From drugs to deprivation: a Bayesian framework for understanding models of psychosis
Philip R. Corlett, Chris Frith, Paul C. Fletcher
Psychopharmacology May 27, 2009 DOI: 10.1007/s00213-009-1561-0 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Theoretical or philosophical paper Peer reviewed |
|---|---|
| Citations | 392 |
| Key points | Argues that Bayesian formulations of brain information processing provide a framework linking neural circuitry to psychotic symptoms, explaining similarities and differences across drug models and highlighting sensory deprivation as a relevant model. |
Abstract
Introduction: Various experimental manipulations, usually involving drug administration, have been used to produce symptoms of psychosis in healthy volunteers. Different drugs produce both common and distinct symptoms. A challenge is to understand how apparently different manipulations can produce overlapping symptoms. We suggest that current Bayesian formulations of information processing in the brain provide a framework that maps onto neural circuitry and gives us a context within which we can relate the symptoms of psychosis to their underlying causes. This helps us to understand the similarities and differences across the common models of psychosis.
Materials and Methods: The Bayesian approach emphasises processing of information in terms of both prior expectancies and current inputs. A mismatch between these leads us to update inferences about the world and to generate new predictions for the future. According to this model, what we experience shapes what we learn, and what we learn modifies how we experience things.
Discussion: This simple idea gives us a powerful and flexible way of understanding the symptoms of psychosis where perception, learning and inference are deranged. We examine the predictions of the cognitive model in light of what we understand about the neuropharmacology of psychotomimetic drugs and thereby attempt to account for the common and the distinctive effects of NMDA receptor antagonists, serotonergic hallucinogens, cannabinoids and dopamine agonists.
Conclusion: By acknowledging the importance of perception and perceptual aberration in mediating the positive symptoms of psychosis, the model also provides a useful setting in which to consider an under-researched model of psychosis-sensory deprivation.
Citations in the library
Cited by 92
- The Predictive Coding Account of Psychosis. Biological Psychiatry May 25, 2018
- The default-mode, ego-functions and free-energy: a neurobiological account of Freudian ideas Brain February 28, 2010
- Ego-Dissolution and Psychedelics: Validation of the Ego-Dissolution Inventory (EDI) Frontiers in Human Neuroscience June 14, 2016
- Unifying Theories of Psychedelic Drug Effects Frontiers in Pharmacology March 2, 2018
- Drug models of schizophrenia. Therapeutic Advances in Psychopharmacology February 1, 2015
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Cites 26
- Subanesthetic Effects of the Noncompetitive NMDA Antagonist, Ketamine, in Humans Archives of General Psychiatry March 1, 1994
- Recent advances in the phencyclidine model of schizophrenia American Journal of Psychiatry October 1, 1991
- Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. American Journal of Psychiatry 2003
- Activation of Glutamatergic Neurotransmission by Ketamine: A Novel Step in the Pathway from NMDA Receptor Blockade to Dopaminergic and Cognitive Disruptions Associated with the Prefrontal Cortex Journal of Neuroscience April 15, 1997
- The dissociative anaesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurones by N‐methyl‐aspartate British Journal of Pharmacology June 1, 1983
and 21 more in the library