We propose that the six mechanisms identified by Juslin & Vll (J&V) fall into two categories: signal detection and amplification. Signal detection mechanisms are unmediated and induce emotion by directly detecting emotive signals in music. Amplifiers act in conjunction with signal detection mechanisms. We also draw attention to theoretical and empirical challenges associated with the proposed mechanisms.

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)

t. 1. Dialog s V. V. Davydovym -- t. 2. Nereshennye problemy razvivai︠u︡shchego obrazovanii︠a︡.

In this article, we propose a pluralistic approach to the explanation of social understanding that integrates literature from social psychology with the theory of mind debate. Social understanding in everyday life is achieved in various ways. As a rule of thumb we propose that individuals make use of whatever procedure is cognitively least demanding to them in a given context. Aside from theory and simulation, associations of behaviors with familiar agents play a crucial role in social understanding. This role has (...) been neglected so far. We illustrate the roles of fluency and associations in social understanding in false belief tasks. (shrink)

Delusional beliefs have sometimes been considered as rational inferences from abnormal experiences. We explore this idea in more detail, making the following points. Firstly, the abnormalities of cognition which initially prompt the entertaining of a delusional belief are not always conscious and since we prefer to restrict the term “experience” to consciousness we refer to “abnormal data” rather than “abnormal experience”. Secondly, we argue that in relation to many delusions (we consider eight) one can clearly identify what the abnormal cognitive (...) data are which prompted the delusion and what the neuropsychological impairment is which is responsible for the occurrence of these data; but one can equally clearly point to cases where this impairments is present but delusion is not. So the impairment is not sufficient for delusion to occur. A second cognitive impairment, one which impairs the ability to evaluate beliefs, must also be present. Thirdly (and this is the main thrust of our chapter) we consider in detail what the nature of the inference is that leads from the abnormal data to the belief. This is not deductive inference and it is not inference by enumerative induction; it is abductive inference. We offer a Bayesian account of abductive inference and apply it to the explanation of delusional belief. (shrink)

This paper seeks to differentiate negative properties from positive properties, with the aim of providing the groundwork for further discussion about whether there is anything that corresponds to either of these notions. We differentiate negative and positive properties in terms of their functional role, before drawing out the metaphysical implications of proceeding in this fashion. We show that if the difference between negative and positive properties tabled here is correct, then negative properties are metaphysically contentious entities, entities that many philosophers (...) will be unwilling to countenance. (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)

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)

INTRODUCTION: In accounts of the two-factor theory of delusional belief, the second factor in this theory has been referred to only in the most general terms, as a failure in the processes of hypothesis evaluation, with no attempt to characterise those processes in any detail. Coltheart and Davies attempted such a characterisation, proposing a detailed eight-step model of how unexpected observations lead to new beliefs based on the concept of abductive inference as introduced by Charles Sanders Peirce. METHODS: In (...) this paper, we apply that model to the explanation of various forms of delusional belief. RESULTS: We provide evidence that in cases of delusion there is a specific failure of the seventh step in our model: the step at which predictions from hypotheses are considered in the light of relevant evidence. CONCLUSIONS: In the two-factor theory of delusional belief, the second factor consists of a failure to reject hypotheses in the face of disconfirmatory evidence. (shrink)

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.

Models of the architecture of mature cognitive systems can inform the study of normal and disordered cognitive development, if one distinguishes between proximal and distal causes of performance. The assumption of residual normality need not be made in order to apply adult models to performance early in development, because these models can be modified to reflect the results of compensatory processing.

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.

Some delusional patients exhibit only a single delusional belief (or several delusional beliefs concerning a single theme): this is monothematic delusion. It contrasts with polythematic delusion, where the patient exhibits a variety of delusions concerning a variety of different themes. The neuropsychological bases of various monothematic delusions are rather well understood, and there is a well-worked-out general neuropsychological theory of monothematic delusion, the two-factor theory. Whether polythematic delusion might be explained in a similar way is an open question: I sketch (...) some possible ways in which a comparable two-factor account might be developed for polythematic (‘psychiatric’) delusional conditions such as delusions of reference. (shrink)

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)

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)

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)

Are there universals of reading? There are three ways of construing this question. Is the region of the brain where reading is implemented identical regardless of what writing system the reader uses? Is the mental information-processing system used for reading the same regardless of what writing system the reader uses. Do the word's writing systems share certain universal features? Dehaene offers affirmative answers to all three questions in his book. Here I suggest instead that the answers should be negative. And (...) I ask: if reading is not universal in any sense, what does this imply about Dehaene's Neuronal Recycling hypothesis for reading? (shrink)