Elisabeth Pacherie is a research fellow in philosophy at Institut Jean Nicod, Paris. Her main research and publications are in the areas of philosophy of mind, psychopathology and action theory. Her publications include a book on intentionality (_Naturaliser_ _l'intentionnalité_, Paris, PUF, 1993) and she is currently preparing a book on action and agency.

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)

Cognitive neuropsychiatry (CN) is the explanation of psychiatric disorder by the methods of cognitive neuropsychology. Within CN there are, broadly speaking, two approaches to delusion. The first uses a one-stage model, in which delusions are explained as rationalizations of anomalous experiences via reasoning strategies that are not, in themselves, abnormal. Two-stage models invoke additional hypotheses about abnormalities of reasoning. In this paper, I examine what appears to be a very strong argument, developed within CN, in favor of a two-stage explanation (...) of the difference in content between the Capgras and Cotard delusions. That explanation treats them as alternative rationalizations of essentially the same phenomenology. I show, however, that once we distinguish the phenomenology (and the neuroetiology), a one-stage model is adequate. In the final section I make some more general remarks on the one- and two-stage models. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 11.1 (2004) 65-70 [Access article in PDF] Top-Down and Bottom-Up in Delusion Formation Jakob Hohwy Keywords delusions, top-down, bottom-up, predictive coding Some delusions may arise as responses to unusual experiences (Davies et al. 2001; Maher 1974;). The implication is that delusion formation in some cases involves some kind of bottom-up mechanism—roughly, from perception to belief. Delusion formation may also involve some kind of top-down mechanism. (...) This could be in the shape of a patient's flawed background beliefs, or biases, which somehow modulate perception or ensure delusional interpretations of experience. There is little agreement about what kind of mechanism is primary in delusion formation, or, indeed, what the particular mechanisms and their neural substrates might be.In the evaluation of top-down and bottom-up mechanisms in delusion formation, a number of conceptual questions should be addressed (Davies and Coltheart 2000). For example, if there is an experiential component, why is a hypothesis with a delusional explanation of the unusual experience seen as relevant? Why do the subjects come to believe it tenaciously? How come some unusual experiences do not develop into delusions?A number of empirical findings also need to be taken into account: for example, the damage to the autonomic system in Capgras delusion (Ellis et al. 1997), the decreased ability for fast error correction in schizophrenia (Frith and Done 1989), modulation of activity in parietal cortex in delusions of alien control and other passivity experiences (Blakemore, Oakley, and Frith 2003), and also in schizophrenia, the increased sensitivity to self-produced stimuli, such as tickling oneself (Blakemore et al. 2000) and the sound of one's own voice (Ford et al. 2001).Theory choice can also be guided by philosophical doctrines about, for example, the nature of belief, the constitutive role of rationality, and intersubjectivity and the nature of judgements about the external world. It is natural, however, to let beliefs about philosophical doctrine be secondary to empirical findings and conceptual issues.The distinction between bottom-up and top-down mechanisms is particularly sharp in John Campbell's (2001) account of delusions and in Tim Bayne and Elisabeth Pacherie's (2004) discussion of Campbell. In this discussion, top-down approaches are associated with the general philosophical doctrine of rationalism, and bottom-up approaches with the philosophical doctrine of empiricism. Campbell's account is top-down because he posits delusional framework beliefs that arise directly as a result of brain damage or malfunction, and that work in some top-down fashion on the interpretation of experience. Bayne [End Page 65] and Pacherie convincingly defend empiricism against Campbell's rationalist account. Among their many other objections, they briefly puzzle about how a delusional framework belief (e.g., that one's spouse is an impostor) in a top-down fashion could cause the damage to the autonomic system seen in the Capgras and Cotard delusions (2004, 1). I think this is a very important objection because skin conductance data are part of the evidence for the bottom-up hypothesis concerning the Capgras delusion. We could add to this, for example, that it is mysterious how belief in a top-down fashion could cause people with schizophrenia to be worse at fast error correction than normal controls, to be better at tickling themselves than normal controls, and to have an increased response to the sound of their own voice.On the other hand, although the skin conductance response (SCR) evidence suggests a bottom-up approach to the Capgras delusion, it does not explain the character of the subjective experience that is hypothesized to give rise to the delusional belief: reduced SCR is not part of the experience itself (thanks to Ian Gold for discussion of this). Something more is required to give a full account of the type of experience that gives rise to the delusion. Further, as they stand, most bottom-up accounts are unable to account for why reality testing fails for beliefs based on these experiences.Neither rationalism nor empiricism on their own seem able to address the conceptual questions while paying... (shrink)

