Voluntary acts are preceded by electrophysiological (RPs). With spontaneous acts involving no preplanning, the main negative RP shift begins at about200 ms. Control experiments, in which a skin stimulus was timed (S), helped evaluate each subject's error in reporting the clock times for awareness of any perceived event.

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)

Ordinarily, if you say something like “I see a comet,” you might make a mistake about whether it is a comet that you see, but you could not be right about whether it is a comet but wrong about who is seeing it. There cannot be an “error of identification” in this case. In making a judgement like, “I see a comet,” there are not two steps, finding out who is seeing the thing and finding out what it is that (...) is being seen, so that you could go wrong at either step. The only place to go wrong is in your description of what is being seen. We usually take it that the same point applies to present-tense ascriptions to oneself of psychological states in general. You can get it wrong about which psychological state you are in, but you cannot get it right about the psychological state but wrong about whose psychological state it is. In contrast, in a room full of people, I might hear a noise and conclude, “Bill sneezed,” and in this case I could be wrong either about who it was that sneezed or about whether it was a sneeze, rather than say a death-rattle. (shrink)

The abilities to attribute an action to its proper agent and to understand its meaning when it is produced by someone else are basic aspects of human social communication. Several psychiatric syndromes, such as schizophrenia, seem to lead to a dysfunction of the awareness of one’s own action as well as of recognition of actions performed by other. Such syndromes offer a framework for studying the determinants of agency, the ability to correctly attribute actions to their veridical source. Thirty normal (...) subjects and 30 schizophrenic patients with and without hallucinations and/or delusional experiences were required to execute simple finger and wrist movements, without direct visual control of their hand. The image of either their own hand or an alien hand executing the same or a different movement was presented on a TV-screen in real time. The task for the subjects was to discriminate whether the hand presented on the screen was their own or not. Hallucinating and deluded schizophrenic patients were more impaired in discriminating their own hand from the alien one than the non-hallucinating ones, and tended to misattribute the alien hand to themselves. Results are discussed according to a model of action control. A tentative description of the mechanisms leading to action consciousness is proposed. (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)

This paper is concerned with the problem of selfidentification in the domain of action. We claim that this problem can arise not just for the self as object, but also for the self as subject in the ascription of agency. We discuss and evaluate some proposals concerning the mechanisms involved in selfidentification and in agencyascription, and their possible impairments in pathological cases. We argue in favor of a simulation hypothesis that claims that actions, whether overt or covert, are centrally simulated (...) by the neural network, and that this simulation provides the basis for action recognition and attribution. (shrink)

This paper offers a framework for consciousness of internal reality. Recent PET experiments are reviewed, showing partial overlap of cortical activation during self-produced actions and actions observed from other people. This overlap suggests that representations for actions may be shared by several individuals, a situation which creates a potential problem for correctly attributing an action to its agent. The neural conditions for correct agency judgments are thus assigned a key role in self/other distinction and self-consciousness. A series of behavioral experiments (...) that demonstrate, in normal subjects, the poor monitoring of action-related signals and the difficulty in recognizing self-produced actions are described. In patients presenting delusions, this difficulty dramatically increases and actions become systematically misattributed. These results point to schizophrenia and related disorders as a paradigmatic alteration of a ''Who?'' system for self-consciousness. (shrink)

In the past dozen years a number of theoretical models of schizophrenic symptoms have been proposed, often inspired by advances in the cognitive sciences, and especially cognitive neuroscience. Perhaps the most widely cited and influential of these is the neurocognitive model proposed by Christopher Frith (1992). Frith's influence reaches into psychiatry, neuroscience, and even philosophy. The philosopher John Campbell (1999a), for example, has called Frith's model the most parsimonious explanation of how self-ascriptions of thoughts are subject to errors of identification. (...) "On reflection, it also seems that this is not just one possible theory; it is the simplest theory which has any prospect of explaining the sense of agency, and we ought to work from it, introducing complications only as necessary" (1999a, p. 612). Not everyone agrees. In their recent analysis of alien voices and inserted thoughts in schizophrenia, Stephens and Graham (2000) offer a critique of Frith. Their criticism, however, although serious, is neither deep nor extensive. They outline three points. First, Frith fails to provide an adequate account of why a subject who experiences thought insertion would misattribute that thought to some other agent. Second, Frith does not clarify the distinction between thought insertion and thought influence. And third, Frith fails to explain how a subject can claim both that he is thinking the thought and that the thought is someone else's thought (Stephens and Graham.. (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)

Organisms engage in various activities that are directed at objects, whether real or imagined. Such activities may be termed “intentional relations.” We present a four-level framework of social understanding that organizes the ways in which social organisms represent the intentional relations of themselves and other agents. We presuppose that the information available to an organism about its own intentional relations (or first person information) is qualitatively different from the information available to that organism about other agents’ intentional relations (or third (...) person information). However, through the integration of these two sources of information, it is possible to generate representations of intentional relations that are uniformly applicable to the activities of both self and other. The four levels of the framework differ in the extent to which such integration occurs and in the degree to which imagination is involved in generating these representations. Most animals exist at the lowest level, at which integration of first and third person sources of information does not occur. Of nonhuman species, only great apes exhibit social understanding at intermediate levels, at which integration of these sources of information provides uniform representations of intentional relations. Only humans attain the highest level, at which it is possible to represent intentional relations with mental objects. We propose that with the development of the imagination, children progress through three stages, equivalent to the later three levels of the framework. The abnormalities in social understanding of autistic individuals are hypothesized to result from a failure to develop integrated representations of intentional relations. (shrink)

