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)

Wegner and colleagues have offered an explanation of the sense of agency over one’s bodily actions. If the orthodox view is correct and there is a sense of agency deficit associated with delusions of alien control, then Wegner and colleagues’ model ought to extend to an explanation of this deficit. Data from intentional binding studies opens up the possibility that an abnormality in representing the timing of mental events leads to a violation of the principle of priority in (...) those suffering from delusions of alien control. However, the model ultimately fails as it is unable to accommodate action monitoring deficits associated with delusions of alien control, in particular the theory of mind deficiencies predicted by such accounts have not materialised. There are theory of mind problems associated with schizophrenia but they are not associated with delusions of alien control. Such accounts thereby fail to adequately explain delusions of alien control. (shrink)

Monothematic delusions are delusions whose contents pertain to a single subject matter. Examples include Capgras delusion, the delusion that a loved one has been replaced by an impostor, and Cotard delusion, the delusion that one is dead or does not exist. Two-factor accounts of such delusions hold that they are the result of both an experiential deficit, for instance flattened affect, coupled with an aberrant cognitive response to that deficit. In this paper we develop (...) a new expressivist two-factor account of delusion. In contrast to existing endorsement and explanationist accounts, which treat delusions as either explanations or endorsements of the contents of these disordered experiences, we hold that delusional beliefs have an expressive function: they characterize, in impressionistic terms, what the subject’s experience is like for them. We show how our account improves upon existing two-factor views in explaining the central features of monothematic delusions, in particular the way in which delusional subjects fall short of the ideal of rationality. (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)

Delusions are explanations of anomalous experiences. A theory of delusion requires an explanation of both the anomalous experience _and _the apparently irrational explanation generated by the delusional subject. Hence, we require a model of rational belief formation against which the belief formation of delusional subjects can be evaluated. _Method. _I first describe such a model, distinguishing procedural from pragmatic rationality. Procedural rationality is the use of rules or procedures, deductive or inductive, that produce an inferentially coherent set of propositions. (...) Pragmatic rationality is the use of procedural rationality _in context_. I then apply the distinction to the explanation of the Capgras and the Cotard delusions. I then argue that delusions are failures of pragmatic rationality. I examine the nature of these failures employing the distinction between performance and competence familiar from Chomskian linguistics. _Results. _This approach to the irrationality of delusions reconciles accounts in which the explanation of the anomalous experience exhausts the explanation of delusion, accounts that appeal to further deficits within the reasoning processes of delusional subjects, and accounts that argue that delusions are not beliefs at all. (Respectively, one-stage, two-stage, and expressive accounts.) _Conclusion. _In paradigm cases that concern cognitive neuropsychiatry the irrationality of delusional subjects should be thought of as a performance deficit in pragmatic rationality. (shrink)

In their target article, McKay & Dennett (M&D) conclude that only “positive illusions” are adaptive misbeliefs. Relying on overly strict conceptual schisms (deficit vs. motivational, functional vs. organic, perception vs. belief), they prematurely discount delusions asbiologicallyadaptive. In contrast to their view that “motivation” plays a psychological but not a biological function in a two-factor model of the forming and maintenance of delusions, we propose asingleimpairment in prediction-error–driven (i.e., motivational) learning in three stages in which delusions play a biologically adaptive (...) role. (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)

In psychiatry some disorders of cognition are distinguished from instances of normal cognitive functioning and from other disorders in virtue of their surface features rather than in virtue of the underlying mechanisms responsible for their occurrence. Aetiological considerations often cannot play a significant classificatory and diagnostic role, because there is no sufficient knowledge or consensus about the causal history of many psychiatric disorders. Moreover, it is not always possible to uniquely identify a pathological behaviour as the symptom of a certain (...) disorder, as disorders that are likely to differ both in their causal histories and in their overall manifestations may give rise to very similar patterns of behaviour. -/- Consider delusions as an example. It wouldn’t be correct to define delusions as those beliefs people form as a result of a neurobiological deficit and a hypothesis-evaluation deficit (as some versions of the two-factor theory of delusions suggest), because for some delusions no neurobiological deficit may be found, and reasoning biases and motivational factors may be contributors to the formation of the delusion (e.g. McKay et al., 2005). Moreover, it would be a mistake to define delusions as symptoms of schizophrenia alone, because they occur also in other disorders, including dementia, amnesia, and delusional disorders. Thus, aetiological considerations may appear in the description and analysis of delusions, but do not feature prominently in their definition. -/- In this paper I argue that the surface features used as criteria for the classification and diagnosis of disorders of cognition are often epistemic in character. I shall offer two examples: confabulations and delusions are defined as beliefs or narratives that fail to meet standards of accuracy and justification. Although classifications and diagnoses based on features of people’s observable behaviour are necessary at these early stages of neuropsychiatric research, given the variety of conditions in which certain phenomena appear, I shall attempt to show that current epistemic accounts of confabulations and delusions have limitations. Epistemic criteria can guide both research and clinical practice, but fail to provide sufficient conditions for the identification of delusions and confabulations, and fail to demarcate pathological from non-pathological narratives or beliefs. -/- Another limitation of current epistemic accounts – which I shall not address here – is the excessive focus on epistemic faults of confabulations and delusions at the expense of their epistemically neutral or advantageous features (see Bortolotti and Cox, 2009). This may lead to a misconception of delusions and confabulations, and to an oversimplification in the assessment of the needs of people who require clinical treatment for their psychotic symptoms. (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 (...) class='Hi'>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)

In this paper we review two debates in the current literature on clinical delusions. One debate is about what delusions are. If delusions are beliefs, why are they described as failing to play the causal roles that characterise beliefs, such as being responsive to evidence and guiding action? The other debate is about how delusions develop. What processes lead people to form delusions and maintain them in the face of challenges and counter-evidence? Do the formation and maintenance of delusions require (...) abnormal experience alone, or also reasoning biases or deficits? We hope to show that the focus on delusions has made a substantial contribution to the philosophy of the mind and continues to raise issues that are central to defining the concept of belief and gaining a better understanding of how people process information and learn about the world. (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 (...) class='Hi'>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)

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)

Delusions are usually defined as false beliefs about the state of affairs in the public world. Taking this premise as unquestionable, the debate in cognitive science tends to oscillate between the so-called 'rationalist approach'- proposing some breakdown in the central intellective modules embodying human rationality - and the 'empiricist approach' - proposing a primary peripheral deficit , followed by explanatory efforts in the form of delusions. In this article the foundational assumption about delusion is questioned. Especially in the (...) case of schizophrenia, delusions are not epistemic statements about external world but metaphorical reports of altered structure of experiencing . Delusions as epistemic statements or beliefs occur paradigmatically in delusional disorder . These two types of delusions are compared from a primarily phenomenological stance. (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)

