Basal ganglia dysfunction in OCD: subthalamic neuronal activity correlates with symptoms severity and predicts high-frequency stimulation efficacy.
Identifieur interne : 000973 ( PubMed/Corpus ); précédent : 000972; suivant : 000974Basal ganglia dysfunction in OCD: subthalamic neuronal activity correlates with symptoms severity and predicts high-frequency stimulation efficacy.
Auteurs : M-L Welter ; P. Burbaud ; S. Fernandez-Vidal ; E. Bardinet ; J. Coste ; B. Piallat ; M. Borg ; S. Besnard ; P. Sauleau ; B. Devaux ; B. Pidoux ; P. Chaynes ; S. Tézenas Du Montcel ; A. Bastian ; N. Langbour ; A. Teillant ; W. Haynes ; J. Yelnik ; C. Karachi ; L. MalletSource :
- Translational psychiatry [ 2158-3188 ] ; 2011.
English descriptors
- KwdEn :
- Adult, Basal Ganglia (pathology), Basal Ganglia (physiopathology), Basal Ganglia (surgery), Deep Brain Stimulation (instrumentation), Deep Brain Stimulation (methods), Electrodes, Implanted, Humans, Neurons (pathology), Obsessive-Compulsive Disorder (pathology), Obsessive-Compulsive Disorder (physiopathology), Obsessive-Compulsive Disorder (therapy), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Severity of Illness Index, Treatment Outcome.
- MESH :
- instrumentation : Deep Brain Stimulation.
- methods : Deep Brain Stimulation.
- pathology : Basal Ganglia, Neurons, Obsessive-Compulsive Disorder, Parkinson Disease.
- physiopathology : Basal Ganglia, Obsessive-Compulsive Disorder, Parkinson Disease.
- surgery : Basal Ganglia.
- therapy : Obsessive-Compulsive Disorder, Parkinson Disease.
- Adult, Electrodes, Implanted, Humans, Severity of Illness Index, Treatment Outcome.
Abstract
Functional and connectivity changes in corticostriatal systems have been reported in the brains of patients with obsessive-compulsive disorder (OCD); however, the relationship between basal ganglia activity and OCD severity has never been adequately established. We recently showed that deep brain stimulation of the subthalamic nucleus (STN), a central basal ganglia nucleus, improves OCD. Here, single-unit subthalamic neuronal activity was analysed in 12 OCD patients, in relation to the severity of obsessions and compulsions and response to STN stimulation, and compared with that obtained in 12 patients with Parkinson's disease (PD). STN neurons in OCD patients had lower discharge frequency than those in PD patients, with a similar proportion of burst-type activity (69 vs 67%). Oscillatory activity was present in 46 and 68% of neurons in OCD and PD patients, respectively, predominantly in the low-frequency band (1-8 Hz). In OCD patients, the bursty and oscillatory subthalamic neuronal activity was mainly located in the associative-limbic part. Both OCD severity and clinical improvement following STN stimulation were related to the STN neuronal activity. In patients with the most severe OCD, STN neurons exhibited bursts with shorter duration and interburst interval, but higher intraburst frequency, and more oscillations in the low-frequency bands. In patients with best clinical outcome with STN stimulation, STN neurons displayed higher mean discharge, burst and intraburst frequencies, and lower interburst interval. These findings are consistent with the hypothesis of a dysfunction in the associative-limbic subdivision of the basal ganglia circuitry in OCD's pathophysiology.
