Subthalamic neuronal firing in obsessive‐compulsive disorder and Parkinson disease
Identifieur interne : 000A37 ( Main/Corpus ); précédent : 000A36; suivant : 000A38Subthalamic neuronal firing in obsessive‐compulsive disorder and Parkinson disease
Auteurs : Brigitte Piallat ; Mircea Polosan ; Valérie Fraix ; Laurent Goetz ; Olivier David ; Albert Fenoy ; Napoleon Torres ; Jean-Louis Quesada ; Eric Seigneuret ; Pierre Pollak ; Paul Krack ; Thierry Bougerol ; Alim L. Benabid ; Stéphan ChabardèsSource :
- Annals of Neurology [ 0364-5134 ] ; 2011-05.
Abstract
Objective: Although electrophysiologic dysfunction of the subthalamic nucleus is putative, deep brain stimulation of this structure has recently been reported to improve obsessions and compulsions. In Parkinson disease, sensorimotor subthalamic neurons display high‐frequency burst firing, which is considered as an electrophysiologic signature of motor loop dysfunction. We addressed whether such neuronal dysfunction of the subthalamic nucleus also exists in the nonmotor loops involved in patients with obsessive‐compulsive disorder. Methods: We compared the neuronal activity of the subthalamic nucleus recorded in 9 patients with obsessive‐compulsive disorder with that of 11 patients with Parkinson disease measured during intraoperative exploration for deep brain stimulation. Results: The mean subthalamic neuron discharge rate was statistically lower in patients with obsessive‐compulsive disorder than in patients with Parkinson disease (20.5 ± 11.0 Hz, n = 100 and 30.8 ± 15.6 Hz, n = 93, respectively, p < 0.001). The relative proportion of burst neurons did not differ significantly between the 2 diseases (75% vs 73%). Interestingly, burst neurons were predominantly left‐sided in obsessive‐compulsive disorder. Interpretation: The recording of burst neurons within the nonmotor subthalamic nucleus in patients with obsessive‐compulsive disorder is a novel finding that suggests the existence of deregulation of the nonmotor basal ganglia loop, possibly left‐sided. Potentially, burst activity might interfere with normal processes occurring within nonmotor loops. Ann Neurol 2010.
Url:
DOI: 10.1002/ana.22222
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Psychiatry, University Hospital of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Fraix, Valerie" sort="Fraix, Valerie" uniqKey="Fraix V" first="Valérie" last="Fraix">Valérie Fraix</name><affiliation><mods:affiliation>Grenoble University, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Hospital of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Goetz, Laurent" sort="Goetz, Laurent" uniqKey="Goetz L" first="Laurent" last="Goetz">Laurent Goetz</name><affiliation><mods:affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</mods:affiliation></affiliation></author><author><name sortKey="David, Olivier" sort="David, Olivier" uniqKey="David O" first="Olivier" last="David">Olivier David</name><affiliation><mods:affiliation>Grenoble University, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neuroradiology, University Hospital of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Fenoy, Albert" sort="Fenoy, Albert" uniqKey="Fenoy A" first="Albert" last="Fenoy">Albert Fenoy</name><affiliation><mods:affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</mods:affiliation></affiliation></author><author><name sortKey="Torres, Napoleon" sort="Torres, Napoleon" uniqKey="Torres N" first="Napoleon" last="Torres">Napoleon Torres</name><affiliation><mods:affiliation>Atomic Energy Commission of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Quesada, Jean Ouis" sort="Quesada, Jean Ouis" uniqKey="Quesada J" first="Jean-Louis" last="Quesada">Jean-Louis Quesada</name><affiliation><mods:affiliation>Grenoble University, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Center of Clinical Investigation and INSERM‐003, University Hospital of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Seigneuret, Eric" sort="Seigneuret, Eric" uniqKey="Seigneuret E" first="Eric" last="Seigneuret">Eric Seigneuret</name><affiliation><mods:affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurosurgery, University Hospital of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Pollak, Pierre" sort="Pollak, Pierre" uniqKey="Pollak P" first="Pierre" last="Pollak">Pierre Pollak</name><affiliation><mods:affiliation>Grenoble University, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Hospital of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Krack, Paul" sort="Krack, Paul" uniqKey="Krack P" first="Paul" last="Krack">Paul Krack</name><affiliation><mods:affiliation>Grenoble University, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University Hospital of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Bougerol, Thierry" sort="Bougerol, Thierry" uniqKey="Bougerol T" first="Thierry" last="Bougerol">Thierry Bougerol</name><affiliation><mods:affiliation>Grenoble University, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry, University Hospital of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Benabid, Alim L" sort="Benabid, Alim L" uniqKey="Benabid A" first="Alim L." last="Benabid">Alim L. Benabid</name><affiliation><mods:affiliation>Grenoble University, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Atomic Energy Commission of Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Chabardes, Stephan" sort="Chabardes, Stephan" uniqKey="Chabardes S" first="Stéphan" last="Chabardès">Stéphan Chabardès</name><affiliation><mods:affiliation>Grenoble University, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurosurgery, University Hospital of