In this paper I discuss an intriguing and relatively little studied symptomatic expression of schizophrenia known as experiences of activity in which patients form the delusion that they can control some external events by the sole means of their mind. I argue that experiences of activity result from patients being prone to aberrantly infer causal relations between unrelated events in a retrospective way owing to widespread predictive deficits. Moreover, I suggest that such deficits may, in addition, lead to an (...) aberrant intentional binding effect i.e., the subjective compression of the temporal interval between an intentional action and its external effects. In particular, it might be that patient’s thoughts are bound to the external events they aimed to control producing, arguably, a temporal contiguity between these two components. Such temporal contiguity would reinforce or sustain the feeling that the patient mind is directly causally efficient. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:The Background Theory of Delusion and Existential PhenomenologyRichard G. T. Gipps (bio) and John Rhodes (bio)KeywordsPhenomenology, psychological explanation, epistemology, schizophreniaSituating and Clarifying the PaperThe commentaries of Nassir Ghaemi and Giovanni Stanghellini help to sketch out the intellectual landscape of philosophical perspectives in psychiatry, and situate our paper within it. A happy convergence between the analytical philosophy perspective from which we were writing, and the existential–phenomenological paradigm described by (...) both authors, is the result. Stanghellini in particular carefully describes three main theories of existential deformations, tracing delusion formation back to either (i) a disturbance of meaning synthesis conceived as a dysfunction of a Husserlian consciousness, (ii) a disturbance of pre-reflective self-consciousness resulting in a kind of paralyzing hyperreflexivity, and (iii) (Stanghellini’s preferred model) a disturbance of embodiment. This final account views delusion as springing from a failure in the subject’s corporeal and praxical being-in-the-world. As the subject’s practical, pre-reflective grip on the world is loosened, so their minds become unconstrained by that understanding and practical rationality immanent within that grip, and thought, now unconstrained, starts to travel through delusional worlds. Stanghellini accordingly views our model as an example of a disembodiment theory, which allows it to overcome the disadvantages of the first two models, which may both, in their own ways, overvalue the rôle of (disturbances of) reflective consciousness in the formation (and delusional deformation) of everyday understanding.Being situated within a preexisting landscape has both its benefits and its disbenefits, the principle example of the latter being the potential assimilation of anything new to what has already been said. Thus, although we are grateful to our commentators for placing us on the larger historical and conceptual map, it may be helpful to briefly rehearse our motivations for drawing on the philosophical ideas of the Bedrock and Background in our theory of delusion. Our paper was primarily motivated by a concern that current, psychologically mainstream, cognitive models of delusion, although helpfully drawing our attention to common reasoning and perceptual deficits in the person with psychosis, fail to adequately account for what is delusional about delusions. It was, in [End Page 321] particular, to account for the certainty with which the deluded person clings to often quite extraordinary beliefs that we drew on the epistemological notion of the background. And although this epistemological notion fits quite neatly with ontological concerns regarding the embodied and praxical character of human existence, it is the particular epistemic rôle that it played in our theory—to do with the extraratiocinative constraint on judgement provided by the Background—that we wish to stress here.We return to this shortly, but first wish to comment briefly on two specific considerations raised by the commentaries. The first concerns Stanghellini’s claim that, for us, “when studying delusions, the focus should be on providing an adequate framework for understanding, rather than providing empirical hypotheses to be tested” (2008, 311–314). It seems to us, however, that both are equally important. What we wished to stress, however, was that empirical hypothesis testing may be led astray if it is not informed by an adequate framework for understanding. For example, most cognitive psychological experiments on delusions concern themselves with the individual’s ability to make appropriate guesses (e.g., regarding the color of beads in a bag), and their tendency to jump to conclusions; they do not concern themselves with the kinds of extraordinary conviction and certainty met with in delusion. The risk run by empirical researchers of cognitive factors in delusion is that a lack of a prior adequate theorization of delusion makes for accounts that are ultimately only of the formation, not of delusion in particular but rather of false or unusual beliefs more generally. An analytical approach, however, can help to explicate the ways in which the psychiatric concept of delusion fails to be adequately characterized by the quite general ‘external criteria’ of delusion (as Jaspers [1963] called them: falsity, stubbornness, uncommon), and aids in the construction of empirical hypotheses this time constrained by an understanding of the true ‘internal criteria’ of psychotic belief. Such an approach helps to spell out the... (shrink)

The conscious experiences we have during sleep have the potential to improve our empathetic response to those who experience delusions and psychosis by supplying a virtual reality simulation of mental illness. Empathy for those with mental illness is lacking and there has been little improvement in the last decades despite efforts made to increase awareness. Our lack of empathy, in this case, may be due to an inability to accurately mentally simulate what it’s like to have a particular cognitive disorder. (...) Dreaming can help mitigate these deficits by placing the dreamer directly into a realistic virtual simulation and thus increase their capacity for empathy. Increasing empathy would go some way towards reducing the stigma and discrimination faced by people in this group. Recent work suggests that virtual reality can increase empathy towards a variety of marginalised groups, however, this technology is limited in its ability to simulate mental illnesses such as delusions. Dreams, however, are at times virtual reality delusion simulators. They can replicate, to a reasonable degree, delusions and psychosis, and through these experiences, we can learn ‘what it’s like’ to have these conditions. It is essential that we recognise these experiences for what they are, attempt to remember and reflect on them. Instead of disregarding dreams due to their unusualness and bizarreness, we can learn from these experiences and expand our understanding of the human condition and its many forms. (shrink)

