Are Hallucinations Due to an Imbalance Between Excitatory and Inhibitory Influences on the Brain?
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.
Univ Lille, CNRS UMR 9193, SCALab (psyCHIC Team) & CHU Lille, Psychiatry Department (CURE), Lille, France; renaud.jardri@chru-lille.fr.
Renaud
R
Jardri
Department of Biological and Medical Psychology, University of Bergen; Department of Radiology, Division of Psychiatry, Haukeland University Hospital, Bergen, Norway;
Kenneth
K
Hugdahl
Brain & Psychological Sciences Centre, Swinburne University of Technology, Melbourne, Victoria, Australia;
Matthew
M
Hughes
Centre Interdisciplinaire de Recherche en Réadaptation et en Intégration Sociale (CIRRIS), Université Laval, Québec City, Québec, Canada; Université Lyon 1, INSERM U1028 & CNRS 5292, Lyon Neuroscience Research Centre (ΨR2 Team), Centre Hospitalier Le Vinatier, Lyon, France;
Jérôme
J
Brunelin
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;
Flavie
F
Waters
Department of Psychology, Durham University, Durham, UK;
Ben
B
Alderson-Day
School of Health and Social Sciences, Leeds Trinity University, Leeds, UK;
Dave
D
Smailes
Department of Psychiatry and Psychotherapy, Campus Charité Mitte, Charité - Universtätsmedizin Berlin, Berlin, Germany;
Philipp
P
Sterzer
Department of Psychiatry, Yale University, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, New Haven, CT;
Philip R
PR
Corlett
Group for Neural Theory, INSERM U960, Institute of Cognitive Studies, École Normale Supérieure, Paris, France;
Pantelis
P
Leptourgos
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;
Martin
M
Debbané
Laboratoire de Psychologie du Développement et de l'Éducation de l'Enfant, UMR 8240, CNRS & Université Paris-Descartes (Sorbonne-Paris-Cité), Paris, France.
Arnaud
A
Cachia
Group for Neural Theory, INSERM U960, Institute of Cognitive Studies, École Normale Supérieure, Paris, France;
Sophie
S
Denève
D001921:Brain / Q000378:metabolism / Q000503:physiopathology*; D006212:Hallucinations / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D009433:Neural Inhibition / Q000502:physiology*
Bayesian; GABA; NMDA; glutamate; hallucination; inhibition; oscillation; sensory gating