Brains, it has recently been argued, are essentially prediction machines. They are bundles of cells that support perception and action by constantly attempting to match incoming sensory inputs with top-down expectations or predictions. This is achieved using a hierarchical generative model that aims to minimize prediction error within a bidirectional cascade of cortical processing. Such accounts offer a unifying model of perception and action, illuminate the functional role of attention, and may neatly capture the special contribution of cortical processing to (...) adaptive success. This target article critically examines this approach, concluding that it offers the best clue yet to the shape of a unified science of mind and action. Sections 1 and 2 lay out the key elements and implications of the approach. Section 3 explores a variety of pitfalls and challenges, spanning the evidential, the methodological, and the more properly conceptual. The paper ends (sections 4 and 5) by asking how such approaches might impact our more general vision of mind, experience, and agency. (shrink)

Does the formation of delusions involve abnormal reasoning? According to the prominent ‘two-factor’ theory of delusions (e.g. Coltheart, 2007), the answer is yes. The second factor in this theory is supposed to affect a deluded individual's ability to evaluate candidates for belief. However, most published accounts of the two-factor theory have not said much about the nature of this second factor. In an effort to remedy this shortcoming, Coltheart, Menzies and Sutton (2010) recently put forward a Bayesian account of inference (...) in delusions. I outline some criticisms of this important account, and sketch an alternative account of delusional inference that, I argue, avoids these criticisms. Specifically, I argue that the second factor in delusion formation involves a systematic deviation from Bayesian updating, a deviation that may be characterized as a bias towards ‘explanatory adequacy’. I present a numerical model of this idea and show that my alternative account is broadly consistent with prominent prediction error models of delusion formation (e.g. Corlett, Murray et al., 2007). (shrink)

Bortolotti’s Delusions and Other Irrational Beliefs defends the view that delusions are beliefs on a continuum with other beliefs. A different view is that delusions are more like illusions, that is, they arise from faulty perception. This view, which is not targeted by the book, makes it easier to explain why delusions are so alien and disabling but needs to appeal to forensic aspects of functioning.

“Mad belief” (in analogy with Lewisian “mad pain”) would be a belief state with none of the causal role characteristic of belief—a state not caused or apt to have been caused by any of the sorts of events that usually cause belief and involving no disposition toward the usual behavioral or other manifestations of belief. On token-functionalist views of belief, mad belief in this sense is conceptually impossible. Cases of delusion—or at least some cases of delusion—might be cases of belief (...) gone half-mad, cases in which enough of the functional role characteristic of belief is absent that the subject is in an “in-between” state regarding the delusive content, such that it is neither quite right to say the subject determinately believes the delusive content nor quite right to say that she determinately fails to believe that content. Although Bortolotti (2010) briefly mentions such “sliding scale” approaches to the relationship of delusion and belief, she dismisses such approaches on rather thin grounds and then later makes some remarks that seem consonant with sliding scale approaches. (shrink)

Delusional beliefs have sometimes been considered as rational inferences from abnormal experiences. We explore this idea in more detail, making the following points. Firstly, the abnormalities of cognition which initially prompt the entertaining of a delusional belief are not always conscious and since we prefer to restrict the term “experience” to consciousness we refer to “abnormal data” rather than “abnormal experience”. Secondly, we argue that in relation to many delusions (we consider eight) one can clearly identify what the abnormal cognitive (...) data are which prompted the delusion and what the neuropsychological impairment is which is responsible for the occurrence of these data; but one can equally clearly point to cases where this impairments is present but delusion is not. So the impairment is not sufficient for delusion to occur. A second cognitive impairment, one which impairs the ability to evaluate beliefs, must also be present. Thirdly (and this is the main thrust of our chapter) we consider in detail what the nature of the inference is that leads from the abnormal data to the belief. This is not deductive inference and it is not inference by enumerative induction; it is abductive inference. We offer a Bayesian account of abductive inference and apply it to the explanation of delusional belief. (shrink)

In this paper we defend the doxastic conception of delusions against the metacognitive account developed by Greg Currie and collaborators. According to the metacognitive model, delusions are imaginings that are misidentified by their subjects as beliefs: the Capgras patient, for instance, does not believe that his wife has been replaced by a robot, instead, he merely imagines that she has, and mistakes this imagining for a belief. We argue that the metacognitive account is untenable, and that the traditional conception of (...) delusions as beliefs should be retained. (shrink)

Recreative Minds develops a philosophical theory of imagination that draws upon the latest work in psychology. This theory illuminates the use of imagination in coming to terms with art, its role in enabling us to live as social beings, and the psychological consequences of disordered imagination. The authors offer a lucid exploration of a fascinating subject.

