Introduction: Cotard delusion—the delusional belief “I am dead”—is named after the French psychiatrist who first described it: Jules Cotard (1880, 1882). Ramachandran and Blakeslee (1998) proposed that the idea “I am dead” comes to mind when a neuropathological condition has resulted in complete abolition of emotional responsivity to the world. The idea would arise as a putative explanation: if “I am dead” were true, there would be no emotional responsivity to the world. Methods: We scrutinised the literature (...) on people who expressed the delusional belief “I am dead”, looking for data on whether such patients are reported as entirely lacking in emotional responsivity. Results: In numerous cases, patients with Cotard delusion are described as experiencing emotions including anxiety, fear, guilt, distress, euphoria and worry. Conclusions: We conclude that complete absence of emotional responsivity cannot be what prompts the delusional idea that one is dead. We propose that, in at least some cases, the idea “I am dead” comes to mind in response to symptoms of depersonalisation or derealisation, often present in cases of Cotard delusion, and give examples of Cotard patients with abnormalities in various neural areas that could be responsible for the presence of such symptoms. (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)

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)

The initial cause of Cotard delusion is pervasive dyshomeostasis (dysregulation of basic bodily function).This explanation draws on interoceptive active inference account of self‐representation. In this framework, the self is an hierarchical predictive model made by the brain to facilitate homeostatic regulation. The account I provide is an alternative to two factor accounts of the Cotard delusion that treat depersonalisation experience as the first factor in genesis of the Cotard delusion. I argue that depersonalisation experience (...) and the Cotard delusion are produced by different breakdowns in the process of self‐modelling. (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)

Discussion on the Cotard delusion often focuses on the patient’s delusional belief that he/she is dead. Of interest to this paper, however, is the little referred to claim made by some Cotard patients that they are immortal. How might one explain the juxta-position of death and immortality evident in patients sharing the same clinical diagnosis, and how might these delusional beliefs inform our understanding of patient phenomenology, particularly regarding experiences of existential change? This paper sets out to (...) explain delusions of death and immortality in Cotard patients with reference to changes in their experience of being, owed in part to a conflict in recognition evident in other delusional disorders such as the Capgras and Frégoli delusions. This experiential change is positioned within an interactionist framework of bottom-up and top-down processing that is also compatible with explanationist and endorsement approaches to delusions. (shrink)

Discussion on the Cotard delusion often focuses on the patient’s delusional belief that he/she is dead. Of interest to this paper, however, is the little referred to claim made by some Cotard patients that they are immortal. How might one explain the juxta-position of death and immortality evident in patients sharing the same clinical diagnosis, and how might these delusional beliefs inform our understanding of patient phenomenology, particularly regarding experiences of existential change? This paper sets out to (...) explain delusions of death and immortality in Cotard patients with reference to changes in their experience of being, owed in part to a conflict in recognition evident in other delusional disorders such as the Capgras and Frégoli delusions. This experiential change is positioned within an interactionist framework of bottom-up and top-down processing that is also compatible with explanationist and endorsement approaches to delusions. (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)

Monothematic delusions are delusions whose contents pertain to a single subject matter. Examples include Capgras delusion, the delusion that a loved one has been replaced by an impostor, and Cotard delusion, the delusion that one is dead or does not exist. Two-factor accounts of such delusions hold that they are the result of both an experiential deficit, for instance flattened affect, coupled with an aberrant cognitive response to that deficit. In this paper we develop a (...) new expressivist two-factor account of delusion. In contrast to existing endorsement and explanationist accounts, which treat delusions as either explanations or endorsements of the contents of these disordered experiences, we hold that delusional beliefs have an expressive function: they characterize, in impressionistic terms, what the subject’s experience is like for them. We show how our account improves upon existing two-factor views in explaining the central features of monothematic delusions, in particular the way in which delusional subjects fall short of the ideal of rationality. (shrink)