Although a common clinical phenomenon, delusions are difficult to explain and have a problematic conceptual status. Advances in understanding delusions have come from studies which involve detailed investigation of particular types of delusion. Some of this work is summarised, with the Capgras and Cotard delusions as specific examples. These are used to high-highlight questions for which there is the potential for fruitful dialogue with philosophers. Such questions include the criteria for deciding that a statement represents a belief, the extent to (...) which we integrate our beliefs into a coherent web, and the nature and limits of human rationality. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 9.1 (2002) 65-72 [Access article in PDF] Multiple Paths to Delusion Philip Gerrans Response to Phillips JAMES PHILLIPS COMMENTS are summarized in four recommendations. Clarify the Relationship of the Cognitive Model to its Neuroscientific Base The cognitive approach postulates a cognitive entity whose information-processing properties explain a symptom or unify a set of symptoms. The key idea is that we can use a model of (...) normal cognitive functioning to explain a disorder in terms of failure of a component of the model. In the case under discussion, the symptom is the loss of affect, which is part of the clinical profile of both the Capgras and Cotard delusions. The body of neuropsychological data concerning links between recognitional and affective processes extends back at least to Charcot's patient M. X. whose affective responses to familiar situations were lost, together with his visual episodic memory. M. X described his phenomenology this way: A remarkable consequence of this loss of mental ability is, as I have said, the change in my personality and impressions. I am much less affected by sorrow or grief. I can tell you that, after losing one of my relatives with whom I was very close, I experienced a much less intense grief than if I had still been able to image the features of that relative, the stages of the illness he went through, or especially if I had been able to picture to myself [voir interieurement] the outward effect of this untimely death on the members of my family. (Young and van de Wal 1996) (It is interesting to note that M. X. retained insight into his condition and explained it in a lucid, rational way rather than forming a delusional belief. Initial evidence for a two-stage theory, one might have thought).Given convergent evidence that the limbic system is the basis of affective states, the hypothesis that the delusions under discussion are rationalizations of unusual affective experiences consequent on abnormal limbic function or loss of connection between limbic and other functions is an inference to the best explanation. The Young-Ellis model is a cognitive model that describes cognitive function at what Dennett calls the design level, intermediate between what Marr called the computational level and level of representation and algorithm. As such it implies only that the boxes and arrows are implemented neurally, but endorses no hypotheses about the nature of that implementation.It is correct of Phillips to observe that the crucial inference about the link between affective and cognitive function is grounded in a background theory of the relationship between cognitive models, clinical symptoms, and neurobiology. If Phillips' complaint is that the model cannot be sheeted home to a neurobiological substrate, [End Page 65] this is true. Implementation theories are thin on the ground in cognitive science because they would require a theory of biological computation that, despite partisan claims, is elusive. Nonetheless, information-processing models and partial implementation theories for specific functions such as perception, language, face recognition, and the affective systems do exist. The allusion to cognitive structure remains sound as long as it accounts for observable clinical and experimental data and makes verifiable predictions.The fact that the Young-Ellis model of face recognition can account for both normal function and a variety of forms of prosopagnosia together (under assumptions about the relation between belief and experience) with delusions of misidentification counts in its favor (Ellis 1998).Phillips objection to cognitive theories is stronger when we turn to models of belief and rationality. In the case of functions such as face recognition or language, there is a variety of convergent evidence, especially from deficit studies, to support a model of normal cognitive function. For example, we know that face recognition activates schemas concerning orientation, features, emotions, and gender because these components can be selectively damaged (Young 1998). However, we lack a model of normal human reasoning other than "folk theory" of belief-desire psychology. Cognitive theories of belief formation are often forced to use models derived from philosophy such as logic, probability theory, or decision theory, which are amenable to... (shrink)

After presenting and criticizing recent theoretical work on the nature of delusional belief, I argue that the works of the later Wittgenstein and Donald Davidson offer heretofore underappreciated insights into delusional belief. I distinguish two general kinds of delusion: pedestrian and stark. The former can be explained as cognitive mistakes of various kinds, whereas the latter I argue are necessarily inexplicable. This thesis requires the denial of the Davidsonian dogma that rationality is constitutive of mental content. I claim that the (...) dogma holds only for normal cognition and is violated precisely in the case of stark delusion. (shrink)

