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

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)

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

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are misidentified by their subjects as beliefs: the Capgras patient, for instance, does not believe that his wife has been replaced by a robot, instead, he merely imagines that she has, and mistakes this imagining for a belief.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

After 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)

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) 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)

Psychologists have recently turned their attention to the nature of the recognition involved in judgment of familiarity. It has been suggested that, apart from judging a stimulus to be familiar when one is able to recall a context in which it was previously perceived, subjects are also able to judge that something is familiar merely on the basis of its faster perceptual processing.

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)

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

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)

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)

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

In 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)

Subjective feelings of familiarity associated with a stimulus tend to be strongest when specific information about the previous encounter with the stimulus is difficult to retrieve . Recognizing: The judgment of previous occurrence. Psychological Review, 87, 252–271.]). When a stimulus has been encountered previously and the circumstances of the encounter cannot be recollected, additional cognitive resources may be directed toward recollection processes; this resource allocation is accompanied by autonomic arousal [Dawson, M. E., Filion, D. L., & Schell, A. M. . (...) Is elicitation of the autonomic orienting response associated with allocation of processing resources?. Psychophysiology, 26, 560–572]. One easily measurable index of autonomic arousal is the skin conductance response . In the present study, participants studied lists of words and then gave recognition ratings to briefly displayed and masked studied and nonstudied test words while their SCRs were monitored. Results revealed a relationship between recognition ratings and the temporal characteristics of the SCR, supporting the idea that feelings of familiarity are indeed “feelings” in that they stem from autonomic arousal associated with cognitive resource allocation. (shrink)