Patients suffering from the Cotard syndrome can deny being alive, having guts, thinking or even existing. They can also complain that the world or time have ceased to exist. In this article, I argue that even though the leading neurocognitive accounts have difficulties meeting that task, we should, and we can, make sense of these bizarre delusions. To that effect, I draw on the close connection between the Cotard syndrome and a more common condition known as depersonalisation. Even (...) though they are not delusional, depersonalised patients seem to have experiences that are quite similar to those of Cotard patients. I argue that these experiences are essentially characterised by a lack of subjective character and of two other structural features of experience, which I call ‘the present character’ and ‘the actual character’. Cotard's nihilistic delusions simply consist in taking these anomalous experiences at face value. (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)

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)

Delusions play a fundamental role in the history of psychology, philosophy and culture, dividing not only the mad from the sane but reason from unreason. Yet the very nature and extent of delusions are poorly understood. What are delusions? How do they differ from everyday errors or mistaken beliefs? Are they scientific categories? In this superb, panoramic investigation of delusion Jennifer Radden explores these questions and more, unravelling a fascinating story that ranges from Descartes’s demon to famous first-hand accounts (...) of delusion, such as Daniel Schreber’s Memoirs of My Nervous Illness. Radden places delusion in both a clinical and cultural context and explores a fascinating range of themes: delusions as both individually and collectively held, including the phenomenon of folies á deux ; spiritual and religious delusions, in particular what distinguishes normal religious belief from delusions with religious themes; how we assess those suffering from delusion from a moral standpoint; and how we are to interpret violent actions when they are the result of delusional thinking. As well as more common delusions, such as those of grandeur, she also discusses some of the most interesting and perplexing forms of clinical delusion, such as Cotard and Capgras. (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)

Current models of delusion converge in proposing that delusional beliefs are based on unusual experiences of various kinds. For example, it is argued that the Capgras delusion (the belief that a known person has been replaced by an impostor) is triggered by an abnormal affective experience in response to seeing a known person; loss of the affective response to a familiar person’s face may lead to the belief that the person has been replaced by an impostor (Ellis & (...) Young, 1990). Similarly, the Cotard delusion (which involves the belief that one is dead or unreal in some way) may stem from a general.. (shrink)

Delusions are explanations of anomalous experiences. A theory of delusion requires an explanation of both the anomalous experience _and _the apparently irrational explanation generated by the delusional subject. Hence, we require a model of rational belief formation against which the belief formation of delusional subjects can be evaluated. _Method. _I first describe such a model, distinguishing procedural from pragmatic rationality. Procedural rationality is the use of rules or procedures, deductive or inductive, that produce an inferentially coherent set of propositions. (...) Pragmatic rationality is the use of procedural rationality _in context_. I then apply the distinction to the explanation of the Capgras and the Cotard delusions. I then argue that delusions are failures of pragmatic rationality. I examine the nature of these failures employing the distinction between performance and competence familiar from Chomskian linguistics. _Results. _This approach to the irrationality of delusions reconciles accounts in which the explanation of the anomalous experience exhausts the explanation of delusion, accounts that appeal to further deficits within the reasoning processes of delusional subjects, and accounts that argue that delusions are not beliefs at all. (Respectively, one-stage, two-stage, and expressive accounts.) _Conclusion. _In paradigm cases that concern cognitive neuropsychiatry the irrationality of delusional subjects should be thought of as a performance deficit in pragmatic rationality. (shrink)

Derek Bolton has claimed that extant philosophical theories of mind imply accounts of mental disorder, via their accounts of intentionality. The purpose of this paper is to extend Bolton’s claims, by exploring what an embodied/situated theory of mind might imply about mental disorder. I argue that, unlike the more traditional views Bolton considers, embodied/situated accounts can (in principle) provide an observer-independent criterion for distinguishing mental health from disorder in cases of Capgras and Cotard delusions.

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 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)

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)

People suffering from severe monothematic delusions, such as Capgras, Fregoli, or Cotard patients, regularly assert extraordinary and unlikely things. For example, some say that their loved ones have been replaced by impostors. A popular view in philosophy and cognitive science is that such monothematic delusions aren't beliefs because they don't guide behaviour and affect in the way that beliefs do. Or, if they are beliefs, they are somehow anomalous, atypical, or marginal beliefs. We present evidence from five studies that (...) folk psychology unambiguously views monothematic delusions as stereotypical beliefs. This calls into question widespread assumptions in the professional literature about belief's stereotypical functional profile. We also show that folk psychology views delusional patients as holding contradictory beliefs. And we show that frequent assertion is a powerful cue to belief ascription, more powerful than even a robust and consistent track record of non-verbal behaviour. (shrink)

Cotard's syndrome is a psychotic condition that includes delusion of a supernatural nature. Based on insights from recovered patients who were convinced of being immortal, we can (1) distinguish biographical experiences from cultural and evolutionary backgrounds; (2) show that cultural significance dominates biographical experiences; and (3) support Bering's view of a cognitive system dedicated to forming illusory representations of immortality.