Some monothematic types of delusions may arise because subjects have unusual experiences. The role of this experiential component in the pathogenesis of delusion is still not understood. Focussing on delusions of alien control, we outline a model for reality testing competence on unusual experiences. We propose that nascent delusions arise when there are local failures of reality testing performance, and that monothematic delusions arise as normal responses to these. In the course of this we address questions concerning the tenacity with (...) which delusions are maintained, their often bizarre content, the patients' inability to dismiss them, and their often circumscribed character. (shrink)

A popular approach to monothematic delusions in the recent literature has been to argue that monothematic delusions involve broadly rational responses to highly unusual experiences. Campbell calls this the empiricist approach to monothematic delusions, and argues that it cannot account for the links between meaning and rationality. In place of empiricism Campbell offers a rationalist account of monothematic delusions, according to which delusional beliefs are understood as Wittgensteinian framework propositions. We argue that neither Campbell's attack on empiricism nor his rationalist (...) alternative to empiricism is successful. (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)

Elisabeth Pacherie is a research fellow in philosophy at Institut Jean Nicod, Paris. Her main research and publications are in the areas of philosophy of mind, psychopathology and action theory. Her publications include a book on intentionality (_Naturaliser_ _l'intentionnalité_, Paris, PUF, 1993) and she is currently preparing a book on action and agency.

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)

People experiencing alien control report that their thoughts, movements, actions, and emotions have been replaced by those of an "other." The latter is commonly a perceived persecutor of the patient. Here I describe the clinical phenomenology of alien control, mechanistic models that have been used to explain it, problems inherent in these models, the brain deficits and functional abnormalities associated with this symptom, and the means by which disordered agency may be examined in this perplexing condition. Our current state of (...) knowledge implicates potentially reversible dysfunction in certain key brain regions (especially the right parietal cortex), which is temporally related to the presence of symptoms. Alien control is quintessentially a disorder of agency. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 9.1 (2002) 65-72 [Access article in PDF] Multiple Paths to Delusion Philip Gerrans Response to Phillips JAMES PHILLIPS COMMENTS are summarized in four recommendations. Clarify the Relationship of the Cognitive Model to its Neuroscientific Base The cognitive approach postulates a cognitive entity whose information-processing properties explain a symptom or unify a set of symptoms. The key idea is that we can use a model of (...) normal cognitive functioning to explain a disorder in terms of failure of a component of the model. In the case under discussion, the symptom is the loss of affect, which is part of the clinical profile of both the Capgras and Cotard delusions. The body of neuropsychological data concerning links between recognitional and affective processes extends back at least to Charcot's patient M. X. whose affective responses to familiar situations were lost, together with his visual episodic memory. M. X described his phenomenology this way: A remarkable consequence of this loss of mental ability is, as I have said, the change in my personality and impressions. I am much less affected by sorrow or grief. I can tell you that, after losing one of my relatives with whom I was very close, I experienced a much less intense grief than if I had still been able to image the features of that relative, the stages of the illness he went through, or especially if I had been able to picture to myself [voir interieurement] the outward effect of this untimely death on the members of my family. (Young and van de Wal 1996) (It is interesting to note that M. X. retained insight into his condition and explained it in a lucid, rational way rather than forming a delusional belief. Initial evidence for a two-stage theory, one might have thought).Given convergent evidence that the limbic system is the basis of affective states, the hypothesis that the delusions under discussion are rationalizations of unusual affective experiences consequent on abnormal limbic function or loss of connection between limbic and other functions is an inference to the best explanation. The Young-Ellis model is a cognitive model that describes cognitive function at what Dennett calls the design level, intermediate between what Marr called the computational level and level of representation and algorithm. As such it implies only that the boxes and arrows are implemented neurally, but endorses no hypotheses about the nature of that implementation.It is correct of Phillips to observe that the crucial inference about the link between affective and cognitive function is grounded in a background theory of the relationship between cognitive models, clinical symptoms, and neurobiology. If Phillips' complaint is that the model cannot be sheeted home to a neurobiological substrate, [End Page 65] this is true. Implementation theories are thin on the ground in cognitive science because they would require a theory of biological computation that, despite partisan claims, is elusive. Nonetheless, information-processing models and partial implementation theories for specific functions such as perception, language, face recognition, and the affective systems do exist. The allusion to cognitive structure remains sound as long as it accounts for observable clinical and experimental data and makes verifiable predictions.The fact that the Young-Ellis model of face recognition can account for both normal function and a variety of forms of prosopagnosia together (under assumptions about the relation between belief and experience) with delusions of misidentification counts in its favor (Ellis 1998).Phillips objection to cognitive theories is stronger when we turn to models of belief and rationality. In the case of functions such as face recognition or language, there is a variety of convergent evidence, especially from deficit studies, to support a model of normal cognitive function. For example, we know that face recognition activates schemas concerning orientation, features, emotions, and gender because these components can be selectively damaged (Young 1998). However, we lack a model of normal human reasoning other than "folk theory" of belief-desire psychology. Cognitive theories of belief formation are often forced to use models derived from philosophy such as logic, probability theory, or decision theory, which are amenable to... (shrink)