This paper explores the phenomenology of the Capgras and Cotard delusions. The former is generally characterised as the belief that relatives or friends have been replaced by impostors, and the latter as the conviction that one is dead or has ceased to exist. A commonly reported feature of these delusions is an experienced ''defamiliarisation'' or even ''derealisation'' of things, which is associated with an absence or distortion of affect. I suggest that the importance attributed to affect by current explanations of (...) delusional experience can serve to make explicit the manner in which we ordinarily experience the world under a taken-for-granted aspect of affective familiarity. This implicit feeling is, I argue, partly constitutive of our sense of reality. However, so-called ''folk psychology,'' which is generally adopted by philosophers as an initial interpretive backdrop for delusional beliefs and for beliefs more generally, fails to accommodate it. As a consequence, some pervasive philosophical assumptions concerning the manner in which we experience and understand the world, ourselves, and each other are called into question. (shrink)

In this book, psychologists and philosophers describe and discuss a range of case studies of delusional beliefs, drawing out general lessons both for the cognitive architecture of the mind and for the notion of rationality, and exploring connections between the delusional beliefs that occur in schizophrenia and the flawed understanding of beliefs that is characteristic of autism.

An elegant theory in cognitive neuropsychiatry explains the Capgras and Cotard delusions as resulting from the same type of anomalous phenomenal experience explained in different ways by different sufferers. ‘Although the Capgras and Cotard delusions are phenomenally distinct, we thus think that they represent patients’ attempts to make sense of fundamentally similar experiences’ (Young and Leafhead, 1996, p. 168). On the theory proposed by Young and Leafhead, the anomalous experience results from damage to an information processing subsystem which associates an (...) affect of ‘familiarity’ with overt recognition of faces, and, sometimes, scenes and objects. When the normal affect of familiarity is absent the subject experiences an unusual feeling of derealization or depersonalization. The Cotard and Capgras patients adopt different, delusional, explanations of this unusual qualitative state, for reasons to do with ‘attributional style’. It is part of this attribution hypothesis that delusional subjects, like normal people, interpret perceptual phenomena in the light of a set of background beliefs whose structure is a product of social/contextual influences and individual psychological dispositions. That structure predisposes people to reason in certain ways, to discount or reinterpret evidence and to favour certain hypoth-. (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)

Psychiatric treatment and diagnosis rests upon a richer conception of normativity than, for example, cognitive neuropsychology. This paper explores the role that considerations of rationality can play in defining this richer conception of normativity. It distinguishes two types of rationality and considers how each type can break down in different ways in delusional psychiatric disorders.

Some monothematic types of delusions may arise because subjects have unusual experiences. The role of this experiential component in the pathogenesis of delusion is still not understood. Focussing on delusions of alien control, we outline a model for reality testing competence on unusual experiences. We propose that nascent delusions arise when there are local failures of reality testing performance, and that monothematic delusions arise as normal responses to these. In the course of this we address questions concerning the tenacity with (...) which delusions are maintained, their often bizarre content, the patients’ inability to dismiss them, and their often circumscribed character. (shrink)

Face perception, perhaps the most highly developed visual skill in humans, is mediated by a distributed neural system in humans that is comprised of multiple, bilateral regions. We propose a model for the organization of this system that emphasizes a distinction between the representation of invariant and changeable aspects of faces. The representation of invariant aspects of faces underlies the recognition of individuals, whereas the representation of changeable aspects of faces, such as eye gaze, expression, and lip movement, underlies the (...) perception of information that facilitates social communication. The model is also hierarchical insofar as it is divided into a core system and an extended system. The core system is comprised of occipitotemporal regions in extrastriate visual cortex that mediate the visual analysis of faces. In the core system, the representation of invariant aspects is mediated more by the face-responsive region in the fusiform gyrus, whereas the representation of changeable aspects is mediated more by the face-responsive region in the superior temporal sulcus. The extended system is comprised of regions from neural systems for other cognitive functions that can be recruited to act in concert with the regions in the core system to extract meaning from faces. (shrink)