The text concerns the role of emotions in delusion formation. Provided are definitions from DSM-V and DSM-IV-R and the problems found in those definitions. One of them, the problem of delusion formation, is described when providing cognitive theories of delusions. The core of the paper is a presentation of the emotional and affective disorders in delusions, especially Capgras delusion and Cotard delusion. The author provides a comparison of the kinds of delusions and the conclusions taken (...) from neuroimaging studies. As a result of the fact that an explanation of delusion formation focusing on emotional problems turns out to be insufficient, the author provides examples of the reasoning impairments which coexist with them. At the end of the article, some hypotheses are proposed concerning the role of emotions and reasoning in delusion formation and the relation between belief disorders and emotional disorders. (shrink)

Young’s paper (2012) offers an interesting and fruitful extension to recent work on Cotard’s syndrome, and in particular, a philosophical investigation of how and why beliefs around death and non-existence frequently co-occur with beliefs around immortality. In this brief response, we discuss a few issues from the paper. Namely, the issue of Cotard delusion being a natural kind, the seeming paradox of death and immortality and its relation to wider culture and literature, and the utility of the (...) concept of misplaced being. (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 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)

“Identity disorders” constitute a large class of psychiatric disturbances that, due to deviant forms of self-modeling, result in dramatic changes in the patients’ phenomenal experience of their own personal identity. The phenomenal experience of selfhood and transtemporal identity can vary along an extremely large number of dimensions: There are simple losses of content. There are also various typologies of phenomenal disintegration as in schizophrenia, in depersonalization disorders and in_ Dissociative Identity Disorder_, sometimes accompanied by multiplications of the phenomenal self within (...) one and the same physical system. It is important to not only analyze these state-classes in terms of functional deficits or phenomenology alone, but as _self-representational _content as well. For instance, in the second type of cases just mentioned, we confront major redistributions of the phenomenal property of "mineness” in representational space, of what is sometimes also called the “sense of ownership”. Finally, there are at least four different delusions of misidentification. Being a philosopher, I will discuss two particular types of identity disorder _ 2 _ in this contribution - disorders, which are of direct philosophical relevance: A specific form of DM, and the Cotard delusion. Why should philosophers do this? And why should psychiatrists care? (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 9.1 (2002) 61-63 [Access article in PDF] Arguing from Neuroscience in Psychiatry James Phillips PHILIP GERRANS "A One-stage Explanation of the Cotard Delusion" provides an elegant example of the application of neuroscientific findings to known clinical phenomena in psychiatry. Gerrans argues that, in the cases of the Cotard and Capgras delusions, a one-stage explanation is sufficient to account for the clinical phenomena. (...) That is, the neuroanatomic defect and the consequent anomalous experience are sufficient to produce the delusion. According to Gerrans, we do not need to postulate that the delusion will emerge only if the anomalous experience is filtered through a faulty reasoning process (a two-stage explanation). Against the argument of Young and Leafhead (1996) that Cotard and Capgras delusions stem from the same neuroanatomic deficit and differentiate only in being processed differently—thus requiring a two-stage explanation—Gerrans argues that the respective neuroanatomic defects are in fact different, and that, therefore, the two delusional syndromes differ at the first stage and do not require the two-stage explanation suggested by Young and Leafhead.I do not have an opinion as to who is right in this disagreement, and I will devote these remarks to explaining why I do not have an opinion. In developing this explanation I will touch on what I find problematic in many discussions of neuroscience, neurocognitive models, and clinical psychiatry; I will thus use this article to highlight those problems.On the face of it, one would think that the issue raised by Gerrans should admit of a simple resolution. He argues that Capgras and Cotard delusions derive from different neural defects. Young and Leafhead, on the other hand, base their two-stage argument on the argument that the two delusions derive from the same neural defect. So which is it? Neuroscientists should be able to settle the issue and end the dispute. Gerrans remarks "that we need to look more closely at the CN [cognitive neuropsychiatric] explanation of the Capgras delusion." As he describes it, face recognition involves two components, a cognitive and an affective component, with separate neuroanatomic substrates. An individual successfully recognizes the face of a friend or acquaintance when she matches the cognitive recognition (cognitive component) with the affective tone of familiarity (second component). When there is a lesion in the neural substrate of the affective component, she may recognize the face but without the tone of familiarity. In her effort to understand her affective experience of the face as alien rather than as familiar, she may conclude that her friend has been replaced by a double. Thus we have the Capgras delusion.Let us now unpack this explanation. According to Gerrans, researchers have hypothesized [End Page 61] two anatomatically distinct pathways involved in face recognition. He writes: "Initially... these separate neuroanatomic substrates were hypothesized to lie in separate dorsal and ventral processing pathways, but the most persuasive hypothesis is that of Breen et al. that face recognition is performed in the ventral visual processing pathway, whereas covert [affective] recognition effects result from the activation of pathways connecting the ventral pathway and the limbic system. It is damage to these latter pathways that gives rise to the Capgras delusion."In other words, the explanation of Capgras delusions depends on a neurocognitive model, itself based on an unspecified base of neuroanatomic data. When Gerrans writes that "[t]he Capgras delusion arises in cases where, following a neurological accident, the pathways connecting the FRU [Face Recognition Unit] to the limbic system are damaged leaving ventral pathways and hence overt recognition unimpaired...," he means that the Capgras delusion arises in that manner if the proposed model bears any relation to the reality of the living brain and if real Capgras patients have suffered the hypothesized lesion. At this point the reader is struggling with the following questions: (1) What are the hard neuroanatomic data underpinning the neurocognitive model? (2) What is the argument for developing this model (single Face Recognition Unit with independent pathways to cognitive and affective components of face recognition) out of the hard data? (3) What is the evidence... (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)