DOI: 10.1038/tp.2011.5
PubMed: 22832400
Links to Exploration step
pubmed:22832400Le document en format XML
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Burbaud</name></author><author><name sortKey="Fernandez Vidal, S" sort="Fernandez Vidal, S" uniqKey="Fernandez Vidal S" first="S" last="Fernandez-Vidal">S. Fernandez-Vidal</name></author><author><name sortKey="Bardinet, E" sort="Bardinet, E" uniqKey="Bardinet E" first="E" last="Bardinet">E. Bardinet</name></author><author><name sortKey="Coste, J" sort="Coste, J" uniqKey="Coste J" first="J" last="Coste">J. Coste</name></author><author><name sortKey="Piallat, B" sort="Piallat, B" uniqKey="Piallat B" first="B" last="Piallat">B. Piallat</name></author><author><name sortKey="Borg, M" sort="Borg, M" uniqKey="Borg M" first="M" last="Borg">M. Borg</name></author><author><name sortKey="Besnard, S" sort="Besnard, S" uniqKey="Besnard S" first="S" last="Besnard">S. Besnard</name></author><author><name sortKey="Sauleau, P" sort="Sauleau, P" uniqKey="Sauleau P" first="P" last="Sauleau">P. Sauleau</name></author><author><name sortKey="Devaux, B" sort="Devaux, B" uniqKey="Devaux B" first="B" last="Devaux">B. Devaux</name></author><author><name sortKey="Pidoux, B" sort="Pidoux, B" uniqKey="Pidoux B" first="B" last="Pidoux">B. Pidoux</name></author><author><name sortKey="Chaynes, P" sort="Chaynes, P" uniqKey="Chaynes P" first="P" last="Chaynes">P. Chaynes</name></author><author><name sortKey="Tezenas Du Montcel, S" sort="Tezenas Du Montcel, S" uniqKey="Tezenas Du Montcel S" first="S" last="Tézenas Du Montcel">S. Tézenas Du Montcel</name></author><author><name sortKey="Bastian, A" sort="Bastian, A" uniqKey="Bastian A" first="A" last="Bastian">A. Bastian</name></author><author><name sortKey="Langbour, N" sort="Langbour, N" uniqKey="Langbour N" first="N" last="Langbour">N. Langbour</name></author><author><name sortKey="Teillant, A" sort="Teillant, A" uniqKey="Teillant A" first="A" last="Teillant">A. Teillant</name></author><author><name sortKey="Haynes, W" sort="Haynes, W" uniqKey="Haynes W" first="W" last="Haynes">W. Haynes</name></author><author><name sortKey="Yelnik, J" sort="Yelnik, J" uniqKey="Yelnik J" first="J" last="Yelnik">J. Yelnik</name></author><author><name sortKey="Karachi, C" sort="Karachi, C" uniqKey="Karachi C" first="C" last="Karachi">C. Karachi</name></author><author><name sortKey="Mallet, L" sort="Mallet, L" uniqKey="Mallet L" first="L" last="Mallet">L. Mallet</name></author></analytic><series><title level="j">Translational psychiatry</title><idno type="eISSN">2158-3188</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Basal Ganglia (pathology)</term><term>Basal Ganglia (physiopathology)</term><term>Basal Ganglia (surgery)</term><term>Deep Brain Stimulation (instrumentation)</term><term>Deep Brain Stimulation (methods)</term><term>Electrodes, Implanted</term><term>Humans</term><term>Neurons (pathology)</term><term>Obsessive-Compulsive Disorder (pathology)</term><term>Obsessive-Compulsive Disorder (physiopathology)</term><term>Obsessive-Compulsive Disorder (therapy)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Severity of Illness Index</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" qualifier="instrumentation" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Neurons</term><term>Obsessive-Compulsive Disorder</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Obsessive-Compulsive Disorder</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Basal Ganglia</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Obsessive-Compulsive Disorder</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Electrodes, Implanted</term><term>Humans</term><term>Severity of Illness Index</term><term>Treatment Outcome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Functional and connectivity changes in corticostriatal systems have been reported in the brains of patients with obsessive-compulsive disorder (OCD); however, the relationship between basal ganglia activity and OCD severity has never been adequately established. We recently showed that deep brain stimulation of the subthalamic nucleus (STN), a central basal ganglia nucleus, improves OCD. Here, single-unit subthalamic neuronal activity was analysed in 12 OCD patients, in relation to the severity of obsessions and compulsions and response to STN stimulation, and compared with that obtained in 12 patients with Parkinson's disease (PD). STN neurons in OCD patients had lower discharge frequency than those in PD patients, with a similar proportion of burst-type activity (69 vs 67%). Oscillatory activity was present in 46 and 68% of neurons in OCD and PD patients, respectively, predominantly in the low-frequency band (1-8 Hz). In OCD patients, the bursty and oscillatory subthalamic neuronal activity was mainly located in the associative-limbic part. Both OCD severity and clinical improvement following STN stimulation were related to the STN neuronal activity. In patients with the most severe OCD, STN neurons exhibited bursts with shorter duration and interburst interval, but higher intraburst frequency, and more oscillations in the low-frequency bands. In patients with best clinical outcome with STN stimulation, STN neurons displayed higher mean discharge, burst and intraburst frequencies, and lower interburst interval. These findings are consistent with the hypothesis of a dysfunction in the associative-limbic subdivision of the basal ganglia circuitry in OCD's pathophysiology.