Functional imaging of subthalamic nucleus deep brain stimulation in Parkinson's disease
Identifieur interne : 000190 ( Main/Corpus ); précédent : 000189; suivant : 000191Functional imaging of subthalamic nucleus deep brain stimulation in Parkinson's disease
Auteurs : Tessel Boertien ; Ludvic Zrinzo ; Joshua Kahan ; Marjan Jahanshahi ; Marwan Hariz ; Laura Mancini ; Patricia Limousin ; Thomas FoltynieSource :
- Movement Disorders [ 0885-3185 ] ; 2011-08-15.
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Abstract
Deep brain stimulation of the subthalamic nucleus is an accepted treatment for the motor complications of Parkinson's disease. The therapeutic mechanism of action remains incompletely understood. Although the results of deep brain stimulation are similar to the results that can be obtained by lesional surgery, accumulating evidence from functional imaging and clinical neurophysiology suggests that the effects of subthalamic nucleus‐deep brain stimulation are not simply the result of inhibition of subthalamic nucleus activity. Positron emission tomography/single‐photon emission computed tomography has consistently demonstrated changes in cortical activation in response to subthalamic nucleus‐deep brain stimulation. However, the technique has limited spatial and temporal resolution, and therefore the changes in activity of subcortical projection sites of the subthalamic nucleus (such as the globus pallidus, substantia nigra, and thalamus) are not as clear. Clarifying whether clinically relevant effects from subthalamic nucleus‐deep brain stimulation in humans are mediated through inhibition or excitation of orthodromic or antidromic pathways (or both) would contribute to our understanding of the precise mechanism of action of deep brain stimulation and may allow improvements in safety and efficacy of the technique. In this review we discuss the published evidence from functional imaging studies of patients with subthalamic nucleus‐deep brain stimulation to date, together with how these data inform the mechanism of action of deep brain stimulation. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23788
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Clarifying whether clinically relevant effects from subthalamic nucleus‐deep brain stimulation in humans are mediated through inhibition or excitation of orthodromic or antidromic pathways (or both) would contribute to our understanding of the precise mechanism of action of deep brain stimulation and may allow improvements in safety and efficacy of the technique. In this review we discuss the published evidence from functional imaging studies of patients with subthalamic nucleus‐deep brain stimulation to date, together with how these data inform the mechanism of action of deep brain stimulation. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Tessel Boertien</name><affiliations><json:string>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</json:string><json:string>Faculty of Medicine, University of Amsterdam, Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Ludvic Zrinzo MD, FRCS</name><affiliations><json:string>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</json:string><json:string>Victor Horsley Department of Neurosurgery, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Joshua Kahan</name><affiliations><json:string>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Marjan Jahanshahi PhD</name><affiliations><json:string>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Marwan Hariz MD, PhD</name><affiliations><json:string>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</json:string><json:string>Victor Horsley Department of Neurosurgery, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Laura Mancini PhD</name><affiliations><json:string>Lysholm Department of Neuroradiology, National Hospital for Neurology & Neurosurgery, UCLH NHS Foundation Trust, Queen Square, London, United Kingdom</json:string><json:string>Academic Neuroradiological Unit, Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, Queen Square, London, United Kingdom</json:string><json:string>Queen Square Imaging Centre, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Patricia Limousin MD, PhD</name><affiliations><json:string>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Thomas Foltynie MRCP, PhD</name><affiliations><json:string>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</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>functional imaging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>functional magnetic resonance imaging; deep brain stimulation; subthalamic nucleus</value></json:item></subject><articleId><json:string>MDS23788</json:string></articleId><language><json:string>eng</json:string></language><abstract>Deep brain stimulation of the subthalamic nucleus is an accepted treatment for the motor complications of Parkinson's disease. The therapeutic mechanism of action remains incompletely understood. Although the results of deep brain stimulation are similar to the results that can be obtained by lesional surgery, accumulating evidence from functional imaging and clinical