The cognitive science of belief is a burgeoning field, with insights ranging from detailing the fundamental structure of the mind, to explaining the spread of fake news. Here we highlight how new insights into belief acquisition, storage, and change can transform our understanding of psychiatric disorders. Although we focus on monothematic delusions, the conclusions apply more broadly. -/- .

Experiences of thought-insertion are a first-rank, diagnostically central symptom of schizophrenia. Schizophrenic patients who undergo such delusional mental states report being first-personally aware of an occurrent conscious thought which is not theirs, but which belongs to an external cognitive agent. Patients seem to be right about what they are thinking but mistaken about who is doing the thinking. It is notoriously difficult to make sense of such delusions. One general approach to explaining the etiology of monothematic delusions has come to (...) be known as the endorsement model. This model claims that the patient holds her delusional belief because she simply trusts her bizarre experience and takes it at face value. The content of the bizarre experience thus plays a central role in the etiology of delusions. Despite being widely discussed with respect to delusions like Capgras and Cotard, an endorsement model of thought-insertion has not yet been formulated. This article seeks to fill this void by fleshing out and defending the endorsement approach to delusions of inserted thoughts. It aims to show that such an approach can be defended against objections that have been raised in the literature. In particular, it will be argued that there is nothing wrong with the idea of being first-personally aware of a thought which is presented in consciousness as being someone else's. The upshot is that with respect to delusions of thought-insertion, the endorsement model turns out to be a viable account of why patients come to believe that someone else is inserting thoughts into their minds. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 11.1 (2004) 35-41 [Access article in PDF] The Rationality of Psychosis and Understanding the Deluded Matthew R. Broome Campbell's important and influential paper (Campbell 2001) has framed the debate that Bayne and Pacherie (2004) most explicitly, and Klee (2004) and Georgaca (2004) more implicitly, engage in. Campbell has offered two broad ways of thinking about explanations of delusions—the empirical and the rational. He offers some (...) criticism of the former and an endorsement of the latter. Campbell uses examples from clinical psychopathology to illustrate his argument and Bayne and Pacherie in turn employ these. Campbell discusses the eponymously named delusions of Capgras and Cotard—the former a subtype of delusional misidentification and the latter a delusion whose content is colored predominantly with nihilistic and possibly hypochondriacal themes. Campbell, Bayne and Pacherie, and Klee discuss the empirical data in relation to such delusions and as an aid to discussing the empirical model more generally. It does seem a little unfortunate that these delusions, which are less than typical, become the focus of Campbell's paper, and Bayne and Pacherie's criticism of his work. Delusions are remarkably heterogeneous; this indeed may be part of the reason why there is so much difficulty in reaching a definition as Klee discusses, and occur in a wide variety of mental and neurological illnesses. The most common delusions are those of persecution and reference (World Health Organization [WHO] 1973) and typically occur in schizophrenia. By contrast, delusional misidentification occurs most commonly in patients with dementia, delirium, and focal cognitive impairment, but can occur in other functional psychoses such as an affective or schizophrenic psychosis. The most common form of delusional misidentification is not that of either the exotic Capgras or Fregoli syndromes but delusional misidentification for place; thus, although Bayne and Pacherie's arguments against Campbell may still hold, delusional misidentification tends to occur in the context of a patient believing that they are at home or on holiday rather than in hospital and may not necessarily involve close family members or other intimate relationships. Similarly, Cotard's syndrome