In this paper I consider a theory developed within cognitive neuropsychiatry to explain two delusions of misidentification, the Capgras and the Cotard delusions. These delusions are classified together with others in which the subject misidentifies persons, places or objects, including parts of her own body. Strictly speaking, the Cotard may not, at the level of content, be a delusion of misidentification, but I have described it as such because the theory I discuss treats it as sharing a causal and a (...) conceptual structure with the Capgras delusion. That theory, associated particularly with the work of Andy Young, raises a Wittgensteinian echo in its claim that, at the subpersonal, information-processing, level, perceptual recognition of familiar faces and scenes is laden with affect. Where affect is absent or distorted as a result of neurological damage the subject “feels” strange in the presence of familiar scenes or people. Thus Young and Leafhead in their discussion of the Cotard delusion: “What the patients often give as evidence of their nonexistence or death is that they don’t have proper feeling.”. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 11.1 (2004) 65-70 [Access article in PDF] Top-Down and Bottom-Up in Delusion Formation Jakob Hohwy Keywords delusions, top-down, bottom-up, predictive coding Some delusions may arise as responses to unusual experiences (Davies et al. 2001; Maher 1974;). The implication is that delusion formation in some cases involves some kind of bottom-up mechanism—roughly, from perception to belief. Delusion formation may also involve some kind of top-down mechanism. (...) This could be in the shape of a patient's flawed background beliefs, or biases, which somehow modulate perception or ensure delusional interpretations of experience. There is little agreement about what kind of mechanism is primary in delusion formation, or, indeed, what the particular mechanisms and their neural substrates might be.In the evaluation of top-down and bottom-up mechanisms in delusion formation, a number of conceptual questions should be addressed (Davies and Coltheart 2000). For example, if there is an experiential component, why is a hypothesis with a delusional explanation of the unusual experience seen as relevant? Why do the subjects come to believe it tenaciously? How come some unusual experiences do not develop into delusions?A number of empirical findings also need to be taken into account: for example, the damage to the autonomic system in Capgras delusion (Ellis et al. 1997), the decreased ability for fast error correction in schizophrenia (Frith and Done 1989), modulation of activity in parietal cortex in delusions of alien control and other passivity experiences (Blakemore, Oakley, and Frith 2003), and also in schizophrenia, the increased sensitivity to self-produced stimuli, such as tickling oneself (Blakemore et al. 2000) and the sound of one's own voice (Ford et al. 2001).Theory choice can also be guided by philosophical doctrines about, for example, the nature of belief, the constitutive role of rationality, and intersubjectivity and the nature of judgements about the external world. It is natural, however, to let beliefs about philosophical doctrine be secondary to empirical findings and conceptual issues.The distinction between bottom-up and top-down mechanisms is particularly sharp in John Campbell's (2001) account of delusions and in Tim Bayne and Elisabeth Pacherie's (2004) discussion of Campbell. In this discussion, top-down approaches are associated with the general philosophical doctrine of rationalism, and bottom-up approaches with the philosophical doctrine of empiricism. Campbell's account is top-down because he posits delusional framework beliefs that arise directly as a result of brain damage or malfunction, and that work in some top-down fashion on the interpretation of experience. Bayne [End Page 65] and Pacherie convincingly defend empiricism against Campbell's rationalist account. Among their many other objections, they briefly puzzle about how a delusional framework belief (e.g., that one's spouse is an impostor) in a top-down fashion could cause the damage to the autonomic system seen in the Capgras and Cotard delusions (2004, 1). I think this is a very important objection because skin conductance data are part of the evidence for the bottom-up hypothesis concerning the Capgras delusion. We could add to this, for example, that it is mysterious how belief in a top-down fashion could cause people with schizophrenia to be worse at fast error correction than normal controls, to be better at tickling themselves than normal controls, and to have an increased response to the sound of their own voice.On the other hand, although the skin conductance response (SCR) evidence suggests a bottom-up approach to the Capgras delusion, it does not explain the character of the subjective experience that is hypothesized to give rise to the delusional belief: reduced SCR is not part of the experience itself (thanks to Ian Gold for discussion of this). Something more is required to give a full account of the type of experience that gives rise to the delusion. Further, as they stand, most bottom-up accounts are unable to account for why reality testing fails for beliefs based on these experiences.Neither rationalism nor empiricism on their own seem able to address the conceptual questions while paying... (shrink)

