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)

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)

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.

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)

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 twostage 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 oneand two-stage models. (shrink)

Detailed studies of people who have experienced the Capgras delusion (the delusion that certain other people, usually close relatives, have been replaced by impostors) have led to advances in constructing an account which can deal with the basic symptomatology, testing alternative possibilities, generating and testing non‐trivial predictions, and broadening the scope of the basic account to encompass other delusions. This paper outlines these developments. It uses them to explore implications for understanding the formation and maintenance of beliefs, and to discuss (...) basic principles of what has come to be known as cognitive neuropsychiatry. (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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

Explanations of Capgras delusion and prosopagnosia typically incorporate a dual-route approach to facial recognition in which a deficit in overt or covert processing in one condition is mirror-reversed in the other. Despite this double dissociation, experiences of either patient-group are often reported in the same way – as lacking a sense of familiarity toward familiar faces. In this paper, deficits in the facial processing of these patients are compared to other facial recognition pathologies, and their experiential characteristics mapped onto the (...) dual-route model in order to provide a less ambiguous link between facial processing and experiential content. The paper concludes that the experiential states of Capgras delusion, prosopagnosia, and related facial pathologies are quite distinct, and that this descriptive distinctiveness finds explanatory equivalence at the level of anatomical and functional disruption within the face recognition system. The role of skin conductance response as a measure of ‘familiarity’ is also clarified. (shrink)

Emotions and bodily feelings -- Existential feelings -- The phenomenology of touch -- Body and world -- Feeling and belief in the Capgras delusion -- Feelings of deadness and depersonalization -- Existential feeling in schizophrenia -- What William James really said -- Stance, feeling, and belief -- Pathologies of existential feeling.

The paper discusses the role affective factors may play in explaining why, in Capgras'delusion, the delusional belief once formed is maintained and argues that there is an important link between the modularity of the relevant emotional system and the persistence of the delusional belief.