RESUMEN Desde 1980, C. D. Frith investiga la esquizofrenia, y explica sus síntomas centrales como las alucinaciones, con miras a aclarar cuál es el déficit originario de este trastorno mental. Frith propone una hipótesis centrada en el concepto de conciencia, que ha elaborado como parte del desarrollo científico contemporáneo. En primer lugar, como parte de la aplicación de modelos neurocognitivos de control motor, según los cuales el déficit se atribuye al concepto de copia eferente y su función. En segundo lugar, (...) la actualiza y complementa con evidencia de imagen cerebral de la atenuación de la actividad cortical parietal, como efecto derivado de la copia eferente. En tercer lugar, adiciona el concepto de sentido de agencia, y el componente de cognición social, intentando integrar la experiencia del paciente y la relevancia del ámbito intersubjetivo a su propuesta. Este artículo hace una revisión crítica de la hipótesis de Frith y se divide en cuatro partes: primero, se presenta una síntesis de la evolución de la hipótesis; segundo, se sintetiza su argumentación; tercero, se presentan los principales puntos críticos y, por último, se derivan unas conclusiones generales. ABSTRACT Since 1980, C. D. Frith has been working on schizophrenia, and explaining central symptoms such as hallucinations, in an attempt to clarify the basic deficits of this mental disorder. Frith has put forth a hypothesis based on the concept of consciousness, and has been adjusting it alongside contemporary scientific developments. In first place, it begins with the use of neurocognitive models of motor control, according to which the deficit is attributable to the concept of efferent copy and its function. In second place, he updated the model by including neuroimaging evidence of attenuation in parietal activity, as a consequence of the efferent copy. In third place, he added the concept of sense of agency, and the social cognition component, trying to integrate to his proposal the patient's experience and the relevance of the inter-subjective aspect. The current paper, which critically reviews Frith's hypothesis, it's divided in four parts: First, the hypothesis' evolution is synthesized; second, the main arguments are summarized; third, the main critical points are presented; and, finally, some general conclusions are drawn. (shrink)

Popular two-factor accounts of thought insertion hold that this symptom of psychosis is caused by two elements working in tandem: an anomalous experience of some kind (the first factor) and a reasoning deficit or bias (the second factor). This chapter develops a very different alternative to explaining and treating thought insertion—one that views thought insertion as a form persecutory delusion. If this thesis is correct, clinical interventions for persecutory delusions may be successful for thought insertion as well. The (...) chapter begins by presenting several difficulties for two-factor accounts of thought insertion and for two-factor accounts of delusions more generally. It then discusses positive reasons for seeing thought insertion as a form of persecutory delusion. The positive case begins with reflection on first-person descriptions of thought insertion gleaned from online discussion forums. It continues by considering ways in which clinical diagnostic tools may create the appearance of deep differences between symptoms such as thought insertion and persecutory delusions where there are none. This case is bolstered by evidence for considerable variability in the content of delusions patients present with over time. Implications for the treatment of thought insertion are then considered. (shrink)

How do I know that I am the person who is moving? According to Wittgenstein (1958), the sense of agency involves a primitive notion of the self used as subject, which does not rely on any prior perceptual identification and which is immune to error through misidentification. However, the neuroscience of action and the neuropsychology of schizophrenia show the existence of specific cognitive processes underlying the sense of agency—the ‘‘Who'' system (Georgieff & Jeannerod, 1998) which is disrupted in delusions of (...) control (Frith, 1992). Yet, we have to be careful in the interpretation of such clinical symptoms, which cannot be so easily reduced to deficit of action monitoring or to lack of action awareness. Moreover, we should refine the definition of the sense of agency by distinguishing the sense of initiation and the sense of one's own movements. A conceptual analysis of the empirical data will lead us to establish the taxonomy of the different levels of action representations. (shrink)

This paper proposes an integrated account of the etiology of OCD that accommodates both dysfunctional cognitions and sensorimotor features of compulsive action. It is argued that cognitive/metacognitive theories do not aspire to address all obsessive-compulsive phenomenal properties and that empirical evidence concerning some of these requires the incorporation of motor deficits as an independent factor in a plausible conception of OCD. The difference in agency attribution between obsessive-compulsive persons and schizophrenia patients with delusions of control is also accounted for in (...) terms of bottom-up processes. (shrink)

Explanations of Capgras delusion and prosopagnosia typically incorporate a dual-route approach to facial recognition in which a deficit in overt or covert processing in one condition is mirror-reversed in the other. Despite this double dissociation, experiences of either patient-group are often reported in the same way – as lacking a sense of familiarity toward familiar faces. In this paper, deficits in the facial processing of these patients are compared to other facial recognition pathologies, and their experiential characteristics mapped (...) onto the dual-route model in order to provide a less ambiguous link between facial processing and experiential content. The paper concludes that the experiential states of Capgras delusion, prosopagnosia, and related facial pathologies are quite distinct, and that this descriptive distinctiveness finds explanatory equivalence at the level of anatomical and functional disruption within the face recognition system. The role of skin conductance response as a measure of ‘familiarity’ is also clarified. (shrink)

Patients with psychotic disorders experience a range of reality distortions. These often include auditory-verbal hallucinations, and thought insertion to a lesser degree; however, their mechanisms and relationships between each other remain largely elusive. Here we attempt to establish a integrative model drawing from the phenomenology of both AVHs and TI and argue that they in fact can be seen as ‘spectra’ of experiences with varying degrees of agency and ownership, with ‘silent and internal own thoughts’ on one extreme and ‘fully (...) external and clearly audible voices’ in the absence of a speaker on the other. We believe a spectral model will add emphasis to the continuity of experience and help to better understand how one type of psychotic symptom may interact with another, and put forward the argument that the experience of TI itself is not sufficient to classify as a delusion. In addition we aim to discuss some of the conceptual issues surrounding AVHs and TI with first-person accounts and current philosophical and neuropsychological theories in mind. We propose that the mechanisms behind AVHs and TI are more complex than source-monitoring deficits; indeed, to understand such phenomena one must appreciate that their very ‘existence’ and ‘reality’ as experienced by the individual have much deeper implications and meaning, both philosophically and clinically. (shrink)

