This new edition of the classic Contemporary Theories of Knowledge has been significantly updated to include analyses of the recent literature in epistemology.

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

Article copyright 2002. We provide a battery of examples of delusions against which theoretical accounts can be tested. Then we identify neuropsychological anomalies that could produce the unusual experiences that may lead, in turn, to the delusions in our battery. However, we argue against Maher's view that delusions are false beliefs that arise as normal responses to anomalous experiences. We propose, instead, that a second factor is required to account for the transition from unusual experience to delusional belief. The second (...) factor in the etiology of delusions can be described superficially as a loss of the ability to reject a candidate for belief on the grounds of its implausibility and its inconsistency with everything else that the patient knows, but we point out some problems that confront any attempt to say more about the nature of this second factor. (shrink)

In 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)

This paper is concerned with the problem of selfidentification in the domain of action. We claim that this problem can arise not just for the self as object, but also for the self as subject in the ascription of agency. We discuss and evaluate some proposals concerning the mechanisms involved in selfidentification and in agencyascription, and their possible impairments in pathological cases. We argue in favor of a simulation hypothesis that claims that actions, whether overt or covert, are centrally simulated (...) by the neural network, and that this simulation provides the basis for action recognition and attribution. (shrink)

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

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)

According to social constructionism factuality, the establishment of accounts as corresponding to an objective external reality, is an interactional accomplishment ordinarily achieved in everyday conversations. In cases of disagreement regarding the interpretation and nature of events, however, not only the plausibility of the account, but also the rationality, integrity, and accountability of the participants is at stake. Delusions present extreme cases of such disagreement. This paper analyzes extracts from an interview with an individual diagnosed as delusional focusing on the factualization (...) devices used in the negotiation of accounts. The question of whether the observation of conversational rules documented in the interview is sufficient to establish the plausibility of an account and the rationality of its teller leads to arguments around the necessity of shifting the focus from the grounded micro-analysis of talk to wider social and institutional processes. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 11.1 (2004) 71-80 [Access article in PDF] Some Reflections on the (Analytic) Philosophical Approach to Delusion Louis A. Sass There are more things in heaven and earth, Horatio, Than are dreamt of in your philosophy." —Hamlet, Act I, Scene 5 The peculiar, often problematic phenome na of psychopathology have been attract ing the attention of analytic philosophers in recent years. The topic of delusion has (...) been a particular draw, with a number of analytic philosophers attempting to use their conceptual tools, usually combined with ideas from cognitive neuroscience, to criticize the traditional understanding and to clarify the nature of this central psychiatric topic. It is useful to have this kind of interdisciplinary dialogue. Indeed, there is good reason to hope that concepts honed in the philosophy of mind and other philosophical subfields will help to sort out our understanding of a phenomenon (or set of phenomena) for which contemporary psychiatric definitions and conceptualizations are clearly inadequate and, in some respects, downright misleading (see Parnas and Sass 2001; Spitzer 1990).1Here, however, I would like to call attention to some weaknesses that, it seems to me, are rather common (I do not say universal) in many analytic philosophical approaches to psychopathology. In my opinion, there is a tendency to formulate issues and arguments in overly polarized, even dichotomous terms, and then to rely too uncritically on these essentialistic formulations in exploring the domain of inquiry. Although this polarizing tendency sometimes has the salutary effect of clarifying conceptual domains, it can, when taken too far, actually hamper our understanding of phenomena that are often fraught with ambiguities and complexities that defy many standard conceptualizations.The relationship between philosophy and psychopathology is obviously a two-way street—we are familiar, for example, with disorders that challenge deep philosophical assumptions about self and mind (e.g., blindsight, split-brain phenomena, perhaps also Dissociative Identity Disorder, and the first rank symptoms of schizophrenia). I am suggesting that, in their work on delusions, philosophers may need to put more emphasis on moving from the natural phenomena [End Page 71] of psychopathology and to the domain of philosophical analysis.I believe that a greater sensitivity to the modes of knowing associated with the phenomenological tradition, and to the forms of conceptual self-critique fostered by Ludwig Wittgenstein, are crucial ingredients for any adequate approach to delusion as well as many other topics in psychopathology. In my opinion, the work of many analytic philosophers interested in psychopathology would be enriched if they spent more time trying to discover and imagine what it might be like to experience certain kinds of abnormal psychiatric conditions, and also speculating about what implications such experiential modalities might have for action and verbal expression. I believe they would also be wise to spend more time questioning, and attempting to transcend, the philosophically derived conceptual distinctions and dichotomies that appear to organize their conceptual universes. Phenomenological imagination and Wittgensteinian critique can show how to move outside the conceptual capsule and into the rich and strange realms of actual experience, both normal and abnormal.So far I have offered only slogans. Let me use the articles by Tim Bayne and Elisabeth Pacherie (2004) and Robert Klee (2004) to flesh out the criticisms I have offered. There is much that is intelligent and much that is worthwhile in both their articles. (For example, I was largely convinced by the criticisms of John Campbell and of Donald Davidson that are central to the articles by Bayne and Pacherie and by Klee, respectively.) Here, however, I will focus only on issues that illustrate the above-mentioned tendencies—tendencies that, in my view, tend to infect even the best writings on the (analytic) philosophy of psychiatry. I will also make some remarks about the works of Campbell and Davidson, the two philosophers criticized in the articles by Bayne and Pacherie and by Klee. Because the article by Eugenie Georgaca (2004) is in a different tradition, I will say only a few words about it at the end. Bayne and Pacherie on the Preservation-Of-meaning... (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)

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)

© 2004 by The Johns Hopkins University Press.