tends to occur in the context of a severe depressive illness with mood-congruent psychotic symptoms, typically in an elderly individual. It does not have to have the content that the deluded is dead, but can include beliefs, for example, that the world no longer exists or that their internal organs are not present. Thus, a patient with either Capgras' or Cotard's syndrome is likely to differ from patients with delusions of persecution. They would [End Page 35] have different diagnoses, probably be older, and have a greater likelihood of structural abnormalities of the brain on imaging and consequent neuropsychological dysfunction. That is not to say that patients with schizophrenia have normal cerebral anatomy and neuropsychology, but rather that the Capgras' and Cotard's patients are likely to have neurological quality to their presentation that is clinically relevant, rather than what commonly the case in schizophrenia and the other functional psychoses, where the neurological abnormalities are only currently important at the level of academic research. Empirical Models of Delusion Formation Different delusions may not have that much in common, nor may the patients who believe in them. This in turn relates to the empirical paradigm that both Campbell and Bayne and Pacherie discuss. It is true that current research, and indeed the clinical practice of cognitive behavioral therapy for psychosis, is indebted to the work of Maher and it is within his legacy which we work. This, however, is not to say that we think his initial formulation was correct. Maher's (1988, 1992) work focused attempts in explaining delusions—both to support and refute his thesis that delusions are the consequence of normal cognitive mechanisms seeking to explain an anomalous sensory experience. Such a view initially led to work demonstrating delusions in the absence of anomalous perceptions, the presence of reasoning biases in the deluded population, and the possibility that abnormal sensory experience may be consequent upon biased cognitive processes (Garety and Freeman 1999). More recent work has demonstrated the prevalence of... (shrink)

: Self-consciousness is considered in a framework comprising four dimensions which are theoretically defined and supported by clinical neuropsychological evidence. Self-monitoring is defined as the ability to reflect on one’s own behaviour, with supporting evidence for deficits in this capacity noted in anosognosia syndrome. Self-feeling is defined as the capacity to feel all sensations related to one’s own body, with supporting evidence from deficiencies occurring in alexithymia, psychosomatic states and Cotard’s delusion. Identity refers to the capacity to recognize (...) an object as identical to oneself, based on autobiographic memory; pathological conditions related to this dimension include delusions of identity and the Zelig syndrome. Ownership is the capacity to perceive the status of ones’ own body, and is clinically altered in somatoparaphrenia. All four dimensions are related to specific brain networks. Keywords: Self-Monitoring; Self-Feeling; Identity; Ownership; Neurocognitive Dimensions Le dimensioni neurocognitive dell’autocoscienza Riassunto: L’autocoscienza viene inquadrata in base a quattro dimensioni, determinate in via teorica e supportate da evidenze cliniche di carattere neuropsicologico. L’automonitoraggio è definito quale capacità di riflettere sul proprio comportamento ed è sostenuto da evidenze che derivano da quella sindrome denominata anosognosia. Il sentire il proprio sé è la capacità di avvertire tutte le sensazioni del corpo proprio ; questa dimensione è supportata da evidenze derivanti da condizioni cliniche quali l’alessitimia, le affezioni psicosomatiche e il delirio di Cotard. L’identità si riferisce alla capacità di riconoscere come identico a se stesso un oggetto, fondata sulla memoria autobiografica; le condizioni patologiche legate a questa dimensione sono il delirio di identità e la sindrome di Zelig. Il possesso di sé è la capacità di percepire lo stato del proprio corpo, condizione che risulta alterata nella somatoparafrenia. Tutte queste quattro dimensioni sono collegate a specifici network cerebrali. Parole chiave: Automonitoraggio; Sentimento di sé; Identità; Padronanza di sé; Dimensioni neurocognitive. (shrink)