Despite the diagnostic relevance of thought insertion for disorders such as schizophrenia, the debates about its aetiology are far from resolved. This paper claims that in paying exclusive attention to the perceptual and cognitive impairments leading to delusional experiences in general, current deficit approaches overlook the role that affective disturbances might play in giving rise to cases of thought insertion. In the context of psychosis, affective impairments are often characterized as a consequence of the stress and anxiety caused by (...) delusional episodes. However, here I explore some of the conceptual and empirical reasons to think that affective problems might in fact play a crucial doxastic role in the aetiology of thought insertion. Finally, I conclude by proposing a way of integrating the main insights of my analysis with the current ‘two-factor’ deficit approach to thought insertion and I explore the potential adaptive role that some delusions might have within this framework. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Lack of Autonomy: A View From the InsideSteve Weiner (bio)Keywordsagency, autonomy, deficit, determinismThe most vivid and truly overwhelming response I have to all arguments stressing agency/autonomy, that is, what lay people call free will, is this: that I’ve never had the sensation of acting autonomously since the onset of my mental illness on August 28, 1965. I have never been comfortable with saying that “I made a choice,” (...) or with other people either lecturing me or attempting to reassure me, often at the same time, by saying that I acted with autonomy/primary agency, as it were. That is my overwhelming subjective experience. I usually refrain from attempting to make a general case for determinism about myself or the universe in general, although, again, I feel far more determined than free. (I would note that Mary Midgley [2006] points out that the word determined and the concept, by extension, of determinism have two different meanings in say, social theory and geometry.)One strong criticism of this article I would put forward is that the Davidson and Shahan seemed to mention only depression among many diagnoses to make their case, although their French mentors/ co-thinkers apparently focused on schizophrenia, however unusually defined by them. In obsessive-compulsive disorder, we all have the very strong impression of the obsessive thoughts having been forced into our mind by something or someone else. My impression is that we all engage in our warding-off rituals, especially in the later, most frequent, most ritualistic repetitions, “against our will.”My most frequent diagnoses over the decades have been paranoid schizophrenia and schizoaffective disorder, and I more or less agree most of the time with those labels. I find Louis Sass’ “discovery” that our delusions are better thought of as semi-delusions with our simultaneously believing and not believing them, and our usual failure to take action on them, pretty well describes my own long-term experience. I know he is insistent on ascribing some degree of agency/whole personality involvement to us as compared with the standard National Alliance on Mental Illness/biological model, but I feel that he is getting closer to most of the “truth” when he talks about a subtle interweaving of affliction/deficit and agency.The authors’ reliance on French thinkers almost inevitably sends me back to a once-prominent French intellectual, one of my favorite writers Albert Memmi, the Tunisian-Jewish born socialist and Zionist. In a book that mentions The Story of O, (Memmi 1984) a story of extreme sexual submission or masochism, he makes the striking remark that the mentally ill are “oppressed from within.” I have spoken of this often because it seems to touch perfectly on my experience and that of fellow mentally ill people I have met. From the perspective of the outsider, it seems that the whole [End Page 237] and integrated person is involved in every behavior. What looks like agency to others, especially when it comes to undesirable behaviors, when experienced from within, is actually a situation of affliction from a seemingly autonomous place. We experience this as coming, yes, from within us, but not ultimately of us.I cannot be sure, but a belief in some degree of metaphysical choice from the beginning of one’s life seems to me the only way the authors of this article can firmly, enthusiastically come down on the side of agency as opposed to deficit/malfunction in trying to explain human problems. In contrast, I suppose I could be called a physicalist. I have noticed that physical substances (alcohol, caffeine, psychiatric drugs) have such a vivid and consistent effect on my mind that it makes sense to me to conclude that yes, mind is probably ultimately reducible to brain/body/experience of the senses. That is my private opinion based on experience as mediated through knowledge/intellect.One final point: Despite the (almost certainly) radical left politics of the authors, as an officially disabled person almost completely dependent on the welfare state, I fear that in competitive individualist America, the authors’ hoped-for far greater emphasis on autonomy will feed into popular “blame the victim” ideology. I believe... (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 9.1 (2002) 55-59 [Access article in PDF] One Stage Is Not Enough Andrew W. Young and Karel W. de Pauw Keywords: delusions, Cotard delusion, Capgras delusion, cognitive neuropsychiatry. WE WELCOME THE OPPORTUNITY to offer our reflections on Philip Gerrans' interesting paper. Our opinion is that on fundamental issues we agree quite a bit—but there are clear differences when it comes to details.The most (...) basic issue concerns the nature of the enterprise. Like Gerrans, we think that it is possible to create testable accounts of the formation and maintenance of what would otherwise seem bizarre and inexplicable delusions, and that these accounts should be grounded in theoretical models of factors that underpin our everyday perception and reasoning. This general approach certainly forms part of what has been called cognitive neuropsychiatry. However, we disagree with Gerrans in that we see cognitive neuropsychiatry as an attempt to draw on the underlying logic of cognitive neuropsychology, rather than (as Gerrans implies) its current methods. The underlying logic of cognitive neuropsychological approaches has been to try to understand the effects of brain injury in terms of disruption of different components of theoretical models of normal abilities. In this approach, a model of normal performance is tested by its ability to account for the effects of brain injury. Where the model of normal performance also provides a convincing account of brain injury it is retained, and when it fails to account for effects of brain injury, it is revised or abandoned. In cognitive neuropsychiatry, the key theoretical move has been to argue that an adequate model of normal performance should be able to account for any disordered pattern (Ellis and Young 1990). The same logic of seeking to explain disordered performance by reference to models of normal function is then attempted, but for disorders that would usually fall within the province of psychiatry.In our opinion, however, cognitive neuropsychiatry will not simply involve importing the methods of cognitive neuropsychology into the new domain; they will need to be developed and adapted to fit the new agenda (Young 2000).In cognitive neuropsychology, progress has often come from the careful investigation of people with stable, selective deficits of fundamental cognitive functions involved in sensory analysis, memory, and verbal or motor output. In contrast, delusional beliefs can be relatively unstable; often they are only held for a few weeks or even days. When the delusions change, patients may modify or abandon them as suddenly as they seemed to form them, or they may give them up much more slowly and reluctantly. At the very least, this creates difficulties in the timing of investigations and in interpreting the relation of deficits and symptoms, which may be recorded on separate dates. These methodological problems [End Page 55] are exacerbated by the fact that deficits linked to complex abnormal experiences such as delusions may be multifaceted and diffuse, even when the delusions themselves have a specific content or theme. Such complications do not invalidate cognitive neuropsychiatry, but they do mean it will need to develop its own methods for dealing with them and making appropriate inferences.One of the key complexities that has surfaced already involves the idea that delusional beliefs might reflect the interaction of two or more contributory factors. Gerrans discusses a particular variant of this idea, which had been suggested by Young and Leafhead (1996) as an approach to understanding the Cotard delusion: The Cotard delusion represents a depressed person's attempt to account for abnormal perceptual experiences. It follows that the delusion is based on an unfortunate interaction between different contributory factors. One set of factors creates the abnormal perceptual experiences, which are characterised by lack of emotional responses and feelings of emptiness, depersonalisation and derealisation. The other factors result in a misinterpretation of these perceptual changes, in which the patients' depressed moods lead them correctly to attribute the changes to themselves, but to exaggerate their consequences. (Young and Leafhead, 1996, 166) Gerrans describes this as a two-stage account, but argues that a one-stage account based only on abnormal perceptual... (shrink)

