Four detailed cases of delusions of misidentification (DM) are presented: two cases of misidentification of the reflected self, one of reverse intermetamorphosis, and one of reduplicative paramnesia. The cases are discussed in the context of three levels of interpretation: neurological, cognitive and phenomenological. The findings are compared to previous work with DM patients, particularly the work of Ellis and Young (1990; Young, 1998) who found that loss of the normal affective response to familiar faces was a contributing factor in the (...) Capgras delusion. The four cases presented suggest that this particular deficit is not a critical factor in the development of other forms of DM. (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are misidentified by their subjects as beliefs: the Capgras patient, for instance, does not believe that his wife has been replaced by a robot, instead, he merely imagines that she has, and mistakes this imagining for a belief.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)

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

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

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

Circumscribed delusional beliefs can follow brain injury. We suggest that these involve anomalous perceptual experiences created by a deficit to the person's perceptual system, and misinterpretation of these experiences due to biased reasoning. We use the Capgras delusion (the claim that one or more of one's close relatives has been replaced by an exact replica or impostor) to illustrate this argument. Our account maintains that people voicing this delusion suffer an impairment that leads to faces being perceived as drained of (...) their normal affective significance, and an additional reasoning bias that leads them to put greater weight on forming beliefs that are observationally adequate rather than beliefs that are a conservative extension of their existing stock. We show how this position can integrate issues involved in the philosophy and psychology of belief, and examine the scope for mutually beneficial interaction. (shrink)

After 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)

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)

Localizing the self in the brain has been the goal of consciousness research for centuries. Recently, there has been an increase in attention to the localization of the self. Here we present data from patients suffering from a loss of self in an attempt to understand the neural correlates of consciousness. Focusing on delusional misidentification syndrome , we find that frontal regions, as well as the right hemisphere appear to play a significant role in DMS and DMS related disorders. These (...) data are placed in the context of neuroimaging findings. (shrink)