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

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

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)

The work reported in this paper investigated the putative functional dependence of pragmatic language skills on general mind‐reading capacity by testing theory‐of‐mind abilities and understanding of non‐literal speech in patients with schizophrenia and in healthy controls. Patients showed difficulties with inferring mental states on a false‐belief picture‐sequencing task and with understanding metaphors and irony on a story‐comprehension task. These difficulties were independent of low verbal IQ and a more generalised problem inhibiting prepotent information. Understanding of metaphors and understanding of irony (...) made significant and independent contributions to discriminating patients from controls, suggesting that metaphor and irony make distinct pragmatic demands. (shrink)

The impact of our desires and preferences upon our ordinary, everyday beliefs is well-documented [Gilovich, T. . How we know what isn’t so: The fallibility of human reason in everyday life. New York: The Free Press.]. The influence of such motivational factors on delusions, which are instances of pathological misbelief, has tended however to be neglected by certain prevailing models of delusion formation and maintenance. This paper explores a distinction between two general classes of theoretical explanation for delusions; the motivational (...) and the deficit. Motivational approaches view delusions as extreme instances of self-deception; as defensive attempts to relieve pain and distress. Deficit approaches, in contrast, view delusions as the consequence of defects in the normal functioning of belief mechanisms, underpinned by neuroanatomical or neurophysiological abnormalities. It is argued that although there are good reasons to be sceptical of motivational theories , recent experiments confirm that motives are important causal forces where delusions are concerned. It is therefore concluded that the most comprehensive account of delusions will involve a theoretical unification of both motivational and deficit approaches. (shrink)

Fregoli delusion is the mistaken belief that some person currently present in the deluded person's environment is a familiar person in disguise. The stranger is believed to be psychologically identical to this known person even though the deluded person perceives the physical appearance of the stranger as being different from the known person's typical appearance. To gain a deeper understanding of this contradictory error in the normal system for tracking and identifying known persons, we conducted a detailed survey of all (...) the Fregoli cases reported in the literature since the seminal Courbon and Fail paper. Our preliminary reading of these cases revealed a notable lack of definitional clarity. So, we first formulated a classification scheme of different person misidentification delusions so as to identify those cases that qualified as instances of Fregoli according to the above characterization: the mistaken belief that a known person is present in the environment in a different guise to his or her typical appearance. We identified 38 clear cases of this type and set out to answer a series of questions motivated by current hypotheses about the origin of the Fregoli delusion. We asked whether the patients misidentified particular strangers, made reference to the misidentified known persons using wigs or plastic surgery , misidentified many different strangers or only one, showed other symptoms , and made inferences about the motives of the known persons in disguise. We conclude by discussing the implications of our findings for current hypotheses concerning the origin of the Fregoli delusion. (shrink)

In folie à deux, a ‘primary’ patient transmits a delusional belief to one or more ‘secondary’ patients who then adopt and share the belief. This paper applies the two‐factor theory of delusion to retrospectively analyse published cases of folie à deux. Lessons from this retrospective analysis include, firstly, that two‐factor theorists need to shift their focus from endogenous processes to consider the exogenous source of delusional content in most secondaries. Secondly, secondaries who come to share the belief via normal processes (...) of social contagion only qualify as delusional by virtue of the abnormal persistence of their belief, albeit a temporary persistence in those secondaries who abandon their belief soon after separation from the primary. Underpinning this abnormal persistence may be a form of inhibitory failure—a difficulty with inhibiting a belief to allow reasoning for and against it being true. (shrink)

This volume brings together philosophical perspectives on emotions, imagination and moral reasoning with contributions from neuroscience, cognitive science, social psychology, personality theory, developmental psychology, and abnormal psychology. The book explores what we can learn about the role of emotions and imagination in moral reasoning from psychopathic adults in the general community, from young children, and adolescents with callous unemotional traits, and from normal child development. It discusses the implications for philosophical moral psychology of recent experimental work on moral reasoning in (...) the cognitive sciences and neurosciences. Conversely, it shows what cognitive scientists and neuroscientists have still to learn from philosophical perspectives on moral reasoning, moral reflection, and moral responsibility. Finally, it looks at whether experimental methods used for researching moral reasoning are consistent with the work in social psychology and with philosophical thought on adult moral reasoning in everyday life. The volume's wide-ranging perspectives reflect the varied audiences for the volume, from students of philosophy to psychologists working in cognition, social and personality psychology, developmental psychology, abnormal psychology, and cognitive neuroscience. (shrink)

Over the past century or more, cognitive neuropsychologists have discussed many of the issues raised in this volume. On the basis of this literature, we argue that autism is not a single homogeneous condition, and so can have no single cause. Instead, each of its symptoms has a cause, and the proper study of autism is the separate study of each of these symptoms and its cause. We also offer evidence to support the radical view advanced by Stoljar and Gold (...) in this volume, namely, that in explaining such syndromes the cognitive level of explanation has priority over the neuroscientific. (shrink)