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)

A new theory is taking hold in neuroscience. It is the theory that the brain is essentially a hypothesis-testing mechanism, one that attempts to minimise the error of its predictions about the sensory input it receives from the world. It is an attractive theory because powerful theoretical arguments support it, and yet it is at heart stunningly simple. Jakob Hohwy explains and explores this theory from the perspective of cognitive science and philosophy. The key argument throughout The Predictive Mind is (...) that the mechanism explains the rich, deep, and multifaceted character of our conscious perception. It also gives a unified account of how perception is sculpted by attention, and how it depends on action. The mind is revealed as having a fragile and indirect relation to the world. Though we are deeply in tune with the world we are also strangely distanced from it. (shrink)

The two-factor theory (Davies, Coltheart, Langdon & Breen 2001; Coltheart 2007; Coltheart, Menzies & Sutton 2010) is an influential account of delusion formation. According to the theory, there are two distinct factors that are causally responsible for delusion formation. The first factor is supposed to explain the content of the delusion, while the second factor is supposed to explain why the delusion is adopted and maintained. Recently, another remarkable account of delusion formation has been proposed, in which the notion of (...) “prediction error” plays the central role (Fletcher & Frith 2009; Corlett, Krystal, Taylor & Fletcher 2009; Corlett, Taylor, Wang, Fletcher & Krystal 2010). According to this account, the prediction-error theory, delusions are formed in response to aberrant prediction-error signals, those signals that indicate a mismatch between expectation and actual experience. -/- In this chapter, we examine the relationship between the two-factor theory and the prediction-error theory in some detail. Our view is that the prediction-error theory does not have to be understood as a rival to the two-factor theory. We do not deny that there are some important differences between them. However, those differences are not as significant as they have been presented in the literature. Moreover, the core ideas of the prediction-error theory may be incorporated into the two- factor framework. For instance, the aberrant prediction-error signal that is posited by prediction-error theorists can be (or underlie) the first factor contributing to the formation of some delusions, and help explain the content of those delusions. Alternatively, the aberrant prediction-error signal can be (or underlie) the second factor, and help explain why the delusion is adopted and maintained. (shrink)

It has been argued that schizophrenic delusions are “behaviourally inert.” This is evidence for the phenomenon of “double bookkeeping,” according to which people are not consistent in their commitment to the content of their delusions. The traditional explanation for the phenomenon is that people do not genuinely believe the content of their delusions. In the article, we resist the traditional explanation and offer an alternative hypothesis: people with delusions often fail to acquire or to maintain the motivation to act on (...) their delusional beliefs. This may be due to avolition, to emotional disturbances, or to the fact that, given the peculiar content of some delusions, the surrounding environment does not support the agent’s motivation to act. (shrink)

[About the book]: Neuroscience has long had an impact on the field of psychiatry, and over the last two decades, with the advent of cognitive neuroscience and functional neuroimaging, that influence has been most pronounced. However, many question whether psychopathology can be understood by relying on neuroscience alone, and highlight some of the perceived limits to the way in which neuroscience informs psychiatry. Psychiatry as Cognitive Neuroscience is a philosophical analysis of the role of neuroscience in the study of psychopathology. (...) The book examines numerous cognitive neuroscientific methods, such as neuroimaging and the use of neuropsychological models, in the context of a variety of psychiatric disorders, including depression, schizophrenia, dependence syndrome, and personality disorders. Psychiatry as Cognitive Neuroscience includes chapters on the nature of psychiatry as a science; the compatibility of the accounts of mental illness derived from neuroscience, information-processing, and folk psychology; the nature of mental illness; the impact of methods such as fMRI, neuropsychology, and neurochemistry, on psychiatry; the relationship between phenomenological accounts of mental illness and those provided by naturalistic explanations; the status of delusions and the continuity between delusions and ordinary beliefs; the interplay between clinical and empirical findings in psychopathology and issues in moral psychology and ethics. With contributions from world class experts in philosophy and cognitive science, this book will be essential reading for those who have an interest in the importance and the limitations of cognitive neuroscience as an aid to understanding mental illness. (shrink)

