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)

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)

Article copyright 2002. 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 etiology 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)

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.