This article contrasts the cognitive neuropsychiatric approach with the traditional psychiatric approaches to delusions to develop testable cognitive theories of delusions so as to render the generation of delusions psychologically understandable. It illustrates how cognitive neuropsychiatrists use the Bruce and Young model of face processing to explain the generation of misidentification delusions. The study of facial expression highlights that future cognitive neuropsychiatric study of self and non-self face processing using different representational media in patients with mirrored-self misidentification delusions will likely (...) be informative with regard to advancing scientific understanding of the putative differences between self and non-self recognition. It reviews cognitive neuropsychiatric research into the Capgras delusion and shows the distinction between overt face recognition and person identity authentication, and suggests the need for further modification of Bruce and Young's model to remove direct pathways between the person's identity module and the affective response system and to incorporate a separate integrative device. (shrink)

Mirrored-self misidentification is the delusional belief that one's own reflection in the mirror is a stranger. In two experiments, we tested the ability of hypnotic suggestion to model this condition. In Experiment 1, we compared two suggestions based on either the delusion's surface features (seeing a stranger in the mirror) or underlying processes (impaired face processing). Fifty-two high hypnotisable participants received one of these suggestions either with hypnosis or without in a wake control. In Experiment 2, we examined the extent (...) to which social cues and role-playing could account for participants' behaviour by comparing the responses of 14 hypnotised participants to the suggestion for impaired face processing (reals) with those of 14 nonhypnotised participants instructed to fake their responses (simulators). Overall, results from both experiments confirm that we can use hypnotic suggestion to produce a compelling analogue of mirrored-self misidentification that cannot simply be attributed to social cues or role-playing. (shrink)

Much attention has been paid recently to the role of anomalous experiences in the aetiology of certain types of psychopathology, e.g. in the formation of delusions. We examine, instead, the top-down influence of pre-existing beliefs and affective factors in shaping an individual’s characterisation of anomalous sensory experiences. Specifically we investigated the effects of paranormal beliefs and alexithymia in determining the intensity and quality of an altered state of consciousness . Fifty five participants took part in a sweat lodge ceremony, a (...) traditional shamanic ritual which was unfamiliar to them. Participants reported significant alterations in their state of consciousness, quantified using the ‘APZ’ questionnaire, a standardized measure of ASC experience. Participants endorsing paranormal beliefs compatible with shamanic mythology, and those showing difficulty identifying feelings scored higher on positive dimensions of ASC experience. Our findings demonstrate that variation in an individual’s characterisation of anomalous experiences is nuanced by pre-existing beliefs and affective factors. (shrink)

In their pursuit of adaptively biased misbelief-making systems, McKay & Dennett (M&D) describe a putative doxastic shear-pin system which enables misbeliefs to form in situations of extreme psychological stress. Rather than discussing their argument, I consider how this shear-pin system might combine with both pathological belief-making ( breakdowns caused by neuropathy) and normal belief-making to explain a spectrum of delusions.

Dehaene et al. (2003) showed an absence of conscious, but not masked, conflict effects when patients with schizophrenia performed a number-categorisation priming task. We aimed to replicate these influential results using a different word-categorisation priming task. Counter to Dehaene et al.'s findings, 21 patients and 20 healthy controls showed similar congruence effects for both masked and visible primes. Within patients, a reduced congruence effect for visible primes associated with longer duration of illness and more severe behavioural disorganisation. Patients, unlike controls, (...) were no slower to respond to targets that followed visible compared to masked primes. Conscious conflict effects on priming tasks are not universally reduced in schizophrenia but may associate with chronicity and behavioural disorganisation. That patients were no slower when the preceding primes were clearly visible accords with evidence elsewhere that information processing in schizophrenia is driven more by immediate conscious experience and constrained less by prior events. (shrink)

By conceiving of autism and psychosis as diametrically opposite phenotypes of underactive and overactive mentalizing, respectively, Crespi & Badcock (C&B) commit themselves to a continuum view of intercorrelated mentalizing functions. This view fails to acknowledge dissociations between mentalizing functions and that psychotic people show a mixture of both hypo- and hyper-mentalizing.

In folie à deux, a ‘primary’ patient transmits a delusional belief to one or more ‘secondary’ patients who then adopt and share the belief. This paper applies the two‐factor theory of delusion to retrospectively analyse published cases of folie à deux. Lessons from this retrospective analysis include, firstly, that two‐factor theorists need to shift their focus from endogenous processes to consider the exogenous source of delusional content in most secondaries. Secondly, secondaries who come to share the belief via normal processes (...) of social contagion only qualify as delusional by virtue of the abnormal persistence of their belief, albeit a temporary persistence in those secondaries who abandon their belief soon after separation from the primary. Underpinning this abnormal persistence may be a form of inhibitory failure—a difficulty with inhibiting a belief to allow reasoning for and against it being true. (shrink)