Delusions are a common symptom of schizophrenia and dementia. Though most English dictionaries define a delusion as a false opinion or belief, there is currently a lively debate about whether delusions are really beliefs and indeed, whether they are even irrational. The book is an interdisciplinary exploration of the nature of delusions. It brings together the psychological literature on the aetiology and the behavioural manifestations of delusions, and the philosophical literature on belief ascription and rationality. The thesis of the (...) book is that delusions are continuous with ordinary beliefs, a thesis that could have important theoretical and practical implications for psychiatric classification and the clinical treatment of subjects with delusions. By bringing together recent work in philosophy of mind, cognitive psychology and psychiatry, the book offers a comprehensive review of the philosophical issues raised by the psychology of normal and abnormal cognition, defends the doxastic conception of delusions, and develops a theory about the role of judgements of rationality and of attributions of self-knowledge in belief ascription. Presenting a highly original analysis of the debate on the nature of delusions, this book will interest philosophers of mind, epistemologists, philosophers of science, cognitive scientists, psychiatrists, and mental health professionals. (shrink)

Delusions are standardly defined as attitudes that are not amenable to change in light of conflicting evidence. But what evidence do people with delusion have for and against it? Do delusions really go against their total evidence? How are the answers affected by different conceptions of evidence? -/- This chapter focuses on how delusions relate to evidence. I consider what delusions-relevant evidence people with delusions have. I give some reasons to think that people typically have evidence for their delusions, (...) and that the evidence they have against them is often overstated. I draw on this discussion to consider whether delusions are evidentially supported and epistemically rational. Finally, I discuss implications for the nature of delusion, responsibility, and treatment and suggest directions for future research. Throughout, the discussion is sensitive to different conceptions of evidence and rationality in epistemology. -/- A central upshot is that what we should say about the epistemic standing of delusions depends substantively on our positions in epistemology, in particular, on the debate between internalists and externalists about evidence. If we want clarity on the epistemic standing of delusions, we need to incorporate more sophisticated tools from epistemology. (shrink)

In this paper we ask whether the two-factor theory of delusions is compatible with two claims, that delusions are pathological and that delusions are adaptive. We concentrate on two recent and influential models of the two-factor theory: the one proposed by Max Coltheart, Peter Menzies and John Sutton (2010) and the one developed by Ryan McKay (2012). The models converge on the nature of Factor 1 but diverge about the nature of Factor 2. The differences between the two models are (...) reflected in different accounts of the pathological and adaptive nature of delusions. We will explore such differences, considering naturalist and normativist accounts of the pathological and focusing on judgements of adaptiveness that are informed by the shear-pin hypothesis (McKay and Dennett 2009). After reaching our conclusions about the two models, we draw more general implications for the status of delusions within two-factor theories. Are there good grounds to claim that delusions are pathological? Are delusions ever adaptive? Can delusions be at the same time pathological and adaptive? (shrink)

The imperviousness of delusions to counter-evidence makes it tempting to classify them as imaginings. Bayne and Pacherie argue that adopting a dispositional account of belief can secure the doxastic status of delusions. But dispositionalism can only secure genuinely doxastic status for mental states by giving folk-psychological norms a significant role in the individuation of attitudes. When such norms individuate belief, deluded subjects will not count as believing their delusions. In general, dispositionalism won't confer genuinely doxastic status more often than do (...) competing accounts of belief. (shrink)

