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.
The "two-route model of face recognition" proposed by Bauer (1984) and adopted by Ellis and Young (1990), has become a widely accepted model in studies of face processing disorders, including both prosopagnosia and the delusional misidentification syndromes. We review the origin and application of the two-route model of face recognition in examining both the neuroanatomical pathways and the cognitive pathways to face recognition. With respect to the neuroanatomy, we conclude that face recognition is subserved by a single pathway, the ventral visual pathway, as there is no evidence to suggest that the dorsal visual pathway is capable of visual recognition or of providing an affective response to familiar stimuli. We demonstrate how operation of the ventral visual pathway and its connections to the amygdala can parsimoniously account for the findings in the literature on prosopagnosia and delusional misidentification syndromes. In addition, we propose a cognitive model of face processing stemming from the work of Bruce and Young (1986). Our model involves two pathways subsequent to the system responsible for face recognition: one pathway to a system containing semantic and biographical information about the seen face, and a second pathway to a system responsible for the generation of an affective response to faces that are familiar. We demonstrate how this cognitive model can explain the dissociations between overt and covert recognition observed in prosopagnosia and the Capgras delusion.
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.Delusions of misidentification (DM) include a variety of fascinating disorders in which there is a mistaken belief in the identity of oneself, other people, places or objects. They include: Capgras syndrome-the belief that other people, often close relatives, have been replaced by doubles or impostors; Fregoli syndrome-the belief that strangers are in fact known people in disguise; intermetamorphosis-the belief that someone has changed physically and psychologically into another person; reverse intermetamorphosis-the belief that there has been a physical and psychological change of oneself into another person; and reduplicative paramnesia-the belief that there are doubles of known people or places. This last delusion (reduplicative paramnesia) differs from Capgras delusion in that while reduplication is believed to have occurred, there is no sense of replacement. Thus, the impostor claim is not made in cases of reduplicative paramnesia. Patients with DM traverse the boundaries of psychiatry, neurology and neuropsychology and have been studied from the perspective of all three disciplines. 1 We are very grateful to TH, FE, DB, RZ and their families for their participation in this research. We would also like to thank Matthew Large for insightful discussion about the cases and referral of patient RZ, Virginia Arpadi for referring patient TH, David Sharpe for referring patient FE, and Robyn Langdon and Karalyn Patterson for helpful comments on an earlier draft of this paper.
We present two patients in whom the mirror sign, the inability to recognize one's own reflected image, was a stable and persisting symptom signalling the onset of a progressive dementing illness. Extensive neuropsychological testing was conducted with both patients, with particular emphasis on face processing and the understanding of reflected space. Both patients were also investigated with structural imaging techniques (computed tomography and magnetic resonance imaging). Although the neuroimaging results were not strongly lateralizing for either patient, neuropsychological testing revealed striking right hemisphere dysfunction with relatively intact left hemisphere cognitive function in both patients. Of particular interest was the patients' dissociation on tests of face processing; one patient, FE, had significant face processing deficits while the other patient, TH, had relatively intact face processing. Further testing with TH revealed striking deficits in his ability to interpret reflected space. The results of the face processing tests are discussed in the context of current models of normal face processing, with particular emphasis on the affective component in face recognition. We propose that a combination of cognitive deficits underlie the mirror sign delusion, including perceptual, affective and reasoning impairments, and also discuss the contributions of cortical and subcortical lesions in these two patients and in delusions in general.
Introduction. Despite the prevalence of delusional beliefs there are currently no viable
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