Toward a neurobiology of delusions

Abstract

Delusions are the false and often incorrigible beliefs that can cause severe suffering in mental illness. We cannot yet explain them in terms of underlying neurobiological abnormalities. However, by drawing on recent advances in the biological, computational and psychological processes of reinforcement learning, memory, and perception it may be feasible to account for delusions in terms of cognition and brain function. The account focuses on a particular parameter, prediction error – the mismatch between expectation and experience – that provides a computational mechanism common to cortical hierarchies, frontostriatal circuits and the amygdala as well as parietal cortices. We suggest that delusions result from aberrations in how brain circuits specify hierarchical predictions, and how they compute and respond to prediction errors. Defects in these fundamental brain mechanisms can vitiate perception, memory, bodily agency and social learning such that individuals with delusions experience an internal and external world that healthy individuals would find difficult to comprehend. The present model attempts to provide a framework through which we can build a mechanistic and translational understanding of these puzzling symptoms.

Computational Psychiatry

“…However, deficits in this fMRI prediction error signal among subjects with first episode psychosis strongly correlated with the severity of delusions across subjects (Corlett et al 2007). Thus, false beliefs may be generated through compromised prediction error and sustained as aberrant learning transitions from being represented by model-based to modelfree systems (Corlett et al 2010). …”

Uncomfortably numb: new evidence for suppressed emotional reactivity in response to body-threats in those predisposed to sub-clinical dissociative experiences

“…However, these probabilistic interpretations can become corrupted, and aberrant biases in this process can lead to disorders in the sense of presence, embodiment and self-awareness (Bechara & Naqvi, 2004;Clark, 2013;Critchley et al, 2004;Herbert, Herbert & Pollatos, 2011;Corlett, Frith & Fletcher, 2009;Corlett, Honey, & Fletcher, 2007;Corlett, Taylor, Wang, Fletcher & Krystal, 2010;Friston, 2005;2010;Seth, 2009;Seth et al, 2012;Tsakiris, Tajadura-Jiménez & Costantini, 2011; see also Apps & Tsakiris, 2014). These predictive process are legion, constantly unfolding and occurring throughout a distributed network and at all levels of a hierarchically organised neuromatrix mediating selfconsciousness.…”

Cognitive phenotype of psychotic symptoms in Alzheimer's disease: evidence for impaired visuoperceptual function in the misidentification subtype

“…These findings are comparable with data from patients with schizophrenia and consistent with shared theories regarding the involvement of corticostriatal dopaminergic networks in the origins of delusions (Coltheart, 2010; Corlett et al ., 2010; White and Cummings, 1996). In the same sample, motor speed and sustained visual attention (Reeves et al ., 2010) correlated significantly with D2/3 receptor availability, but the sample size was too small to meaningfully compare performance in psychotic and nonpsychotic groups.…”