Objective: The clinical hallmark of schizophrenia is psychosis. The objective of this overview is to link the neurobiology (brain), the phenomenological experience (mind), and pharmacological aspects of psychosis-in-schizophrenia into a unitary framework. -/- Method: Current ideas regarding the neurobiology and phenomenology of psychosis and schizophrenia, the role of dopamine, and the mechanism of action of antipsychotic medication were integrated to develop this framework. -/- Results: A central role of dopamine is to mediate the "salience" of environmental events and internal representations. (...) It is proposed that a dysregulated, hyperdopaminergic state, at a "brain" level of description and analysis, leads to an aberrant assignment of salience to the elements of one's experience, at a "mind" level. Delusions are a cognitive effort by the patient to make sense of these aberrantly salient experiences, whereas hallucinations reflect a direct experience of the aberrant salience of internal representations. Antipsychotics "dampen the salience" of these abnormal experiences and by doing so permit the resolution of symptoms. The antipsychotics do not erase the symptoms but provide the platform for a process of psychological resolution. However, if antipsychotic treatment is stopped, the dysregulated neurochemistry returns, the dormant ideas and experiences become reinvested with aberrant salience, and a relapse occurs. -/- Conclusions: The article provides a heuristic framework for linking the psychological and biological in psychosis. Predictions of this hypothesis, particularly regarding the possibility of synergy between psychological and pharmacological therapies, are presented. The author describes how the hypothesis is complementary to other ideas about psychosis and also discusses its limitations. (shrink)

In this paper we defend the doxastic conception of delusions against the metacognitive account developed by Greg Currie and collaborators. According to the metacognitive model, delusions are imaginings that are misidentified by their subjects as beliefs: the Capgras patient, for instance, does not believe that his wife has been replaced by a robot, instead, he merely imagines that she has, and mistakes this imagining for a belief. We argue that the metacognitive account is untenable, and that the traditional conception of (...) delusions as beliefs should be retained. (shrink)

Bortolotti argues that the irrationality of many delusions is no different in kind from the irrationality that marks many non-pathological states typically treated as beliefs. She takes this to secure the doxastic status of those delusions. Bortolotti’s approach has many benefits. For example, it accounts for the fact that we can often make some sense of what deluded subjects are up to, and helps explain why some deluded subjects are helped by cognitive behavioral therapy. But there is an alternative approach (...) that secures the same benefits as Bortolotti’s account while bringing additional benefits. The alternative approach treats both many delusions and many of the non-pathological states to which Bortolotti compares them as in-between states. Subjects in in-between states don’t fully believe the beliefs which it is sometimes convenient to ascribe to them. This alternative approach to belief and belief-ascription fits well with an independently attractive account of the varied purposes of our ordinary attitude ascriptions. It also makes it easier to make fine-grained distinctions between intentional attitudes of different kinds. (shrink)

Young and colleagues . Betwixt life and death: case studies of the Cotard delusion. In P. W. Halligan & J. C. Marshall , Method in madness: Case studies in cognitive neuropsychiatry. Mahway, NJ: Lawrence Erlbaum Associates.) have suggested that cases of the Cotard delusion result when a particular perceptual anomaly occurs in the context of an internalising attributional style. This hypothesis has not previously been tested directly. We report here an investigation of attributional style in a 24-year-old woman with Cotard (...) delusion . LU’s attributional style was assessed using the Internal, Personal and Situational Attributions Questionnaire . A new measure of causal locus: the internal, personal and situational attributions questionnaire. Personality and Individual Differences, 20, 261–264.). LU showed a significantly greater proportion of internalising attributions than the control group, both overall and for negative events specifically. The results obtained thus support an association of Cotard delusion with an internalising attributional style, and are therefore consistent with the account of Young and colleagues. The potential brain basis of Cotard delusion is discussed. (shrink)

Subjects with delusions profess to believe some extremely peculiar things. Patients with Capgras delusion sincerely assert that, for example, their spouses have been replaced by impostors. Patients with Cotard’s delusion sincerely assert that they are dead. Many philosophers and psychologists are hesitant to say that delusional subjects genuinely believe the contents of their delusions.2 One way to reinterpret delusional subjects is to say that we’ve misidentified the content of the problematic belief. So for example, rather than believing that his wife (...) is has been replaced by an impostor, we might say that the victim of Capgras delusion believes that it is, in some respects, as if his wife has been replaced by an impostor. Another is to say that we’ve misidentified the attitude that the delusional subject bears to the content of their delusion. So for example, Gregory Currie and co-authors have suggested that rather than believing that his wife has been replaced by an impostor, we should say that the victim of Capgras delusion merely imagines that his wife has been replaced by an impostor.3. (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)

A number of philosophers have argued that psychiatric delusions threaten Donald Davidson's rationalist account of intentional agency. I argue that a careful look at both Davidson's account and psychiatric delusions shows that, in fact, the two are perfectly compatible. Indeed, a Davidsonian perspective on psychiatric delusions proves remarkably illuminating.