec><sec><title>Methods</title><p>Patients with PD were studied preoperatively, at 1 month and more than 6 months postoperatively. SAI was tested with median nerve stimulation to the wrist preceding TMS pulse to motor cortex by ∼20 ms and LAI by 200 ms. Proprioception (distance and spatial errors) in the arm was quantitatively assessed. For postoperative assessments, patients were studied in the medication-off/stimulator-off, medication-off/stimulator-on, medication-on/stimulator-off and medication-on/stimulator-on conditions.</p></sec><sec><title>Results</title><p>11 patients with PD and 10 controls were enrolled. Preoperatively, SAI and proprioception was abnormal during the medication-on conditions and LAI was reduced regardless of the medication status. STN DBS had no significant effect on SAI, LAI and proprioception at 1 month. However, at 6 months SAI, LAI and distance errors were normalised in the medication-on/stimulator-on condition. Spatial error was normalised with DBS on and off.</p></sec><sec><title>Conclusions</title><p>Chronic STN DBS in PD normalises sensorimotor integration and proprioception, likely through long-term plastic changes in the basal ganglia thalamocortical circuit.</p></sec></abstract><kwd-group><kwd>PARKINSON'S DISEASE</kwd><kwd>NEUROPHYSIOLOGY</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception</title><partName>Research paper</partName></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception</title><partName>Research paper</partName></titleInfo><name type="personal"><namePart type="given">Aparna</namePart><namePart type="family">Wagle Shukla</namePart><affiliation>Center for Movement Disorders and Neurorestoration, University of Florida, Gainesville, Florida, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elena</namePart><namePart type="family">Moro</namePart><affiliation>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</affiliation><affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carolyn</namePart><namePart type="family">Gunraj</namePart><affiliation>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andres</namePart><namePart type="family">Lozano</namePart><affiliation>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mojgan</namePart><namePart type="family">Hodaie</namePart><affiliation>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anthony</namePart><namePart type="family">Lang</namePart><affiliation>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</affiliation><affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert</namePart><namePart type="family">Chen</namePart><affiliation>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario, Canada</affiliation><affiliation>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada</affiliation><affiliation>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2013-09</dateIssued><dateCreated encoding="w3cdtf">2013-04-24</dateCreated><copyrightDate encoding="w3cdtf">2013</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>Objective Sensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used to measure sensorimotor integration. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been found to restore these abnormalities, but the time course of these changes is not known. We prospectively evaluated the short-term and long-term effects of STN DBS on SAI, LAI and proprioception. We hypothesised plasticity changes induced by chronic stimulation are necessary to normalise sensorimotor integration and proprioception. Methods Patients with PD were studied preoperatively, at 1 month and more than 6 months postoperatively. SAI was tested with median nerve stimulation to the wrist preceding TMS pulse to motor cortex by ∼20 ms and LAI by 200 ms. Proprioception (distance and spatial errors) in the arm was quantitatively assessed. For postoperative assessments, patients were studied in the medication-off/stimulator-off, medication-off/stimulator-on, medication-on/stimulator-off and medication-on/stimulator-on conditions. Results 11 patients with PD and 10 controls were enrolled. Preoperatively, SAI and proprioception was abnormal during the medication-on conditions and LAI was reduced regardless of the medication status. STN DBS had no significant effect on SAI, LAI and proprioception at 1 month. However, at 6 months SAI, LAI and distance errors were normalised in the medication-on/stimulator-on condition. Spatial error was normalised with DBS on and off. Conclusions Chronic STN DBS in PD normalises sensorimotor integration and proprioception, likely through long-term plastic changes in the basal ganglia thalamocortical circuit.</abstract><subject><genre>keywords</genre><topic>PARKINSON'S DISEASE</topic><topic>NEUROPHYSIOLOGY</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>2013</date><detail type="volume"><caption>vol.</caption><number>84</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1020</start></extent></part></relatedItem><identifier type="istex">506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30</identifier><identifier type="DOI">10.1136/jnnp-2012-304102</identifier><identifier type="href">jnnp-84-1020.pdf</identifier><identifier type="ArticleID">jnnp-2012-304102</identifier><identifier type="PMID">23616568</identifier><identifier type="local">jnnp;84/9/1020</identifier><accessCondition type="use and reproduction" contentType="copyright">Published by the BMJ Publishing Group Limited. 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