According to one theory, the brain is a sophisticated hypothesis tester: perception is Bayesian unconscious inference where the brain actively uses predictions to test, and then refine, models about what the causes of its sensory input might be. The brain’s task is simply continually to minimise prediction error. This theory, which is getting increasingly popular, holds great explanatory promise for a number of central areas of research at the intersection of philosophy and cognitive neuroscience. I show how the theory can (...) help us understand striking phenomena at three cognitive levels: vision, sensory integration, and belief. First, I illustrate central aspects of the theory by showing how it provides a nice explanation of why binocular rivalry occurs. Then I suggest how the theory may explain the role of the unified sense of self in rubber hand and full body illusions driven by visuotactile conflict. Finally, I show how it provides an approach to delusion formation that is consistent with one-deficit accounts of monothematic delusions. (shrink)

“Identity disorders” constitute a large class of psychiatric disturbances that, due to deviant forms of self-modeling, result in dramatic changes in the patients’ phenomenal experience of their own personal identity. The phenomenal experience of selfhood and transtemporal identity can vary along an extremely large number of dimensions: There are simple losses of content. There are also various typologies of phenomenal disintegration as in schizophrenia, in depersonalization disorders and in_ Dissociative Identity Disorder_, sometimes accompanied by multiplications of the phenomenal self within (...) one and the same physical system. It is important to not only analyze these state-classes in terms of functional deficits or phenomenology alone, but as _self-representational _content as well. For instance, in the second type of cases just mentioned, we confront major redistributions of the phenomenal property of "mineness” in representational space, of what is sometimes also called the “sense of ownership”. Finally, there are at least four different delusions of misidentification. Being a philosopher, I will discuss two particular types of identity disorder _ 2 _ in this contribution - disorders, which are of direct philosophical relevance: A specific form of DM, and the Cotard delusion. Why should philosophers do this? And why should psychiatrists care? (shrink)

The fateful combination of (i) the Dunning‐Kruger effect (ignorance of one's own ignorance) with (ii) the nonlinear dynamics of the echo‐chamber between reviewers and editors fuels a self‐reinforcing collective delusion system that sometimes spirals uncontrollably away from objectivity and truth. Escape from this subconscious meta‐ignorance is a formidable challenge but if achieved will help correct a central deficit of the peer‐review process that stifles innovation and paradigm shifts.

BackgroundParanoia is associated with a multitude of social cognitive deficits, observed in both clinical and subclinical populations. Empathy is significantly and broadly impaired in schizophrenia, yet its relationship with subclinical paranoia is poorly understood. Furthermore, deficits in emotion recognition – a very early component of empathic processing – are present in both clinical and subclinical paranoia. Deficits in emotion recognition may therefore underlie relationships between paranoia and empathic processing. The current investigation aims to add to the literature on social cognition (...) and paranoia by: characterizing the relationship between paranoia and empathy, and testing whether there is an indirect effect of emotion recognition on the relationship between empathy and paranoia.MethodsParanoia, empathy, and emotion recognition were assessed in a non-clinical sample of adults from the Nathan Kline Institute-Rockland dataset. Paranoia was measured using the Peters Delusions Inventory-21. Empathy was measured using the Interpersonal Reactivity Index, a self-report instrument designed to assess empathy using four subscales: Personal Distress, Empathic Concern, Perspective Taking, and Fantasy. Emotion recognition was assessed using the Penn Emotion Recognition Test. Structural equation modeling was used to estimate relationships between paranoia, the four measures of empathy and emotion recognition.ResultsParanoia was associated with the Fantasy subscale of the IRI, such that higher Fantasy was associated with more severe paranoia. No other empathy subscales were associated with paranoia. Fantasy was also associated with the emotion recognition of fear, such that higher Fantasy was correlated with better recognition of fear. Paranoia and emotion recognition were not significantly associated. The Empathic Concern subscale was negatively associated with emotion recognition, with higher empathic concern related to worse overall emotion recognition. All indirect paths through emotion recognition were non-significant.DiscussionThese results suggest that imaginative perspective-taking contributes to paranoia in the general population. These data do not, however, point to robust global relationships between empathy and paranoia or to emotion recognition as an underlying mechanism. Deficits in empathy and emotion recognition observed in schizophrenia may be associated with the broader pathology of schizophrenia, and therefore not detectable with subclinical populations. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Clinical CommentaryChong Siow Ann, Associate ProfessorDr. G appears to experiencing symptoms of schizophrenia, which is arguably the most severe mental disorder and which afflicts about one in a hundred people. This is a psychotic disorder that causes disturbances and distortions in thinking, including neurocognitive impairments, perception and behaviour. There is no cure for this often devastating disorder. Current antipsychotic medications can alleviate some of the symptoms but it often (...) comes at a price as these antipsychotics have burdensome side effects.A feature of this disorder is anosognosia, which is a lack of awareness or “insight” that an illness is present. This lack of insight presents a particular challenge because these individuals would, as in the case of Dr. G, refuse needed treatment as they do not perceive that they are ill. This is not necessarily an all-or-none phenomenon but is rather more complex and multidimensional; there might be an unawareness or recognition on behalf of the patient that they are suffering from a mental illness, the failure to appreciate the necessity of treatment; and/or the inability to recognise and define the psychotic symptoms like unusual thoughts and hallucinations as signs of illness1 and in many instances, all three are present. It is also by no means uncommon. Studies have found that between 60% and 80% of people with schizophrenia lack awareness of their illness to varying degrees.2This phenomenon remains an enigma. Some regard it as a form of psychological defence against the harsh reality of a psychotic illness — awareness of having a chronic and devastating illness might lead to demoralisation, hopelessness and suicide.3 Recent research, however, [End Page 250] indicates that this psychological denial plays a small part, if any, and instead has found an association with certain neuropsychological and neurocognitive deficits,4 as well as functional and structural brain abnormalities in the frontal lobe of the brain.5The prevailing clinical view thus is that this is an intrinsic and organic aspect of the schizophrenic illness which has nothing to do with wilfulness but rather the incapacity to perceive the presence of the illness. Edwin Fuller Torrey, an eminent psychiatrist and executive director of the Stanley Medical Research Foundation, calls anosognosia the “single largest reason why individuals with schizophrenia and bipolar disorder do not take their medications”, and he has remarked that “to keep talking about civil liberty is illogical. Patients are anything but free when they’re at the beck and call of their own delusions”.6It is also this view that it is a product of a brain disorder that some — particularly patients — find unacceptable. At one level, it does not take into context the person’s own experiences, and at a deeper level it calls into question the conception of the self with its capacity to exercise judgements and the autonomy to make decisions.This is a perennial ethical issue in psychiatry when people with severe mental illnesses refuse treatment. This becomes a Catch-22 situation where part of the illness that needs treatment is also preventing any treatment to be given: implicit in the principle of informed consent for treatment is that the person should be aware of the nature and course of their illness and acknowledge the need for treatment. While there are laws for involuntary commitment, the bar is usually high in that there must be a clear and present risk of harm to the person or others. Alan Stone, a professor of law and psychiatry at Harvard University proposed a possible justification for involuntary treatment based on his “thank-you theory” which assumes that patients will become well and subsequently agree that the intervention was in their best interests but research suggests that only half of these patients would admit so.7One suggested mechanism is the use of advance directives — psychiatry’s version of the living will in which people can specify what sort of medical care they would like should they become mentally unwell and unable to exercise appropriate judgement. An intrinsic part of this might include a “Ulysses contract” — just as Ulysess instructed his crew to lash him to the mast of the his ship so that he could... (shrink)

