La maladie de Parkinson en France (serveur d'exploration)

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Subthalamic neuronal firing in obsessive‐compulsive disorder and Parkinson disease

Identifieur interne : 000D61 ( Istex/Corpus ); précédent : 000D60; suivant : 000D62

Subthalamic 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 Chabardès

Source :

RBID : ISTEX:D181E3C67D96B43C1EFC13A3E1D51CBFE627F9B9

Abstract

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.

Url:
DOI: 10.1002/ana.22222

Links to Exploration step

ISTEX:D181E3C67D96B43C1EFC13A3E1D51CBFE627F9B9

Le document en format XML

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<div type="abstract">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.</div>
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<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>
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<affiliation>Department of Neuroradiology, University Hospital of Grenoble, France</affiliation>
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</name>
<name type="personal">
<namePart type="given">Albert</namePart>
<namePart type="family">Fenoy</namePart>
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<namePart type="given">Napoleon</namePart>
<namePart type="family">Torres</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
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<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>
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<name type="personal">
<namePart type="given">Eric</namePart>
<namePart type="family">Seigneuret</namePart>
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<affiliation>Department of Neurosurgery, University Hospital of Grenoble, France</affiliation>
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<namePart type="given">Pierre</namePart>
<namePart type="family">Pollak</namePart>
<namePart type="termsOfAddress">MD</namePart>
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<affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation>
<affiliation>Department of Neurology, University Hospital of Grenoble, France</affiliation>
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<namePart type="family">Krack</namePart>
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<affiliation>Grenoble University, France</affiliation>
<affiliation>INSERM‐U836, Grenoble Institute of Neurosciences, France</affiliation>
<affiliation>Department of Neurology, University Hospital of Grenoble, France</affiliation>
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<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>
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<name type="personal">
<namePart type="given">Alim L.</namePart>
<namePart type="family">Benabid</namePart>
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<affiliation>Grenoble University, France</affiliation>
<affiliation>Atomic Energy Commission of Grenoble, France</affiliation>
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<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>
<affiliation>Grenoble Institut des Neurosciences, INSERM‐U836, Equipe 11, Université Joseph Fourier, Site Sante, La Tronche, BP170, 38042 Grenoble cédex 9, France</affiliation>
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<dateIssued encoding="w3cdtf">2011-05</dateIssued>
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<abstract>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.</abstract>
<abstract>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.</abstract>
<abstract>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.</abstract>
<abstract>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>
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<title>Annals of Neurology</title>
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<title>Ann Neurol.</title>
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<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>
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<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>
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<detail type="issue">
<caption>no.</caption>
<number>5</number>
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<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>
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