neurophysiology suggests that the effects of subthalamic nucleus‐deep brain stimulation are not simply the result of inhibition of subthalamic nucleus activity. Positron emission tomography/single‐photon emission computed tomography has consistently demonstrated changes in cortical activation in response to subthalamic nucleus‐deep brain stimulation. However, the technique has limited spatial and temporal resolution, and therefore the changes in activity of subcortical projection sites of the subthalamic nucleus (such as the globus pallidus, substantia nigra, and thalamus) are not as clear. Clarifying whether clinically relevant effects from subthalamic nucleus‐deep brain stimulation in humans are mediated through inhibition or excitation of orthodromic or antidromic pathways (or both) would contribute to our understanding of the precise mechanism of action of deep brain stimulation and may allow improvements in safety and efficacy of the technique. In this review we discuss the published evidence from functional imaging studies of patients with subthalamic nucleus‐deep brain stimulation to date, together with how these data inform the mechanism of action of deep brain stimulation. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.64</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>3</keywordCount><abstractCharCount>1604</abstractCharCount><pdfWordCount>5501</pdfWordCount><pdfCharCount>37571</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>220</abstractWordCount></qualityIndicators><title>Functional imaging of subthalamic nucleus deep brain stimulation in Parkinson's disease</title><genre><json:string>review-article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>9</total><last>1843</last><first>1835</first></pages><issn><json:string>0885-3185</json:string></issn><issue>10</issue><subject><json:item><value>Review</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23788</json:string></doi><id>BFDDAD346B7406C55DAD01EAE33835B2A617B041</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/BFDDAD346B7406C55DAD01EAE33835B2A617B041/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/BFDDAD346B7406C55DAD01EAE33835B2A617B041/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/BFDDAD346B7406C55DAD01EAE33835B2A617B041/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Functional imaging of subthalamic nucleus deep brain stimulation in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Funding agencies: This work was undertaken at UCL/UCLH and was partly funded by the Department of Health NIHR Biomedical Research Centres funding scheme. The Unit of Functional Neurosurgery, Queen Square, London, is supported by the Parkinson's Appeal.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Functional imaging of subthalamic nucleus deep brain stimulation in Parkinson's disease</title><author><persName><forename type="first">Tessel</forename><surname>Boertien</surname></persName><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><affiliation>Faculty of Medicine, University of Amsterdam, Amsterdam, The Netherlands</affiliation></author><author><persName><forename type="first">Ludvic</forename><surname>Zrinzo</surname></persName><roleName type="degree">MD, FRCS</roleName><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><affiliation>Victor Horsley Department of Neurosurgery, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Joshua</forename><surname>Kahan</surname></persName><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Marjan</forename><surname>Jahanshahi</surname></persName><roleName type="degree">PhD</roleName><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Marwan</forename><surname>Hariz</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><affiliation>Victor Horsley Department of Neurosurgery, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Laura</forename><surname>Mancini</surname></persName><roleName type="degree">PhD</roleName><affiliation>Lysholm Department of Neuroradiology, National Hospital for Neurology & Neurosurgery, UCLH NHS Foundation Trust, Queen Square, London, United Kingdom</affiliation><affiliation>Academic Neuroradiological Unit, Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><affiliation>Queen Square Imaging Centre, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Patricia</forename><surname>Limousin</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation></author><author><persName><forename type="first">Thomas</forename><surname>Foltynie</surname></persName><roleName type="degree">MRCP, PhD</roleName><note type="correspondence"><p>Correspondence: Box 146, National Hospital for Neurology & Neurosurgery, Queen Square, London, WC1N 3BG, UK</p></note><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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Although the results of deep brain stimulation are similar to the results that can be obtained by lesional surgery, accumulating evidence from functional imaging and clinical neurophysiology suggests that the effects of subthalamic nucleus‐deep brain stimulation are not simply the result of inhibition of subthalamic nucleus activity. Positron emission