: Self-consciousness is considered in a framework comprising four dimensions which are theoretically defined and supported by clinical neuropsychological evidence. Self-monitoring is defined as the ability to reflect on one’s own behaviour, with supporting evidence for deficits in this capacity noted in anosognosia syndrome. Self-feeling is defined as the capacity to feel all sensations related to one’s own body, with supporting evidence from deficiencies occurring in alexithymia, psychosomatic states and Cotard’s delusion. Identity refers to the capacity to recognize an (...) object as identical to oneself, based on autobiographic memory; pathological conditions related to this dimension include delusions of identity and the Zelig syndrome. Ownership is the capacity to perceive the status of ones’ own body, and is clinically altered in somatoparaphrenia. All four dimensions are related to specific brain networks. Keywords: Self-Monitoring; Self-Feeling; Identity; Ownership; Neurocognitive Dimensions Le dimensioni neurocognitive dell’autocoscienza Riassunto: L’autocoscienza viene inquadrata in base a quattro dimensioni, determinate in via teorica e supportate da evidenze cliniche di carattere neuropsicologico. L’automonitoraggio è definito quale capacità di riflettere sul proprio comportamento ed è sostenuto da evidenze che derivano da quella sindrome denominata anosognosia. Il sentire il proprio sé è la capacità di avvertire tutte le sensazioni del corpo proprio ; questa dimensione è supportata da evidenze derivanti da condizioni cliniche quali l’alessitimia, le affezioni psicosomatiche e il delirio di Cotard. L’identità si riferisce alla capacità di riconoscere come identico a se stesso un oggetto, fondata sulla memoria autobiografica; le condizioni patologiche legate a questa dimensione sono il delirio di identità e la sindrome di Zelig. Il possesso di sé è la capacità di percepire lo stato del proprio corpo, condizione che risulta alterata nella somatoparafrenia. Tutte queste quattro dimensioni sono collegate a specifici network cerebrali. Parole chiave: Automonitoraggio; Sentimento di sé; Identità; Padronanza di sé; Dimensioni neurocognitive. (shrink)

Synofzik, Vosgerau, and Newen (2008) offer a powerful explanation of the sense of agency. To argue for their model they attempt to show that one of the standard models (the comparator model) fails to explain the sense of agency and that their model offers a more general account than is aimed at by the standard model. Here I offer comment on both parts of this argument. I offer an alternative reading of some of the data they use to argue against (...) the comparator model. I argue that contrary to Synofzik, Vosgerau and Newen’s reading the case of G.L. supports rather than contradicts the comparator model. Next I suggest how the comparator model can differentiate failures of action attribution in patients suffering parietal lobe lesions and delusions of alien control. I also argue that the apparently unexpected phenomenon of ‘‘hyperassociation” is predicted by the comparator model. Finally I suggest that as it stands Synofzik, Vosgerau and Newen’s model is not well specified enough to explain deficits in the sense of agency associated with delusions of thought insertion. Thus they have not met their second argumentative burden of showing how their model is more general than the comparator model. (shrink)