I argue that some cases of delusions show the inadequacy of those theories of interpretation that rely on a necessary rationality constraint on belief ascription. In particular I challenge the view that irrational beliefs can be ascribed only against a general background of rationality. Subjects affected by delusions seem to be genuine believers and their behaviour can be successfully explained in intentional terms, but they do not meet those criteria that according to Davidson (1985a) need to be met for the (...) background of rationality to be in place. (shrink)

Some monothematic types of delusions may arise because subjects have unusual experiences. The role of this experiential component in the pathogenesis of delusion is still not understood. Focussing on delusions of alien control, we outline a model for reality testing competence on unusual experiences. We propose that nascent delusions arise when there are local failures of reality testing performance, and that monothematic delusions arise as normal responses to these. In the course of this we address questions concerning the tenacity with (...) which delusions are maintained, their often bizarre content, the patients' inability to dismiss them, and their often circumscribed character. (shrink)

A popular approach to monothematic delusions in the recent literature has been to argue that monothematic delusions involve broadly rational responses to highly unusual experiences. Campbell calls this the empiricist approach to monothematic delusions, and argues that it cannot account for the links between meaning and rationality. In place of empiricism Campbell offers a rationalist account of monothematic delusions, according to which delusional beliefs are understood as Wittgensteinian framework propositions. We argue that neither Campbell's attack on empiricism nor his rationalist (...) alternative to empiricism is successful. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 9.1 (2002) 55-59 [Access article in PDF] One Stage Is Not Enough Andrew W. Young and Karel W. de Pauw Keywords: delusions, Cotard delusion, Capgras delusion, cognitive neuropsychiatry. WE WELCOME THE OPPORTUNITY to offer our reflections on Philip Gerrans' interesting paper. Our opinion is that on fundamental issues we agree quite a bit—but there are clear differences when it comes to details.The most basic issue (...) concerns the nature of the enterprise. Like Gerrans, we think that it is possible to create testable accounts of the formation and maintenance of what would otherwise seem bizarre and inexplicable delusions, and that these accounts should be grounded in theoretical models of factors that underpin our everyday perception and reasoning. This general approach certainly forms part of what has been called cognitive neuropsychiatry. However, we disagree with Gerrans in that we see cognitive neuropsychiatry as an attempt to draw on the underlying logic of cognitive neuropsychology, rather than (as Gerrans implies) its current methods. The underlying logic of cognitive neuropsychological approaches has been to try to understand the effects of brain injury in terms of disruption of different components of theoretical models of normal abilities. In this approach, a model of normal performance is tested by its ability to account for the effects of brain injury. Where the model of normal performance also provides a convincing account of brain injury it is retained, and when it fails to account for effects of brain injury, it is revised or abandoned. In cognitive neuropsychiatry, the key theoretical move has been to argue that an adequate model of normal performance should be able to account for any disordered pattern (Ellis and Young 1990). The same logic of seeking to explain disordered performance by reference to models of normal function is then attempted, but for disorders that would usually fall within the province of psychiatry.In our opinion, however, cognitive neuropsychiatry will not simply involve importing the methods of cognitive neuropsychology into the new domain; they will need to be developed and adapted to fit the new agenda (Young 2000).In cognitive neuropsychology, progress has often come from the careful investigation of people with stable, selective deficits of fundamental cognitive functions involved in sensory analysis, memory, and verbal or motor output. In contrast, delusional beliefs can be relatively unstable; often they are only held for a few weeks or even days. When the delusions change, patients may modify or abandon them as suddenly as they seemed to form them, or they may give them up much more slowly and reluctantly. At the very least, this creates difficulties in the timing of investigations and in interpreting the relation of deficits and symptoms, which may be recorded on separate dates. These methodological problems [End Page 55] are exacerbated by the fact that deficits linked to complex abnormal experiences such as delusions may be multifaceted and diffuse, even when the delusions themselves have a specific content or theme. Such complications do not invalidate cognitive neuropsychiatry, but they do mean it will need to develop its own methods for dealing with them and making appropriate inferences.One of the key complexities that has surfaced already involves the idea that delusional beliefs might reflect the interaction of two or more contributory factors. Gerrans discusses a particular variant of this idea, which had been suggested by Young and Leafhead (1996) as an approach to understanding the Cotard delusion: The Cotard delusion represents a depressed person's attempt to account for abnormal perceptual experiences. It follows that the delusion is based on an unfortunate interaction between different contributory factors. One set of factors creates the abnormal perceptual experiences, which are characterised by lack of emotional responses and feelings of emptiness, depersonalisation and derealisation. The other factors result in a misinterpretation of these perceptual changes, in which the patients' depressed moods lead them correctly to attribute the changes to themselves, but to exaggerate their consequences. (Young and Leafhead, 1996, 166) Gerrans describes this as a two-stage account, but argues that a one-stage account based only on abnormal perceptual... (shrink)