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22832400</PMID><DateCreated><Year>2012</Year><Month>07</Month><Day>26</Day></DateCreated><DateCompleted><Year>2013</Year><Month>04</Month><Day>04</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>15</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2158-3188</ISSN><JournalIssue CitedMedium="Internet"><Volume>1</Volume><PubDate><Year>2011</Year><Month>May</Month><Day>03</Day></PubDate></JournalIssue><Title>Translational psychiatry</Title><ISOAbbreviation>Transl Psychiatry</ISOAbbreviation></Journal><ArticleTitle>Basal ganglia dysfunction in OCD: subthalamic neuronal activity correlates with symptoms severity and predicts high-frequency stimulation efficacy.</ArticleTitle><Pagination><MedlinePgn>e5</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/tp.2011.5</ELocationID><Abstract><AbstractText>Functional and connectivity changes in corticostriatal systems have been reported in the brains of patients with obsessive-compulsive disorder (OCD); however, the relationship between basal ganglia activity and OCD severity has never been adequately established. We recently showed that deep brain stimulation of the subthalamic nucleus (STN), a central basal ganglia nucleus, improves OCD. Here, single-unit subthalamic neuronal activity was analysed in 12 OCD patients, in relation to the severity of obsessions and compulsions and response to STN stimulation, and compared with that obtained in 12 patients with Parkinson's disease (PD). STN neurons in OCD patients had lower discharge frequency than those in PD patients, with a similar proportion of burst-type activity (69 vs 67%). Oscillatory activity was present in 46 and 68% of neurons in OCD and PD patients, respectively, predominantly in the low-frequency band (1-8 Hz). In OCD patients, the bursty and oscillatory subthalamic neuronal activity was mainly located in the associative-limbic part. Both OCD severity and clinical improvement following STN stimulation were related to the STN neuronal activity. In patients with the most severe OCD, STN neurons exhibited bursts with shorter duration and interburst interval, but higher intraburst frequency, and more oscillations in the low-frequency bands. In patients with best clinical outcome with STN stimulation, STN neurons displayed higher mean discharge, burst and intraburst frequencies, and lower interburst interval. These findings are consistent with the hypothesis of a dysfunction in the associative-limbic subdivision of the basal ganglia circuitry in OCD's pathophysiology.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Welter</LastName><ForeName>M-L</ForeName><Initials>ML</Initials><AffiliationInfo><Affiliation>Centre de Recherche de l'Institut du Cerveau et de Moelle épiniere, Université Pierre et Marie Curie-Paris 6, UMR-S975, Paris, France. marie-laure.welter@psl.aphp.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Burbaud</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Fernandez-Vidal</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Bardinet</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Coste</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Piallat</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Borg</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Besnard</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Sauleau</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Devaux</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Pidoux</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Chaynes</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Tézenas du Montcel</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Bastian</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Langbour</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Teillant</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Haynes</LastName><ForeName>W</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Yelnik</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Karachi</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Mallet</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><CollectiveName>French Stimulation dans Trouble Obsessionnel Compulsif (STOC) Study Group</CollectiveName></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>05</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Transl Psychiatry</MedlineTA><NlmUniqueID>101562664</NlmUniqueID><ISSNLinking>2158-3188</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Int J Psychophysiol. 2006 Oct;62(1):87-92</RefSource><PMID Version="1">16554100</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neural Transm Suppl. 2006;(70):27-30</RefSource><PMID Version="1">17017505</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropsychopharmacology. 2006 Nov;31(11):2384-93</RefSource><PMID Version="1">16855529</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Gen Psychiatry. 2006 Nov;63(11):1225-36</RefSource><PMID 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