tomography/single‐photon emission computed tomography has consistently demonstrated changes in cortical activation in response to subthalamic nucleus‐deep brain stimulation. However, the technique has limited spatial and temporal resolution, and therefore the changes in activity of subcortical projection sites of the subthalamic nucleus (such as the globus pallidus, substantia nigra, and thalamus) are not as clear. Clarifying whether clinically relevant effects from subthalamic nucleus‐deep brain stimulation in humans are mediated through inhibition or excitation of orthodromic or antidromic pathways (or both) would contribute to our understanding of the precise mechanism of action of deep brain stimulation and may allow improvements in safety and efficacy of the technique. In this review we discuss the published evidence from functional imaging studies of patients with subthalamic nucleus‐deep brain stimulation to date, together with how these data inform the mechanism of action of deep brain stimulation. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>functional imaging</term></item><item><term>functional magnetic resonance imaging; deep brain stimulation; subthalamic nucleus</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Review</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-11-17">Received</change><change when="2011-04-17">Registration</change><change when="2011-08-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/BFDDAD346B7406C55DAD01EAE33835B2A617B041/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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affiliationRef="#af1"><personName><givenNames>Joshua</givenNames><familyName>Kahan</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Marjan</givenNames><familyName>Jahanshahi</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Marwan</givenNames><familyName>Hariz</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4 #af5 #af6"><personName><givenNames>Laura</givenNames><familyName>Mancini</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Patricia</givenNames><familyName>Limousin</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Thomas</givenNames><familyName>Foltynie</familyName><degrees>MRCP, PhD</degrees></personName><contactDetails><email>T.Foltynie@ion.ucl.ac.uk</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="NL" type="organization"><unparsedAffiliation>Faculty of Medicine, University of Amsterdam, Amsterdam, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>Victor Horsley Department of Neurosurgery, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="GB" type="organization"><unparsedAffiliation>Lysholm Department of Neuroradiology, National Hospital for Neurology & Neurosurgery, UCLH NHS Foundation Trust, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="GB" type="organization"><unparsedAffiliation>Academic Neuroradiological Unit, Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="GB" type="organization"><unparsedAffiliation>Queen Square Imaging Centre, Queen Square, London, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">functional imaging</keyword><keyword xml:id="kwd3">functional magnetic resonance imaging; deep brain stimulation; subthalamic nucleus</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Deep brain stimulation of the subthalamic nucleus is an accepted treatment for the motor complications of Parkinson's disease. The therapeutic mechanism of action remains incompletely understood. Although the results of deep brain stimulation are similar to the results that can be obtained by lesional surgery, accumulating evidence from functional imaging and clinical neurophysiology suggests that the effects of subthalamic nucleus‐deep brain stimulation are not simply the result of inhibition of subthalamic nucleus activity. Positron emission tomography/single‐photon emission computed tomography has consistently demonstrated changes in cortical activation in response to subthalamic nucleus‐deep brain stimulation. However, the technique has limited spatial and temporal resolution, and therefore the changes in activity of subcortical projection sites of the subthalamic nucleus (such as the globus pallidus, substantia nigra, and thalamus) are not as clear. Clarifying whether clinically relevant effects from subthalamic nucleus‐deep brain stimulation in humans are mediated through inhibition or excitation of orthodromic or antidromic pathways (or both) would contribute to our understanding of the precise mechanism of action of deep brain stimulation and may allow improvements in safety and efficacy of the technique. In this review we discuss the published evidence from functional imaging studies of patients with subthalamic nucleus‐deep brain stimulation to date, together with how these data inform the mechanism of action of deep brain stimulation. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn3"><p><b>Funding agencies:</b> This work was undertaken at UCL/UCLH and was partly funded by the Department of Health NIHR Biomedical Research Centres funding scheme. The Unit of Functional Neurosurgery, Queen Square, London, is supported by the Parkinson's Appeal.