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      The Predictive Coding Account of Psychosis

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          Abstract

          Fueled by developments in computational neuroscience, there has been increasing interest in the underlying neurocomputational mechanisms of psychosis. One successful approach involves predictive coding and Bayesian inference. Here, inferences regarding the current state of the world are made by combining prior beliefs with incoming sensory signals. Mismatches between prior beliefs and incoming signals constitute prediction errors that drive new learning. Psychosis has been suggested to result from a decreased precision in the encoding of prior beliefs relative to the sensory data, thereby garnering maladaptive inferences. Here, we review the current evidence for aberrant predictive coding and discuss challenges for this canonical predictive coding account of psychosis. For example, hallucinations and delusions may relate to distinct alterations in predictive coding, despite their common co-occurrence. More broadly, some studies implicate weakened prior beliefs in psychosis, and others find stronger priors. These challenges might be answered with a more nuanced view of predictive coding. Different priors may be specified for different sensory modalities and their integration, and deficits in each modality need not be uniform. Furthermore, hierarchical organization may be critical. Altered processes at lower levels of a hierarchy need not be linearly related to processes at higher levels (and vice versa). Finally, canonical theories do not highlight active inference—the process through which the effects of our actions on our sensations are anticipated and minimized. It is possible that conflicting findings might be reconciled by considering these complexities, portending a framework for psychosis more equipped to deal with its many manifestations.

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          Most cited references76

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          Neocortical excitation/inhibition balance in information processing and social dysfunction.

          Severe behavioural deficits in psychiatric diseases such as autism and schizophrenia have been hypothesized to arise from elevations in the cellular balance of excitation and inhibition (E/I balance) within neural microcircuitry. This hypothesis could unify diverse streams of pathophysiological and genetic evidence, but has not been susceptible to direct testing. Here we design and use several novel optogenetic tools to causally investigate the cellular E/I balance hypothesis in freely moving mammals, and explore the associated circuit physiology. Elevation, but not reduction, of cellular E/I balance within the mouse medial prefrontal cortex was found to elicit a profound impairment in cellular information processing, associated with specific behavioural impairments and increased high-frequency power in the 30-80 Hz range, which have both been observed in clinical conditions in humans. Consistent with the E/I balance hypothesis, compensatory elevation of inhibitory cell excitability partially rescued social deficits caused by E/I balance elevation. These results provide support for the elevated cellular E/I balance hypothesis of severe neuropsychiatric disease-related symptoms.
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            Rethinking schizophrenia.

            How will we view schizophrenia in 2030? Schizophrenia today is a chronic, frequently disabling mental disorder that affects about one per cent of the world's population. After a century of studying schizophrenia, the cause of the disorder remains unknown. Treatments, especially pharmacological treatments, have been in wide use for nearly half a century, yet there is little evidence that these treatments have substantially improved outcomes for most people with schizophrenia. These current unsatisfactory outcomes may change as we approach schizophrenia as a neurodevelopmental disorder with psychosis as a late, potentially preventable stage of the illness. This 'rethinking' of schizophrenia as a neurodevelopmental disorder, which is profoundly different from the way we have seen this illness for the past century, yields new hope for prevention and cure over the next two decades.
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              Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia.

              The clinical hallmark of schizophrenia is psychosis. The objective of this overview is to link the neurobiology (brain), the phenomenological experience (mind), and pharmacological aspects of psychosis-in-schizophrenia into a unitary framework. Current ideas regarding the neurobiology and phenomenology of psychosis and schizophrenia, the role of dopamine, and the mechanism of action of antipsychotic medication were integrated to develop this framework. A central role of dopamine is to mediate the "salience" of environmental events and internal representations. It is proposed that a dysregulated, hyperdopaminergic state, at a "brain" level of description and analysis, leads to an aberrant assignment of salience to the elements of one's experience, at a "mind" level. Delusions are a cognitive effort by the patient to make sense of these aberrantly salient experiences, whereas hallucinations reflect a direct experience of the aberrant salience of internal representations. Antipsychotics "dampen the salience" of these abnormal experiences and by doing so permit the resolution of symptoms. The antipsychotics do not erase the symptoms but provide the platform for a process of psychological resolution. However, if antipsychotic treatment is stopped, the dysregulated neurochemistry returns, the dormant ideas and experiences become reinvested with aberrant salience, and a relapse occurs. The article provides a heuristic framework for linking the psychological and biological in psychosis. Predictions of this hypothesis, particularly regarding the possibility of synergy between psychological and pharmacological therapies, are presented. The author describes how the hypothesis is complementary to other ideas about psychosis and also discusses its limitations.
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                Author and article information

                Contributors
                Journal
                Biol Psychiatry
                Biol. Psychiatry
                Biological Psychiatry
                Elsevier
                0006-3223
                1873-2402
                01 November 2018
                01 November 2018
                : 84
                : 9
                : 634-643
                Affiliations
                [a ]Department of Psychiatry, Campus Charité Mitte, Charité – Universitätsmedizin Berlin, Berlin, Germany
                [b ]Department of Psychiatry and Psychotherapy, Charité University Medicine and St. Hedwig Hospital, Berlin Center for Advanced Neuroimaging, Humboldt University Berlin, Berlin, Germany
                [c ]Division of Psychiatry, University College London, London, United Kingdom
                [d ]Wellcome Trust Centre for Neuroimaging, University College London, London, United Kingdom
                [e ]Department of Psychiatry, Addenbrooke’s Hospital, University of Cambridge, Cambridge, United Kingdom
                [f ]Wellcome-MRC Behavioral and Clinical Neuroscience Institute, Cambridge and Peterborough Foundation Trust, Cambridge, United Kingdom
                [g ]Center for Clinical and Brain Sciences, Division of Psychiatry, Royal Edinburgh Hospital, University of Edinburgh, Edinburgh, United Kingdom
                [h ]Centre for Cognitive Neuroimaging, Institute of Neuroscience & Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom
                [i ]Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
                [j ]Department of Psychiatry, Yale University, New Haven, Connecticut
                Author notes
                []Address correspondence to Philip R. Corlett, Ph.D., Yale University, Department of Psychiatry, 34 Park St, New Haven, CT 06519. philip.corlett@ 123456yale.edu
                Article
                S0006-3223(18)31532-4
                10.1016/j.biopsych.2018.05.015
                6169400
                30007575
                43ff42da-ad9a-4e82-bdaf-aa5bf52bbdea
                © 2018 Society of Biological Psychiatry. All rights reserved.

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 15 November 2017
                : 14 May 2018
                : 15 May 2018
                Categories
                Article

                Clinical Psychology & Psychiatry
                bayesian brain,cognition,delusions,hallucinations,learning,perception,predictive coding,schizophrenia

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