Grenoble, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-05">2011-05</date><biblScope unit="volume">69</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="793">793</biblScope><biblScope unit="page" to="802">802</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">D181E3C67D96B43C1EFC13A3E1D51CBFE627F9B9</idno><idno type="DOI">10.1002/ana.22222</idno><idno type="ArticleID">ANA22222</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective: Although electrophysiologic dysfunction of the subthalamic nucleus is putative, deep brain stimulation of this structure has recently been reported to improve obsessions and compulsions. In Parkinson disease, sensorimotor subthalamic neurons display high‐frequency burst firing, which is considered as an electrophysiologic signature of motor loop dysfunction. We addressed whether such neuronal dysfunction of the subthalamic nucleus also exists in the nonmotor loops involved in patients with obsessive‐compulsive disorder. Methods: We compared the neuronal activity of the subthalamic nucleus recorded in 9 patients with obsessive‐compulsive disorder with that of 11 patients with Parkinson disease measured during intraoperative exploration for deep brain stimulation. Results: The mean subthalamic neuron discharge rate was statistically lower in patients with obsessive‐compulsive disorder than in patients with Parkinson disease (20.5 ± 11.0 Hz, n = 100 and 30.8 ± 15.6 Hz, n = 93, respectively, p < 0.001). The relative proportion of burst neurons did not differ significantly between the 2 diseases (75% vs 73%). Interestingly, burst neurons were predominantly left‐sided in obsessive‐compulsive disorder. Interpretation: The recording of burst neurons within the nonmotor subthalamic nucleus in patients with obsessive‐compulsive disorder is a novel finding that suggests the existence of deregulation of the nonmotor basal ganglia loop, possibly left‐sided. Potentially, burst activity might interfere with normal processes occurring within nonmotor loops. Ann Neurol 2010.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Brigitte Piallat PhD</name><affiliations><json:string>Grenoble University, France</json:string><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string></affiliations></json:item><json:item><name>Mircea Polosan MD</name><affiliations><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string><json:string>Department of Psychiatry, University Hospital of Grenoble, France</json:string></affiliations></json:item><json:item><name>Valérie Fraix MD, PhD</name><affiliations><json:string>Grenoble University, France</json:string><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string><json:string>Department of Neurology, University Hospital of Grenoble, France</json:string></affiliations></json:item><json:item><name>Laurent Goetz MSc</name><affiliations><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string></affiliations></json:item><json:item><name>Olivier David PhD</name><affiliations><json:string>Grenoble University, France</json:string><json:string>Department of Neuroradiology, University Hospital of Grenoble, France</json:string></affiliations></json:item><json:item><name>Albert Fenoy MD</name><affiliations><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string></affiliations></json:item><json:item><name>Napoleon Torres MD, PhD</name><affiliations><json:string>Atomic Energy Commission of Grenoble, France</json:string></affiliations></json:item><json:item><name>Jean‐Louis Quesada MSc</name><affiliations><json:string>Grenoble University, France</json:string><json:string>Center of Clinical Investigation and INSERM‐003, University Hospital of Grenoble, France</json:string></affiliations></json:item><json:item><name>Eric Seigneuret MD</name><affiliations><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string><json:string>Department of Neurosurgery, University Hospital of Grenoble, France</json:string></affiliations></json:item><json:item><name>Pierre Pollak MD</name><affiliations><json:string>Grenoble University, France</json:string><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string><json:string>Department of Neurology, University Hospital of Grenoble, France</json:string></affiliations></json:item><json:item><name>Paul Krack MD, PhD</name><affiliations><json:string>Grenoble University, France</json:string><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string><json:string>Department of Neurology, University Hospital of Grenoble, France</json:string></affiliations></json:item><json:item><name>Thierry Bougerol MD</name><affiliations><json:string>Grenoble University, France</json:string><json:string>Department of Psychiatry, University Hospital of Grenoble, France</json:string></affiliations></json:item><json:item><name>Alim L. Benabid MD, PhD</name><affiliations><json:string>Grenoble University, France</json:string><json:string>Atomic Energy Commission of Grenoble, France</json:string></affiliations></json:item><json:item><name>Stéphan Chabardès MD</name><affiliations><json:string>Grenoble University, France</json:string><json:string>INSERM‐U836, Grenoble Institute of Neurosciences, France</json:string><json:string>Department of Neurosurgery, University Hospital of Grenoble, France</json:string></affiliations></json:item></author><articleId><json:string>ANA22222</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objective: Although electrophysiologic dysfunction of the subthalamic nucleus is putative, deep brain stimulation of this structure has recently been reported to improve obsessions and compulsions. In Parkinson disease, sensorimotor subthalamic neurons display high‐frequency burst firing, which is considered