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. 2009 Jul 10:3:12.
doi: 10.3389/neuro.09.012.2009. eCollection 2009.

Why do delusions persist?

Affiliations

Why do delusions persist?

Philip R Corlett et al. Front Hum Neurosci. .

Abstract

Delusions are bizarre and distressing beliefs that characterize certain mental illnesses. They arise without clear reasons and are remarkably persistent. Recent models of delusions, drawing on a neuroscientific understanding of learning, focus on how delusions might emerge from abnormal experience. We believe that these models can be extended to help us understand why delusions persist. We consider prediction error, the mismatch between expectancy and experience, to be central. Surprising events demand a change in our expectancies. This involves making what we have learned labile, updating and binding the memory anew: a process of memory reconsolidation. We argue that, under the influence of excessive prediction error, delusional beliefs are repeatedly reconsolidated, strengthening them so that they persist, apparently impervious to contradiction.

Keywords: delusions; extinction; habit; prediction error; reconsolidation; salience.

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Figures

Figure 1
Figure 1
Prediction error responses during learning, extinction and reconsolidation. In these schematics, an upward deflection from the baseline reflects a positive prediction error and a downward deflection represents a negative prediction error (PE). (A) After normal learning – Dopamine neurons come to respond to the conditioned stimulus, the best predictor of the salient outcome (Schultz and Dickinson, 2000). When the CS is presented, the organism is reminded of the salient event (represented in red). (B) During extinction – When the salient event does not occur, a negative prediction error promotes new extinction learning: the formation of a competing CS–NoUs association (represented in blue) (Bouton, ; Eisenhardt and Menzel, 2007). (C) A small number of brief presentations promote reconsolidation over extinction – According to the IRH, brief presentations of the conditioned stimulus serve as a reminder and promote reconsolidation of the CS–US association, which overrides any new extinction learning that occurs when the salient event does not occur (Eisenhardt and Menzel, 2007). (D) Competition between reconsolidation and extinction – This schematic shows the competition between representations of the CS–US association (strengthened by reconsolidation) and the CS–NoUS association (formed during extinction). With brief reminder presentations, reconsolidation dominates over extinction.
Figure 2
Figure 2
Prediction error firing during delusion formation, maintenance and resolution. (A) Aberrant prediction error promotes delusion formation – Aberrant, internally generated prediction error signals imbue mere coincidences (the colors of doors and the sides of the street) with significance which demands explanation (Chadwick, 2001). When an explanation is arrived at, the insight relief may engender dopamine firing which further stamps in the association between the odd experiences and the Organization (Miller, 1993). (B) Aberrant prediction error promotes delusion maintenance – Once the explanatory scheme has been developed, it is invoked any time an aberrant prediction error occurs. These reminders, serve to reconsolidate the belief that odd experiences are a result of the malevolent intervention of The Organization. This reconsolidation overcomes any extinction learning that may occur when no harm comes to the sufferer from The Organization or when others try to convince the sufferer that The Organization is not ministrating against them. (C) Medications target aberrant prediction error – Antipsychotic medications target aberrant prediction error signals, reminders do not occur and as such reconsolidation is blocked. New extinction learning is allowed to prevail and the individual recovers from their delusion. The mechanism for this targeting of prediction error induced reconsolidation may be at the level of neurotransmission in the synapse (e.g., Aripiprazole blocking phasic dopamine signaling (Hamamura et al., 2007) or it may be intracellular, targeting the way in which the experience-explanation belief is stored epigenetically (Bredy and Barad, 2008). (D) Aberrant prediction error promotes delusion maintenance – Prediction errors modulate the representations that govern behavior. Under aberrant prediction error, beliefs reconsolidate rather than extinguish. (E) Medication permits extinction learning by blocking aberrant prediction error – Under antipsychotic medication, aberrant prediction errors are blocked, allowing extinction learning to dominate and the resolution of the delusional belief.

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