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Are Hallucinations Due to an Imbalance Between Excitatory and Inhibitory Influences on the Brain?

Identifieur interne : 002311 ( PubMed/Checkpoint ); précédent : 002310; suivant : 002312

Are Hallucinations Due to an Imbalance Between Excitatory and Inhibitory Influences on the Brain?

Auteurs : Renaud Jardri [France] ; Kenneth Hugdahl [Norvège] ; Matthew Hughes [Australie] ; Jérôme Brunelin [France] ; Flavie Waters [Australie] ; Ben Alderson-Day [Royaume-Uni] ; Dave Smailes [Royaume-Uni] ; Philipp Sterzer [Allemagne] ; Philip R. Corlett [États-Unis] ; Pantelis Leptourgos [France] ; Martin Debbané [Royaume-Uni] ; Arnaud Cachia [France] ; Sophie Denève [France]

Source :

RBID : pubmed:27261492

Descripteurs français

English descriptors

Abstract

This review from the International Consortium on Hallucinations Research intends to question the pertinence of the excitatory-to-inhibitory (E/I) imbalance hypothesis as a model for hallucinations. A large number of studies suggest that subtle impairments of the E/I balance are involved in neurological and psychiatric conditions, such as schizophrenia. Emerging evidence also points to a role of the E/I balance in maintaining stable perceptual representations, suggesting it may be a plausible model for hallucinations. In support, hallucinations have been linked to inhibitory deficits as shown with impairment of gamma-aminobutyric acid transmission, N-methyl-d-aspartate receptor plasticity, reductions in gamma-frequency oscillations, hyperactivity in sensory cortices, and cognitive inhibition deficits. However, the mechanisms by which E/I dysfunctions at the cellular level might relate to clinical symptoms and cognitive deficits remain unclear. Given recent data advances in the field of clinical neuroscience, it is now possible to conduct a synthesis of available data specifically related to hallucinations. These findings are integrated with the latest computational frameworks of hallucinations, and recommendations for future research are provided.

DOI: 10.1093/schbul/sbw075
PubMed: 27261492


Affiliations:


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pubmed:27261492

Le document en format XML

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<title level="j">Schizophrenia bulletin</title>
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<div type="abstract" xml:lang="en">This review from the International Consortium on Hallucinations Research intends to question the pertinence of the excitatory-to-inhibitory (E/I) imbalance hypothesis as a model for hallucinations. A large number of studies suggest that subtle impairments of the E/I balance are involved in neurological and psychiatric conditions, such as schizophrenia. Emerging evidence also points to a role of the E/I balance in maintaining stable perceptual representations, suggesting it may be a plausible model for hallucinations. In support, hallucinations have been linked to inhibitory deficits as shown with impairment of gamma-aminobutyric acid transmission, N-methyl-d-aspartate receptor plasticity, reductions in gamma-frequency oscillations, hyperactivity in sensory cortices, and cognitive inhibition deficits. However, the mechanisms by which E/I dysfunctions at the cellular level might relate to clinical symptoms and cognitive deficits remain unclear. Given recent data advances in the field of clinical neuroscience, it is now possible to conduct a synthesis of available data specifically related to hallucinations. These findings are integrated with the latest computational frameworks of hallucinations, and recommendations for future research are provided.</div>
</front>
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<Year>2016</Year>
<Month>08</Month>
<Day>18</Day>
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<Year>2017</Year>
<Month>07</Month>
<Day>19</Day>
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<Year>2017</Year>
<Month>09</Month>
<Day>02</Day>
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<ISSN IssnType="Electronic">1745-1701</ISSN>
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<Year>2016</Year>
<Month>Sep</Month>
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<Title>Schizophrenia bulletin</Title>
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<ArticleTitle>Are Hallucinations Due to an Imbalance Between Excitatory and Inhibitory Influences on the Brain?</ArticleTitle>
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<ELocationID EIdType="doi" ValidYN="Y">10.1093/schbul/sbw075</ELocationID>
<Abstract>
<AbstractText>This review from the International Consortium on Hallucinations Research intends to question the pertinence of the excitatory-to-inhibitory (E/I) imbalance hypothesis as a model for hallucinations. A large number of studies suggest that subtle impairments of the E/I balance are involved in neurological and psychiatric conditions, such as schizophrenia. Emerging evidence also points to a role of the E/I balance in maintaining stable perceptual representations, suggesting it may be a plausible model for hallucinations. In support, hallucinations have been linked to inhibitory deficits as shown with impairment of gamma-aminobutyric acid transmission, N-methyl-d-aspartate receptor plasticity, reductions in gamma-frequency oscillations, hyperactivity in sensory cortices, and cognitive inhibition deficits. However, the mechanisms by which E/I dysfunctions at the cellular level might relate to clinical symptoms and cognitive deficits remain unclear. Given recent data advances in the field of clinical neuroscience, it is now possible to conduct a synthesis of available data specifically related to hallucinations. These findings are integrated with the latest computational frameworks of hallucinations, and recommendations for future research are provided.</AbstractText>
<CopyrightInformation>© The Author 2016. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.</CopyrightInformation>
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<ForeName>Renaud</ForeName>
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<Affiliation>Univ Lille, CNRS UMR 9193, SCALab (psyCHIC Team) & CHU Lille, Psychiatry Department (CURE), Lille, France; renaud.jardri@chru-lille.fr.</Affiliation>
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<Affiliation>Department of Biological and Medical Psychology, University of Bergen; Department of Radiology, Division of Psychiatry, Haukeland University Hospital, Bergen, Norway;</Affiliation>
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<Affiliation>School of Psychiatry and Clinical Neurosciences, University of Western Australia, and Clinical Research Centre, Graylands Health Campus, North Metropolitan Area Health Service Mental Health, Perth, Western Australia, Australia;</Affiliation>
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<ForeName>Philip R</ForeName>
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<Affiliation>Department of Psychiatry, Yale University, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, New Haven, CT;</Affiliation>
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<LastName>Leptourgos</LastName>
<ForeName>Pantelis</ForeName>
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<Affiliation>Group for Neural Theory, INSERM U960, Institute of Cognitive Studies, École Normale Supérieure, Paris, France;</Affiliation>
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<LastName>Debbané</LastName>
<ForeName>Martin</ForeName>
<Initials>M</Initials>
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<Affiliation>Developmental Clinical Psychology Research Unit, Faculty of Psychology and Educational Sciences, University of Geneva, Geneva, Switzerland; Research Department of Clinical, Educational and Health Psychology, University College London, London, UK;</Affiliation>
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<Affiliation>Laboratoire de Psychologie du Développement et de l'Éducation de l'Enfant, UMR 8240, CNRS & Université Paris-Descartes (Sorbonne-Paris-Cité), Paris, France.</Affiliation>
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<Affiliation>Group for Neural Theory, INSERM U960, Institute of Cognitive Studies, École Normale Supérieure, Paris, France;</Affiliation>
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<Language>eng</Language>
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