as an electrophysiologic signature of motor loop dysfunction. We addressed whether such neuronal dysfunction of the subthalamic nucleus also exists in the nonmotor loops involved in patients with obsessive‐compulsive disorder. Methods: We compared the neuronal activity of the subthalamic nucleus recorded in 9 patients with obsessive‐compulsive disorder with that of 11 patients with Parkinson disease measured during intraoperative exploration for deep brain stimulation. Results: The mean subthalamic neuron discharge rate was statistically lower in patients with obsessive‐compulsive disorder than in patients with Parkinson disease (20.5 ± 11.0 Hz, n = 100 and 30.8 ± 15.6 Hz, n = 93, respectively, p > 0.001). The relative proportion of burst neurons did not differ significantly between the 2 diseases (75% vs 73%). Interestingly, burst neurons were predominantly left‐sided in obsessive‐compulsive disorder. Interpretation: The recording of burst neurons within the nonmotor subthalamic nucleus in patients with obsessive‐compulsive disorder is a novel finding that suggests the existence of deregulation of the nonmotor basal ganglia loop, possibly left‐sided. Potentially, burst activity might interfere with normal processes occurring within nonmotor loops. 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type="first">Mircea</forename><surname>Polosan</surname></persName><roleName type="degree">MD</roleName><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Psychiatry, University Hospital of Grenoble, France</affiliation></author><author><persName><forename type="first">Valérie</forename><surname>Fraix</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurology, University Hospital of Grenoble, France</affiliation></author><author><persName><forename type="first">Laurent</forename><surname>Goetz</surname></persName><roleName type="degree">MSc</roleName><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation></author><author><persName><forename type="first">Olivier</forename><surname>David</surname></persName><roleName type="degree">PhD</roleName><affiliation>Grenoble University, France</affiliation><affiliation>Department of Neuroradiology, University Hospital of Grenoble, France</affiliation></author><author><persName><forename type="first">Albert</forename><surname>Fenoy</surname></persName><roleName type="degree">MD</roleName><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation></author><author><persName><forename type="first">Napoleon</forename><surname>Torres</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Atomic Energy Commission of Grenoble, France</affiliation></author><author><persName><forename type="first">Jean‐Louis</forename><surname>Quesada</surname></persName><roleName type="degree">MSc</roleName><affiliation>Grenoble University, France</affiliation><affiliation>Center of Clinical Investigation and INSERM‐003, University Hospital of Grenoble, France</affiliation></author><author><persName><forename type="first">Eric</forename><surname>Seigneuret</surname></persName><roleName type="degree">MD</roleName><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurosurgery, University Hospital of Grenoble, France</affiliation></author><author><persName><forename type="first">Pierre</forename><surname>Pollak</surname></persName><roleName type="degree">MD</roleName><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurology, University Hospital of Grenoble, France</affiliation></author><author><persName><forename type="first">Paul</forename><surname>Krack</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurology, University Hospital of Grenoble, France</affiliation></author><author><persName><forename type="first">Thierry</forename><surname>Bougerol</surname></persName><roleName type="degree">MD</roleName><affiliation>Grenoble University, France</affiliation><affiliation>Department of Psychiatry, University Hospital of Grenoble, France</affiliation></author><author><persName><forename type="first">Alim L.</forename><surname>Benabid</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Grenoble University, France</affiliation><affiliation>Atomic Energy Commission of Grenoble, France</affiliation></author><author><persName><forename type="first">Stéphan</forename><surname>Chabardès</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Grenoble Institut des Neurosciences, INSERM‐U836, Equipe 11, Université Joseph Fourier, Site Sante, La Tronche, BP170, 38042 Grenoble cédex 9, France</p></note><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurosurgery, University Hospital of Grenoble, France</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-05"></date><biblScope unit="volume">69</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="793">793</biblScope><biblScope unit="page" to="802">802</biblScope></imprint></monogr><idno type="istex">D181E3C67D96B43C1EFC13A3E1D51CBFE627F9B9</idno><idno type="DOI">10.1002/ana.22222</idno><idno 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In Parkinson disease, sensorimotor subthalamic neurons display high‐frequency burst firing, which is considered as an electrophysiologic signature of motor loop dysfunction. We addressed whether such neuronal dysfunction of the subthalamic nucleus also exists in the nonmotor loops involved in patients with obsessive‐compulsive disorder. Methods: We compared the neuronal activity of the subthalamic nucleus recorded in 9 patients with obsessive‐compulsive disorder with that of 11 patients with Parkinson disease measured during intraoperative exploration for deep brain stimulation. Results: The mean subthalamic neuron discharge rate was statistically lower in patients with obsessive‐compulsive disorder than in patients with Parkinson disease (20.5 ± 11.0 Hz, n = 100 and 30.8 ± 15.6 Hz, n = 93, respectively, p < 0.001). The relative proportion of burst neurons did not differ significantly between the 2 diseases (75% vs 73%). Interestingly, burst neurons were predominantly left‐sided in obsessive‐compulsive disorder. Interpretation: The recording of burst neurons within the nonmotor subthalamic nucleus in patients with obsessive‐compulsive disorder is a novel finding that suggests the existence of deregulation of the nonmotor basal ganglia loop, possibly left‐sided. Potentially, burst activity might interfere with normal processes occurring within nonmotor loops. Ann Neurol 2010.