Various psychopathologies of self-awareness, such as somatoparaphrenia and thought insertion in schizophrenia, might seem to threaten the viability of the higher-order thought (HOT) theory of consciousness since it requires a HOT about one’s own mental state to accompany every conscious state. The HOT theory of consciousness says that what makes a mental state a conscious mental state is that there is a HOT to the effect that “I am in mental state M.” I have argued in previous work that a (...) HOT theorist can adequately respond to this concern with respect to somatoparaphrenia and thought insertion. There is also Cotard syndrome which is a rare neuropsychiatric disorder in which people hold the delusional belief that they are dead, do not exist, or have lost their blood or internal organs. In this paper, I argue that HOT theory has nothing to fear from it either and can consistently account for what happens in such unusual cases. I analyze Cotard syndrome in light of my previous discussion of somatoparaphrenia and thought insertion, and argue that HOT theory can provide a somewhat analogous account without the worry of inconsistency. It is crucial to recognize that there are multiple “self-concepts” and levels of HOTs which can help to provide a more nuanced explanation. With regard to the connection between consciousness and self-consciousness, it is proposed that Cotard patients are indeed capable of having some “I-thoughts” about their bodies and mental states. (shrink)

Stanford Encyclopedia Entry on Delusions.

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)

Psychopathological delusions have a number of features that are curiously difficult to explain. Delusions are resistant to counterevidence and impervious to counterargument. Delusions are theoretically, affectively, and behaviorally circumscribed: delusional individuals often do not act on their delusions and often do not update beliefs on the basis of their delusions. Delusional individuals are occasionally able to distinguish their delusions from other beliefs, sometimes speaking of their “delusional reality.” To explain these features, I offer a model according to which, contrary to (...) appearances, delusions are not beliefs at all. Delusions are acceptances that are generated by pathologically powerful cognitive feelings. This model has implications for the way that we should think about non-pathological doxastic states and emotions. (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.

After briefly reviewing some of the empirical and philosophical literature suggesting that there may be an adaptive role for delusion formation, we discuss the results of a recent study consisting of in-depth interviews with people experiencing delusions. We analyse three such cases in terms of the circumstances preceding the development of the delusion; the effects of the development of the delusion on the person’s situation; and the potential protective nature of the delusional belief as seen from the (...) first-person perspective. We argue that the development of the delusional belief can play a short-term protective function and we reflect on the implications that this might have for our understanding of psychotic symptoms, for the stigma associated with mental health issues, and for treatment options. (shrink)

According to the Rationality Constraint, our concept of belief imposes limits on how much irrationality is compatible with having beliefs at all. We argue that empirical evidence of human irrationality from the psychology of reasoning and the psychopathology of delusion undermines only the most demanding versions of the Rationality Constraint, which require perfect rationality as a condition for having beliefs. The empirical evidence poses no threat to more relaxed versions of the Rationality Constraint, which only require only minimal rationality. (...) Nevertheless, we raise problems for all versions of the Rationality Constraint by appealing to more extreme forms of irrationality that are continuous with actual cases of human irrationality. In particular, we argue that there are conceivable cases of “mad belief” in which populations of Lewisian madmen have beliefs that are not even minimally rational. This undermines Lewis’s claim that our ordinary concept of belief is a theoretical concept that is implicitly defined by its role in folk psychology. We argue that introspection gives us a phenomenal concept of belief that cannot be analyzed by applying Lewis’s semantics for theoretical terms. (shrink)

In this paper, I examine a kind of delusion in which the patients judge that their occurrent thoughts are false and try to abandon them precisely because they are false, but fail to do so. I call this delusion transparent, since it is transparent to the sufferer that their thought is false. In explaining this phenomenon, I defend a particular two-factor theory of delusion that takes the proper integration of relevant reasoning processes as vital for thought-evaluation. On (...) this proposal, which is a refinement of Gerrans’s account of delusion as unsupervised by decontextualized processing, I can have all my reasoning processes working reliably and thus judge that my delusion is false but, if I cannot use their outputs when revising the thought itself, the delusion will persist. I also sketch how this framework explains some interesting cases of failed belief-revision in the general population in which people judge that ~p but nonetheless continue to believe that p. (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)