We provide a battery of examples of delusions against which theoretical accounts can be tested. Then, we identify neuropsychological anomalies that could produce the unusual experiences that may lead, in turn, to the delusions in our battery. However, we argue against Maher’s view that delusions are false beliefs that arise as normal responses to anomalous experiences. We propose, instead, that a second factor is required to account for the transition from unusual experience to delusional belief. The second factor in the (...) aetiology of delusions can be described superficially as a loss of the ability to reject a candidate for belief on the grounds of its implausibility and its inconsistency with everything else that the patient knows. But we point out some problems that confront any attempt to say more about the nature of this second factor. (shrink)

Chris Frith has argued that a loss of the sense of agency is central to schizophrenia. This suggests a connection between hallucinations and delusions on the one hand, and the misidentification of the subject’s imaginings as perceptions and beliefs on the other. In particular, understanding the mechanisms that underlie imagination may help us to explain the puzzling phenomena of thought insertion and withdrawal. Frith sometimes states his argument in terms of a loss of metarepresentational capacity in schizophrenia. I argue that (...) this formulation is unhelpful. (shrink)

In their target article, McKay & Dennett (M&D) conclude that only “positive illusions” are adaptive misbeliefs. Relying on overly strict conceptual schisms (deficit vs. motivational, functional vs. organic, perception vs. belief), they prematurely discount delusions asbiologicallyadaptive. In contrast to their view that “motivation” plays a psychological but not a biological function in a two-factor model of the forming and maintenance of delusions, we propose asingleimpairment in prediction-error–driven (i.e., motivational) learning in three stages in which delusions play a biologically adaptive role.

This paper contrasts an interactionist account of delusional misidentification with more traditional one- and two-stage models. Unlike the unidirectional nature of these more traditional models, in which the aetiology of the disorder is said to progress from a neurological disruption via an anomalous experience to a delusional belief, the interactionist account posits the interaction of top-down and bottom-up processes to better explain the maintenance of the delusional belief. In addition, it places a greater emphasis on the patient’s underlying phenomenal experience (...) in accounting for the specificity of the delusional content. The role played by patient phenomenology is examined in light of Ratcliffe’s recent phenomenological account. Similarities and differences are discussed. The paper concludes that a purely phenomenological account is unable to differentiate between non-delusional patient groups, who have what appear to be equivalent phenomenal experiences to patients suffering from delusional misidentification but without the delusional belief, and delusional groups, something the interactionist model is able to do. (shrink)

Circumscribed delusional beliefs can follow brain injury. We suggest that these involve anomalous perceptual experiences created by a deficit to the person's perceptual system, and misinterpretation of these experiences due to biased reasoning. We use the Capgras delusion (the claim that one or more of one's close relatives has been replaced by an exact replica or impostor) to illustrate this argument. Our account maintains that people voicing this delusion suffer an impairment that leads to faces being perceived as drained of (...) their normal affective significance, and an additional reasoning bias that leads them to put greater weight on forming beliefs that are observationally adequate rather than beliefs that are a conservative extension of their existing stock. We show how this position can integrate issues involved in the philosophy and psychology of belief, and examine the scope for mutually beneficial interaction. (shrink)

In this paper I discuss the role played by disturbed phenomenology in accounting for the formation and maintenance of the Capgras delusion. Whilst endorsing a two-stage model to explain the condition, I nevertheless argue that traditional accounts prioritise the role played by some form of second-stage cognitive disruption at the expense of the significant contribution made by the patient’s disturbed phenomenology, which is often reduced to such uninformative descriptions as “anomalous” or “strange”. By advocating an interactionist model, I argue that (...) the delusional belief constitutes an attempt on the part of the patient to explain his/her initially odd and somewhat disturbed phenomenal content and, moreover, that the delusion then structures the patient’s experience such that what he/she perceives is an impostor. This fact is used to explain the delusional belief’s maintenance and resistance to revision. Thus, whilst accepting that second-stage cognitive disruption has a part to play in explaining the Capgras delusion, the emphasis here is placed on the role played by the patient’s changing phenomenal content and its congruence with the delusional belief. Unlike traditional two-stage models, which posit a unidirectional progression from experience to belief, the interactionist model advocates a two-way interaction between bottom-up and top-down processes. The application of this model to other delusional beliefs is also considered. (shrink)