Gut Reactions is an interdisciplinary defense of the claim that emotions are perceptions of changes in the body.

In 1910, Karl Jaspers wrote a seminal essay on morbid jealousy in which he laid the foundation for the psychopathological phenomenology that through his work and the work of Hans Gruhle and Kurt Schneider, among others, would become the ...

Delusions are defined as irrational beliefs that compromise good functioning. However, in the empirical literature, delusions have been found to have some psychological benefits. One proposal is that some delusions defuse negative emotions and protect one from low self-esteem by allowing motivational influences on belief formation. In this paper I focus on delusions that have been construed as playing a defensive function (motivated delusions) and argue that some of their psychological benefits can convert into epistemic ones. Notwithstanding their epistemic costs, (...) motivated delusions also have potential epistemic benefits for agents who have faced adversities, undergone physical or psychological trauma, or are subject to negative emotions and low self-esteem. To account for the epistemic status of motivated delusions, costly and beneficial at the same time, I introduce the notion of epistemic innocence. A delusion is epistemically innocent when adopting it delivers a significant epistemic benefit, and the benefit could not be attained if the delusion were not adopted. The analysis leads to a novel account of the status of delusions by inviting a reflection on the relationship between psychological and epistemic benefits. (shrink)

Article copyright 2002. We provide a battery of examples of delusions against which theoretical accounts can be tested. Then we identify neuropsychological anomalies that could produce the unusual experiences that may lead, in turn, to the delusions in our battery. However, we argue against Maher's view that delusions are false beliefs that arise as normal responses to anomalous experiences. We propose, instead, that a second factor is required to account for the transition from unusual experience to delusional belief. The second (...) factor in the etiology of delusions can be described superficially as a loss of the ability to reject a candidate for belief on the grounds of its implausibility and its inconsistency with everything else that the patient knows, but we point out some problems that confront any attempt to say more about the nature of this second factor. (shrink)

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

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)

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)

Subjects with delusions profess to believe some extremely peculiar things. Patients with Capgras delusion sincerely assert that, for example, their spouses have been replaced by impostors. Patients with Cotard’s delusion sincerely assert that they are dead. Many philosophers and psychologists are hesitant to say that delusional subjects genuinely believe the contents of their delusions.2 One way to reinterpret delusional subjects is to say that we’ve misidentified the content of the problematic belief. So for example, rather than believing that his wife (...) is has been replaced by an impostor, we might say that the victim of Capgras delusion believes that it is, in some respects, as if his wife has been replaced by an impostor. Another is to say that we’ve misidentified the attitude that the delusional subject bears to the content of their delusion. So for example, Gregory Currie and co-authors have suggested that rather than believing that his wife has been replaced by an impostor, we should say that the victim of Capgras delusion merely imagines that his wife has been replaced by an impostor.3. (shrink)

In this book, psychologists and philosophers describe and discuss a range of case studies of delusional beliefs, drawing out general lessons both for the cognitive architecture of the mind and for the notion of rationality, and exploring connections between the delusional beliefs that occur in schizophrenia and the flawed understanding of beliefs that is characteristic of autism.

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)

Does the formation of delusions involve abnormal reasoning? According to the prominent ‘two-factor’ theory of delusions (e.g. Coltheart, 2007), the answer is yes. The second factor in this theory is supposed to affect a deluded individual's ability to evaluate candidates for belief. However, most published accounts of the two-factor theory have not said much about the nature of this second factor. In an effort to remedy this shortcoming, Coltheart, Menzies and Sutton (2010) recently put forward a Bayesian account of inference (...) in delusions. I outline some criticisms of this important account, and sketch an alternative account of delusional inference that, I argue, avoids these criticisms. Specifically, I argue that the second factor in delusion formation involves a systematic deviation from Bayesian updating, a deviation that may be characterized as a bias towards ‘explanatory adequacy’. I present a numerical model of this idea and show that my alternative account is broadly consistent with prominent prediction error models of delusion formation (e.g. Corlett, Murray et al., 2007). (shrink)

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)

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)

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)

"Unsere Literatur ist voll von Klagen über den chaotischen Zustand der Systematik der Psychosen, und jeder Psychiater weiß, daß man sich auf Grund der alten Diagnosen gar nicht genügend verständigen kann. (...) So können sich mit den alten Begriffen nicht einmal die Koryphäen der Wissenschaft verständigen, und viele Patienten tragen genau so viele Diagnosen mit sich herum, als sie Anstalten besucht haben. (...) Irrtümer hindern die Wissenschaft am meisten am Fortschreiten; sie zu beseitigen hat mehr praktischen Wert, als eine neue (...) Erkenntnis zu gewinnen. Und hier ist ein ganzes Chaos von Namen beseitigt worden, hinter denen man fälschlicherweise brauchbare Krankheitsbegriffe suchte, und ein Wald von Grenzpfählen, von denen keiner an einer natürlichen Grenze stand. (...) Mit dem Namen der Dementia praecox oder der Schizophrenie bezeichnen wir eine Psychosengruppe, die bald chronisch, bald in Schüben verläuft, in jedem Stadium Halt machen oder zurückgehen kann, aber wohl keine volle Restitutio ad integrum erlaubt. Sie wird charakterisiert durch eine spezifisch geartete, sonst nirgends vorkommende Alteration des Denkens und Fühlens und der Beziehungen zur Außenwelt.". (shrink)

Here I summarise the main arguments in Delusions and Other Irrational Beliefs [1]. The book addresses the question whether there is a rationality constraint on belief ascription and defends a doxastic account of clinical delusions.

Objective: The clinical hallmark of schizophrenia is psychosis. The objective of this overview is to link the neurobiology (brain), the phenomenological experience (mind), and pharmacological aspects of psychosis-in-schizophrenia into a unitary framework. -/- Method: Current ideas regarding the neurobiology and phenomenology of psychosis and schizophrenia, the role of dopamine, and the mechanism of action of antipsychotic medication were integrated to develop this framework. -/- Results: A central role of dopamine is to mediate the "salience" of environmental events and internal representations. (...) It is proposed that a dysregulated, hyperdopaminergic state, at a "brain" level of description and analysis, leads to an aberrant assignment of salience to the elements of one's experience, at a "mind" level. Delusions are a cognitive effort by the patient to make sense of these aberrantly salient experiences, whereas hallucinations reflect a direct experience of the aberrant salience of internal representations. Antipsychotics "dampen the salience" of these abnormal experiences and by doing so permit the resolution of symptoms. The antipsychotics do not erase the symptoms but provide the platform for a process of psychological resolution. However, if antipsychotic treatment is stopped, the dysregulated neurochemistry returns, the dormant ideas and experiences become reinvested with aberrant salience, and a relapse occurs. -/- Conclusions: The article provides a heuristic framework for linking the psychological and biological in psychosis. Predictions of this hypothesis, particularly regarding the possibility of synergy between psychological and pharmacological therapies, are presented. The author describes how the hypothesis is complementary to other ideas about psychosis and also discusses its limitations. (shrink)