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-03-29">Received</change><change when="2010-08-06">Registration</change><change when="2011-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D181E3C67D96B43C1EFC13A3E1D51CBFE627F9B9/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 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date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst">793</numbering><numbering type="pageLast">802</numbering></numberingGroup><correspondenceTo>Grenoble Institut des Neurosciences, INSERM‐U836, Equipe 11, Université Joseph Fourier, Site Sante, La Tronche, BP170, 38042 Grenoble cédex 9, France</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA22222.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="53"></count><count type="wordTotal" number="5959"></count></countGroup><titleGroup><title type="main" xml:lang="en">Subthalamic neuronal firing in obsessive‐compulsive disorder and Parkinson disease</title><title type="short" xml:lang="en">STN Firing in OCD and PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Brigitte</givenNames><familyName>Piallat</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2 #af3"><personName><givenNames>Mircea</givenNames><familyName>Polosan</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2 #af4"><personName><givenNames>Valérie</givenNames><familyName>Fraix</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Laurent</givenNames><familyName>Goetz</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af5"><personName><givenNames>Olivier</givenNames><familyName>David</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" 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France</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Department of Psychiatry, University Hospital of Grenoble, France</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital of Grenoble, France</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neuroradiology, University Hospital of Grenoble, France</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neurosurgery, University Hospital of Grenoble, France</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="FR" type="organization"><unparsedAffiliation>Center of Clinical Investigation and INSERM‐003, University Hospital of Grenoble, France</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="FR" type="organization"><unparsedAffiliation>Atomic Energy Commission of Grenoble, France</unparsedAffiliation></affiliation></affiliationGroup><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03645134:media:ana22222:ANA_22222_sm_suppinfo"></mediaResource><caption>Supporting Information.</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03645134:media:ana22222:ANA_22222_sm_suppinfofigure_S1"></mediaResource><caption>Supporting Figure 1.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Objective</title><p>Although electrophysiologic dysfunction of the subthalamic nucleus is putative, deep brain stimulation of this structure has recently been reported to improve obsessions and compulsions. In Parkinson disease, sensorimotor subthalamic neurons display high‐frequency burst firing, which is considered as an electrophysiologic signature of motor loop dysfunction. We addressed whether such neuronal dysfunction of the subthalamic nucleus also exists in the nonmotor loops involved in patients with obsessive‐compulsive disorder.</p></section><section xml:id="abs1-2"><title type="main">Methods</title><p>We compared the neuronal activity of the subthalamic nucleus recorded in 9 patients with obsessive‐compulsive disorder with that of 11 patients with Parkinson disease measured during intraoperative exploration for deep brain stimulation.</p></section><section xml:id="abs1-3"><title type="main">Results</title><p>The mean subthalamic neuron discharge rate was statistically lower in patients with obsessive‐compulsive disorder than in patients with Parkinson disease (20.5 ± 11.0 Hz, n = 100 and 30.8 ± 15.6 Hz, n = 93, respectively, <i>p</i> < 0.001). The relative proportion of burst neurons did not differ significantly between the 2 diseases (75% vs 73%). Interestingly, burst neurons were predominantly left‐sided in obsessive‐compulsive disorder.</p></section><section xml:id="abs1-4"><title type="main">Interpretation</title><p>The recording of burst neurons within the nonmotor subthalamic nucleus in patients with obsessive‐compulsive disorder is a novel finding that suggests the existence of deregulation of the nonmotor basal ganglia loop, possibly left‐sided. Potentially, burst activity might interfere with normal processes occurring within nonmotor loops. Ann Neurol 2010.