In recent times, explanations of the Capgras delusion have tended to emphasise the cognitive dysfunction that is believed to occur at the second stage of two-stage models. This is generally viewed as a response to the inadequacies of the one-stage account. Whilst accepting that some form of cognitive disruption is a necessary part of the aetiology of the Capgras delusion, I nevertheless argue that the emphasis placed on this second-stage is to the detriment of the important role played by the (...) phenomenology underlying the disorder, both in terms of the formation and maintenance of the delusional belief. This paper therefore proposes an interactionist two-stage model in which the phenomenal experience of the Capgras patient is examined, emphasised, and its relation to top-down processing discussed. (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)

After reviewing factors implicated in the generation of delusional beliefs, we conclude that whilst a perceptual aberration coupled with a particular type of attri‐butional bias may be necessary to explain the specific thematic content of a bizarre delusion, neither of these factors, whether in isolation or in combination, is sufficient to explain the presence of delusional beliefs. In contrast to bias models (theories which explain delusion formation in terms of extremes of normal reasoning biases), we advocate a deficit model of (...) delusion formation–that is, delusions arise when the normal cognitive system which people use to generate, evaluate, and then adopt beliefs is damaged. Mere bias we think inadequate to explain bizarre delusions which defy commonsense and persist despite overwhelming rational counter‐argument. In particular, we propose that two deficits must be present in the normal cognitive system to explain bizarre delusions: (1) there must be some damage to sensory and/or attentional‐orient‐ing mechanisms which causes an aberrant perception–this explains the bizarre content of the causal hypothesis generated to explain what is happening; and (2) there must also be a failure of normal belief evaluation–this explains why a hypothesis, implausible in the light of general commonsense, is adopted as belief. This latter deficit occurs, we suggest, when an individual is incapable of suspending the natural favoured status of direct first‐person evidence in order to critically evaluate hypotheses, given equal pri‐ority whether based on direct or indirect sources of information. In contrast, delusions with ‘ordinary’ content may arise when a single deficit of normal belief evaluation occurs in the context of an extreme (but normal) attentional bias, thus causing failure to critically evaluate hypotheses based on misperceptions and misintrepretations of ambiguous (but ordinary) first‐person experience. (shrink)

After reviewing factors implicated in the generation of delusional beliefs, we conclude that whilst a perceptual aberration coupled with a particular type of attri‐butional bias may be necessary to explain the specific thematic content of a bizarre delusion, neither of these factors, whether in isolation or in combination, is sufficient to explain the presence of delusional beliefs. In contrast to bias models (theories which explain delusion formation in terms of extremes of normal reasoning biases), we advocate a deficit model of (...) delusion formation–that is, delusions arise when the normal cognitive system which people use to generate, evaluate, and then adopt beliefs is damaged. Mere bias we think inadequate to explain bizarre delusions which defy commonsense and persist despite overwhelming rational counter‐argument. In particular, we propose that two deficits must be present in the normal cognitive system to explain bizarre delusions: (1) there must be some damage to sensory and/or attentional‐orient‐ing mechanisms which causes an aberrant perception–this explains the bizarre content of the causal hypothesis generated to explain what is happening; and (2) there must also be a failure of normal belief evaluation–this explains why a hypothesis, implausible in the light of general commonsense, is adopted as belief. This latter deficit occurs, we suggest, when an individual is incapable of suspending the natural favoured status of direct first‐person evidence in order to critically evaluate hypotheses, given equal pri‐ority whether based on direct or indirect sources of information. In contrast, delusions with ‘ordinary’ content may arise when a single deficit of normal belief evaluation occurs in the context of an extreme (but normal) attentional bias, thus causing failure to critically evaluate hypotheses based on misperceptions and misintrepretations of ambiguous (but ordinary) first‐person experience. (shrink)