RESUMEN La psicopatologia contemporánea sufre de una brecha descriptiva respecto de la experiencia patológica, y la tradición de la psicopatologia contiene un capital descriptivo acumulado que debe ser explotado para la necesaria superación de este déficit. Se argumenta examinando el caso particular de la psicopatologia cognitiva de la esquizofrenia y del contenido de la experiencia del delirio de control, mostrando cómo la teoría de Henri Ey, así como la del automatismo mental del siglo xix en la cual tiene sus raíces, (...) contienen herramientas descriptivas importantes para establecer que la experiencia de un delirio de control es esencialmente diferente de la experiencia de una simple ilusión de control. ABSTRACT This article defends the general view that contemporary psychopathology suffers from a descriptive gap with respect to pathological experience and that the psycho-pathological tradition has accumulated a descriptive capital that should be used in the necessary effort to overcome this gap. This general thesis is argued for by examining the specific case of the cognitive psychopathology of schizophrenia and the experience of the delusion of control, showing how Henri Ey's theory and the 19th century theory of mental automatism in which the former is rooted contain important descriptive tools for establishing that the experience of a delusion of control is fundamentally different from that of a sheer illusion of control. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 9.1 (2002) 61-63 [Access article in PDF] Arguing from Neuroscience in Psychiatry James Phillips PHILIP GERRANS "A One-stage Explanation of the Cotard Delusion" provides an elegant example of the application of neuroscientific findings to known clinical phenomena in psychiatry. Gerrans argues that, in the cases of the Cotard and Capgras delusions, a one-stage explanation is sufficient to account for the clinical phenomena. That is, (...) the neuroanatomic defect and the consequent anomalous experience are sufficient to produce the delusion. According to Gerrans, we do not need to postulate that the delusion will emerge only if the anomalous experience is filtered through a faulty reasoning process (a two-stage explanation). Against the argument of Young and Leafhead (1996) that Cotard and Capgras delusions stem from the same neuroanatomic deficit and differentiate only in being processed differently—thus requiring a two-stage explanation—Gerrans argues that the respective neuroanatomic defects are in fact different, and that, therefore, the two delusional syndromes differ at the first stage and do not require the two-stage explanation suggested by Young and Leafhead.I do not have an opinion as to who is right in this disagreement, and I will devote these remarks to explaining why I do not have an opinion. In developing this explanation I will touch on what I find problematic in many discussions of neuroscience, neurocognitive models, and clinical psychiatry; I will thus use this article to highlight those problems.On the face of it, one would think that the issue raised by Gerrans should admit of a simple resolution. He argues that Capgras and Cotard delusions derive from different neural defects. Young and Leafhead, on the other hand, base their two-stage argument on the argument that the two delusions derive from the same neural defect. So which is it? Neuroscientists should be able to settle the issue and end the dispute. Gerrans remarks "that we need to look more closely at the CN [cognitive neuropsychiatric] explanation of the Capgras delusion." As he describes it, face recognition involves two components, a cognitive and an affective component, with separate neuroanatomic substrates. An individual successfully recognizes the face of a friend or acquaintance when she matches the cognitive recognition (cognitive component) with the affective tone of familiarity (second component). When there is a lesion in the neural substrate of the affective component, she may recognize the face but without the tone of familiarity. In her effort to understand her affective experience of the face as alien rather than as familiar, she may conclude that her friend has been replaced by a double. Thus we have the Capgras delusion.Let us now unpack this explanation. According to Gerrans, researchers have hypothesized [End Page 61] two anatomatically distinct pathways involved in face recognition. He writes: "Initially... these separate neuroanatomic substrates were hypothesized to lie in separate dorsal and ventral processing pathways, but the most persuasive hypothesis is that of Breen et al. that face recognition is performed in the ventral visual processing pathway, whereas covert [affective] recognition effects result from the activation of pathways connecting the ventral pathway and the limbic system. It is damage to these latter pathways that gives rise to the Capgras delusion."In other words, the explanation of Capgras delusions depends on a neurocognitive model, itself based on an unspecified base of neuroanatomic data. When Gerrans writes that "[t]he Capgras delusion arises in cases where, following a neurological accident, the pathways connecting the FRU [Face Recognition Unit] to the limbic system are damaged leaving ventral pathways and hence overt recognition unimpaired...," he means that the Capgras delusion arises in that manner if the proposed model bears any relation to the reality of the living brain and if real Capgras patients have suffered the hypothesized lesion. At this point the reader is struggling with the following questions: (1) What are the hard neuroanatomic data underpinning the neurocognitive model? (2) What is the argument for developing this model (single Face Recognition Unit with independent pathways to cognitive and affective components of face recognition) out of the hard data? (3) What is the evidence... (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 8.4 (2001) 295-298 [Access article in PDF] A Dialectical Conception of Autism Giovanni Stanghellini Some Reasons for the Philosophical Turn in the Psychopathology of Schizophrenia There are many ways to become a schizphrenic. Each individual has her own schizophrenia, coherent with her life history, her problems and alternatives deriving from them (Binswanger 1960). What clinical psychiatry calls "schizophrenia" is not a unitary illness but a (...) common final state—a "syndrome" in the etymological sense, that is, a condition to which different psychopathological pathways may lead. Schizophrenic symptoms, like Schneiderian first-rank symptoms (delusions, hallucinations, experiences of passivity), are nothing but a rather uniform type of reaction. First-rank Schneiderian symptoms may be interpreted as attempts to explain disturbing basic experiences of change in self, body, and world perception (Klosterkoetter 1988) or as the epiphenomena of complex interactions between sensory disorders (aberrations in the perception of self, body, and world), conceptualisation disorders (impairments in the constitution of meanings and intentions), and attitudinal disorders (eccentric structure of values and beliefs) (Stanghellini 2000a). Since the schizophrenic syndrome, as defined by current diagnostic manuals, lacks any authentic core phenomena, and so-called schizophrenic symptoms are not specific (Berner and Kufferle 1982), the clinical diagnosis of schizophrenia finally becomes a diagnosis by exclusion (Maj 1998). This conceptual weakness is obviously unacceptable (not only for old dissenters from operational diagnostic criteria) and is kindling a velvet revolution in nosological studies and a renaissance of philosophically oriented psychopathological research (Parnas and Zahavi 2000). Autism: The Loss of Vital Contact with Reality Eugène Minkowski was a forerunner in the field of philosophical psychopathology: "The psychiatrist and the metaphysician become one in their common research concerning what is human and human experience" (Minkowski 1947). Indeed, his doctoral thesis on autism (Minkowski 1926) was dedicated to his teachers, the psychiatrist E. Bleuler and the philosopher H. Bergson, and his conceptualisation of autism is an ideal example of the link between philosophical perspectives and psychopathological research. The term "autism" was introduced by Bleuler (1911) to describe detachment from outer reality and immersion in inner life. Bleuler's concept of autism relied on Freud's (1905) notion of autoerotism and on associationistic psychology. According to Bleuler, autism was a consequence of the [End Page 295] splitting of psychic functions: a defense mechanism serving to avoid conflicts between desires and reality testing, promoting the shift to inner fantasy life and entailing social withdrawal, emotional indifference, inappropriate behaviors, and idiosyncratic values and beliefs.Minkowski, who was influenced by Bergson and phenomenology, departed from Bleuler's conceptualisation and defined autism as "loss of vital contact with reality" (Minkowski 1926, 1927). For Minkowski, autism is not a symptom, but a global phenomenon investing the whole person. Autism is a way of being whose essential feature is a pragmatic deficit: Autistic activity consists in the reduced capacity to interact with the external world. Autistic thought is characterized by its lack of communicative action. The pragmatic deviance of autistic language is a good example: The autistic person is not interested in communicating her inner world to the others; language is not a means of communication which serves mutual understanding, a cooperative process whose aim is interlacing one's own world with that of others. The autistic person's use of language is much like a soliloquy, the monologue of the solitary thinker more focused on ex-pression—the outward portrayal of immanent contents of consciousness—than on dialogue—the exchange of meanings between speaker and listener. Moreover, each meaning is presented in its manifold profiles or adumbrations and the task of selecting the context-relevant meaning is left to the listener.The pragmatic weakening of the autistic person, according to Minkowski, is not simply a social or occupational dysfunction (APA 1994), that is, a renunciation or refusal to act according to social expectations and standards. It involves the loss of vital contact with reality. The meaning Minkowski attributes to the term "vital" is essential for understanding his philosophical approach to defining the schizophrenic condition. Minkowski assumes that contact with reality is vital when it is established through action (and language... (shrink)

A recent study showed that 78% of global climate science funding flows to European and North American institutions. Dr. Quan-Hoang Vuong gives his perspective on why this is a problem for the planet.