</p></note><note xml:id="fn4"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="fn5"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Functional imaging of subthalamic nucleus deep brain stimulation in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Functional Imaging and STN‐DBS in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Functional imaging of subthalamic nucleus deep brain stimulation in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Tessel</namePart><namePart type="family">Boertien</namePart><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><affiliation>Faculty of Medicine, University of Amsterdam, Amsterdam, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ludvic</namePart><namePart type="family">Zrinzo</namePart><namePart type="termsOfAddress">MD, FRCS</namePart><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><affiliation>Victor Horsley Department of Neurosurgery, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joshua</namePart><namePart type="family">Kahan</namePart><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marjan</namePart><namePart type="family">Jahanshahi</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marwan</namePart><namePart type="family">Hariz</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><affiliation>Victor Horsley Department of Neurosurgery, National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laura</namePart><namePart type="family">Mancini</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Lysholm Department of Neuroradiology, National Hospital for Neurology & Neurosurgery, UCLH NHS Foundation Trust, Queen Square, London, United Kingdom</affiliation><affiliation>Academic Neuroradiological Unit, Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><affiliation>Queen Square Imaging Centre, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patricia</namePart><namePart type="family">Limousin</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Foltynie</namePart><namePart type="termsOfAddress">MRCP, PhD</namePart><affiliation>Unit of Functional Neurosurgery, UCL Institute of Neurology, Queen Square, London, United Kingdom</affiliation><description>Correspondence: Box 146, National Hospital for Neurology & Neurosurgery, Queen Square, London, WC1N 3BG, UK</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-08-15</dateIssued><dateCaptured encoding="w3cdtf">2010-11-17</dateCaptured><dateValid encoding="w3cdtf">2011-04-17</dateValid><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">1</extent><extent unit="references">89</extent><extent unit="words">7210</extent></physicalDescription><abstract lang="en">Deep brain stimulation of the subthalamic nucleus is an accepted treatment for the motor complications of Parkinson's disease. The therapeutic mechanism of action remains incompletely understood. Although the results of deep brain stimulation are similar to the results that can be obtained by lesional surgery, accumulating evidence from functional imaging and clinical neurophysiology suggests that the effects of subthalamic nucleus‐deep brain stimulation are not simply the result of inhibition of subthalamic nucleus activity. Positron emission tomography/single‐photon emission computed tomography has consistently demonstrated changes in cortical activation in response to subthalamic nucleus‐deep brain stimulation. However, the technique has limited spatial and temporal resolution, and therefore the changes in activity of subcortical projection sites of the subthalamic nucleus (such as the globus pallidus, substantia nigra, and thalamus) are not as clear. Clarifying whether clinically relevant effects from subthalamic nucleus‐deep brain stimulation in humans are mediated through inhibition or excitation of orthodromic or antidromic pathways (or both) would contribute to our understanding of the precise mechanism of action of deep brain stimulation and may allow improvements in safety and efficacy of the technique. In this review we discuss the published evidence from functional imaging studies of patients with subthalamic nucleus‐deep brain stimulation to date, together with how these data inform the mechanism of action of deep brain stimulation. © 2011 Movement Disorder Society</abstract><note type="content">*Funding agencies: This work was undertaken at UCL/UCLH and was partly funded by the Department of Health NIHR Biomedical Research Centres funding scheme. The Unit of Functional Neurosurgery, Queen Square, London, is supported by the Parkinson's Appeal.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>functional imaging</topic><topic>functional magnetic resonance imaging; deep brain stimulation; subthalamic nucleus</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Review</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1835</start><end>1843</end><total>9</total></extent></part></relatedItem><identifier type="istex">BFDDAD346B7406C55DAD01EAE33835B2A617B041</identifier><identifier type="DOI">10.1002/mds.23788</identifier><identifier type="ArticleID">MDS23788</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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