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)
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)
There are universals of language; but is it also true, as the target article claims, that there are universals of reading? We believe there are no such universals, and invite others to refute our claim by providing a list of some universals of reading. If there are no universals of reading, there cannot be a universal model of reading.
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.
Anosognosia is literally ‘unawareness of or failure to acknowledge one’s hemi- plegia or other disability’ (OED). Etymology would suggest the meaning ‘lack of knowledge of disease’ so that anosognosia would include any denial of impairment, such as denial of blindness (Anton’s syndrome). But Babinski, who introduced the term in 1914, applied it only to patients with hemiplegia who fail to acknowledge their paralysis. Most commonly, this is failure to acknowledge paralysis of the left side of the body following damage to (...) the right hemisphere of the brain. In this paper, we shall mainly be concerned with anosognosia for hemiplegia. But we shall also use the term ‘anosognosia’ in an inclusive way to encompass lack of knowledge or acknowledgement of any impairment. Indeed, in the construction ‘anosognosia for X’, X might even be anosognosia for some Y. (shrink)
The question posed by Dunn and Kirsner (D&K) is an instance of a more general one: What can we infer from data? One answer, if we are talking about logically valid deductive inference, is that we cannot infer theories from data. A theory is supposed to explain the data and so cannot be a mere summary of the data to be explained. The truth of an explanatory theory goes beyond the data and so is never logically guaranteed by the data. (...) This is not just a point about cognitive neuropsychology, or even about psychology in general. It is a familiar point about all science. (shrink)
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.
Cognitive neuropsychology is that branch of cognitive psychology that investi- gates people with acquired or developmental disorders of cognition. The aim is to learn more about how cognitive systems normally operate or about how they are normally acquired by studying selective patterns of cognitive break- down after brain damage or selective dif?culties in acquiring particular cogni- tive abilities. In the early days of modern cognitive neuropsychology, research focused on rather basic cognitive abilities such as speech comprehension or production at the (...) single-word level, reading and spelling, object and face recognition, and short-term memory. More recently the cognitive-neuro- psychological approach has been applied to the study of rather more complex domains of cognition such as belief ?xation (e.g. Coltheart and Davies, 2000; Langdon and Coltheart, 2000) and pragmatic aspects of communication (e.g. McDonald and Van Sommers, 1993). Our paper concerns the investigation of pragmatic disorders in one clinical group in which such disorders are common, patients with schizophrenia, and what the study of such people can tell us about the normal processes of communication. (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)
who are unrecognizable because they are in disguise. ¼ The person I see in the mirror is not really me. ¼ A person I knew who died is nevertheless in the hospital ward today. ¼ This arm [the speaker’s left arm] is not mine it is yours; you have..
1923; Young, this volume); the Cotard delusion (Cotard, 1882; Berrios and Luque, 1995; Young, this volume); the Fregoli delusion (Courbon and Fail, 1927; de Pauw, Szulecka and Poltock, 1987; Ellis, Whitley and Luaute´, 1994); the delusion of mirrored-self misidentiﬁ- cation (Foley and Breslau, 1982; Breen et al., this volume); a delusion of reduplicative param- nesia (Benson, Gardner and Meadows, 1976; Breen et al., this volume); a delusion sometimes found in patients suffering from unilateral neglect (Bisiach, 1988); and the delusions of (...) alien control and of thought insertion, which are characteristic of schizophrenia (Frith, 1992). (shrink)
O'Brien & Opie believe that some mental representations are evoked by stimuli to which a person is attending, and other mental representations are evoked by stimuli to which attention was not paid. I argue that this is the classical view of consciousness; yet this is the view which they wish to challenge.