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Subthalamic neuronal firing in obsessive‐compulsive disorder and Parkinson disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>STN Firing in OCD and PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Subthalamic neuronal firing in obsessive‐compulsive disorder and Parkinson disease</title></titleInfo><name type="personal"><namePart type="given">Brigitte</namePart><namePart type="family">Piallat</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mircea</namePart><namePart type="family">Polosan</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Psychiatry, University Hospital of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Valérie</namePart><namePart type="family">Fraix</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurology, University Hospital of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laurent</namePart><namePart type="family">Goetz</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olivier</namePart><namePart type="family">David</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Grenoble University, France</affiliation><affiliation>Department of Neuroradiology, University Hospital of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Albert</namePart><namePart type="family">Fenoy</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Napoleon</namePart><namePart type="family">Torres</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Atomic Energy Commission of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Louis</namePart><namePart type="family">Quesada</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Grenoble University, France</affiliation><affiliation>Center of Clinical Investigation and INSERM‐003, University Hospital of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eric</namePart><namePart type="family">Seigneuret</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurosurgery, University Hospital of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Pollak</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurology, University Hospital of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul</namePart><namePart type="family">Krack</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurology, University Hospital of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thierry</namePart><namePart type="family">Bougerol</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Grenoble University, France</affiliation><affiliation>Department of Psychiatry, University Hospital of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alim L.</namePart><namePart type="family">Benabid</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Grenoble University, France</affiliation><affiliation>Atomic Energy Commission of Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stéphan</namePart><namePart type="family">Chabardès</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Grenoble University, France</affiliation><affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation><affiliation>Department of Neurosurgery, University Hospital of Grenoble, France</affiliation><description>Correspondence: Grenoble Institut des Neurosciences, INSERM‐U836, Equipe 11, Université Joseph Fourier, Site Sante, La Tronche, BP170, 38042 Grenoble cédex 9, France</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-05</dateIssued><dateCaptured encoding="w3cdtf">2010-03-29</dateCaptured><dateValid encoding="w3cdtf">2010-08-06</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">4</extent><extent unit="tables">3</extent><extent unit="references">53</extent><extent unit="words">5959</extent></physicalDescription><abstract lang="en">Objective: Although electrophysiologic dysfunction of the subthalamic nucleus is putative, deep brain stimulation of this structure has recently been reported to improve obsessions and compulsions. In Parkinson disease, sensorimotor subthalamic neurons display high‐frequency burst firing, which is considered as an electrophysiologic signature of motor loop dysfunction. We addressed whether such neuronal dysfunction of the subthalamic nucleus also exists in the nonmotor loops involved in patients with obsessive‐compulsive disorder. Methods: We compared the neuronal activity of the subthalamic nucleus recorded in 9 patients with obsessive‐compulsive disorder with that of 11 patients with Parkinson disease measured during intraoperative exploration for deep brain stimulation. Results: The mean subthalamic neuron discharge rate was statistically lower in patients with obsessive‐compulsive disorder than in patients with Parkinson disease (20.5 ± 11.0 Hz, n = 100 and 30.8 ± 15.6 Hz, n = 93, respectively, p < 0.001). The relative proportion of burst neurons did not differ significantly between the 2 diseases (75% vs 73%). Interestingly, burst neurons were predominantly left‐sided in obsessive‐compulsive disorder. Interpretation: The recording of burst neurons within the nonmotor subthalamic nucleus in patients with obsessive‐compulsive disorder is a novel finding that suggests the existence of deregulation of the nonmotor basal ganglia loop, possibly left‐sided. Potentially, burst activity might interfere with normal processes occurring within nonmotor loops. Ann Neurol 2010.</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information. - Supporting Figure 1. - </note><subject><genre>article category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>69</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>793</start><end>802</end><total>10</total></extent></part></relatedItem><identifier type="istex">D181E3C67D96B43C1EFC13A3E1D51CBFE627F9B9</identifier><identifier type="DOI">10.1002/ana.22222</identifier><identifier type="ArticleID">ANA22222</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 American Neurological Association</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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