Delusions are a common symptom of schizophrenia and dementia. Though most English dictionaries define a delusion as a false opinion or belief, there is currently a lively debate about whether delusions are really beliefs and indeed, whether they are even irrational. The book is an interdisciplinary exploration of the nature of delusions. It brings together the psychological literature on the aetiology and the behavioural manifestations of delusions, and the philosophical literature on belief ascription and rationality. The thesis of the (...) book is that delusions are continuous with ordinary beliefs, a thesis that could have important theoretical and practical implications for psychiatric classification and the clinical treatment of subjects with delusions. By bringing together recent work in philosophy of mind, cognitive psychology and psychiatry, the book offers a comprehensive review of the philosophical issues raised by the psychology of normal and abnormal cognition, defends the doxastic conception of delusions, and develops a theory about the role of judgements of rationality and of attributions of self-knowledge in belief ascription. Presenting a highly original analysis of the debate on the nature of delusions, this book will interest philosophers of mind, epistemologists, philosophers of science, cognitive scientists, psychiatrists, and mental health professionals. (shrink)

In chapter 3 of Delusions and Beliefs, Kengo Miyazono argues that, when delusions are pathological beliefs, they are so due to their being both harmful and malfunctional. In this brief commentary, I put pressure on Miyazono’s account of delusions as harmful malfunctioning beliefs. No delusions might satisfy the malfunction criterion and some delusions might fail to satisfy the harmfulness criterion when such conditions are interpreted as criteria for pathological beliefs. In the end, I raise a general concern about attributing pathological (...) status to single beliefs out of context, and gesture towards the idea of pathology as a failure of agency to which some beliefs can contribute but that can only be identified by considering the person as a whole. (shrink)

Psychopathological delusions have a number of features that are curiously difficult to explain. Delusions are resistant to counterevidence and impervious to counterargument. Delusions are theoretically, affectively, and behaviorally circumscribed: delusional individuals often do not act on their delusions and often do not update beliefs on the basis of their delusions. Delusional individuals are occasionally able to distinguish their delusions from other beliefs, sometimes speaking of their “delusional reality.” To explain these features, I offer a model according to which, contrary to (...) appearances, delusions are not beliefs at all. Delusions are acceptances that are generated by pathologically powerful cognitive feelings. This model has implications for the way that we should think about non-pathological doxastic states and emotions. (shrink)

In this paper, I examine a kind of delusion in which the patients judge that their occurrent thoughts are false and try to abandon them precisely because they are false, but fail to do so. I call this delusion transparent, since it is transparent to the sufferer that their thought is false. In explaining this phenomenon, I defend a particular two-factor theory of delusion that takes the proper integration of relevant reasoning processes as vital for thought-evaluation. On (...) this proposal, which is a refinement of Gerrans’s account of delusion as unsupervised by decontextualized processing, I can have all my reasoning processes working reliably and thus judge that my delusion is false but, if I cannot use their outputs when revising the thought itself, the delusion will persist. I also sketch how this framework explains some interesting cases of failed belief-revision in the general population in which people judge that ~p but nonetheless continue to believe that p. (shrink)

In this paper we ask whether the two-factor theory of delusions is compatible with two claims, that delusions are pathological and that delusions are adaptive. We concentrate on two recent and influential models of the two-factor theory: the one proposed by Max Coltheart, Peter Menzies and John Sutton (2010) and the one developed by Ryan McKay (2012). The models converge on the nature of Factor 1 but diverge about the nature of Factor 2. The differences between the two models are (...) reflected in different accounts of the pathological and adaptive nature of delusions. We will explore such differences, considering naturalist and normativist accounts of the pathological and focusing on judgements of adaptiveness that are informed by the shear-pin hypothesis (McKay and Dennett 2009). After reaching our conclusions about the two models, we draw more general implications for the status of delusions within two-factor theories. Are there good grounds to claim that delusions are pathological? Are delusions ever adaptive? Can delusions be at the same time pathological and adaptive? (shrink)

Delusions are standardly defined as attitudes that are not amenable to change in light of conflicting evidence. But what evidence do people with delusion have for and against it? Do delusions really go against their total evidence? How are the answers affected by different conceptions of evidence? -/- This chapter focuses on how delusions relate to evidence. I consider what delusions-relevant evidence people with delusions have. I give some reasons to think that people typically have evidence for their delusions, (...) and that the evidence they have against them is often overstated. I draw on this discussion to consider whether delusions are evidentially supported and epistemically rational. Finally, I discuss implications for the nature of delusion, responsibility, and treatment and suggest directions for future research. Throughout, the discussion is sensitive to different conceptions of evidence and rationality in epistemology. -/- A central upshot is that what we should say about the epistemic standing of delusions depends substantively on our positions in epistemology, in particular, on the debate between internalists and externalists about evidence. If we want clarity on the epistemic standing of delusions, we need to incorporate more sophisticated tools from epistemology. (shrink)

Bortolotti’s Delusions and Other Irrational Beliefs defends the view that delusions are beliefs on a continuum with other beliefs. A different view is that delusions are more like illusions, that is, they arise from faulty perception. This view, which is not targeted by the book, makes it easier to explain why delusions are so alien and disabling but needs to appeal to forensic aspects of functioning.

I argue that some cases of delusions show the inadequacy of those theories of interpretation that rely on a necessary rationality constraint on belief ascription. In particular I challenge the view that irrational beliefs can be ascribed only against a general background of rationality. Subjects affected by delusions seem to be genuine believers and their behaviour can be successfully explained in intentional terms, but they do not meet those criteria that according to Davidson need to be met for the background (...) of rationality to be in place. (shrink)

Empiricist models explain delusional beliefs by identifying the abnormal experiences which ground them. Recently, this strategy has been adopted to explain the false body size beliefs of anorexia nervosa patients. As such, a number of abnormal experiences of body size which patients suffer from have been identified. These oversized experiences convey false information regarding the patients’ own bodies, indicating that they are larger than reality. However, in addition to these oversized experiences, patients are also exposed to significant evidence suggesting their (...) bodies are in fact thin. This situation poses a conundrum: why do patients appear strongly influenced by the former kinds of evidence while the latter has little effect? To solve this conundrum, I suggest a two-factor account. First, I discuss research on the biases patients exhibit in how they gather, attend to and interpret evidence related to their own body size. Such biases in evidence treatment, I suggest, cause oversized experiences to be sought out, attended to and accepted, while veridical body size experiences are ignored or explained away. These biases constitute the second factor for this empiricist model, accounting for the unwarranted conviction with which these beliefs are held. Finally, in line with recent research into self-deception, I propose that, paradoxically, these biases in evidence treatment arise from patients’ own desires. (shrink)