From an evolutionary standpoint, a default presumption is that true beliefs are adaptive and misbeliefs maladaptive. But if humans are biologically engineered to appraise the world accurately and to form true beliefs, how are we to explain the routine exceptions to this rule? How can we account for mistaken beliefs, bizarre delusions, and instances of self-deception? We explore this question in some detail. We begin by articulating a distinction between two general types of misbelief: those resulting from a breakdown in (...) the normal functioning of the belief formation system (e.g., delusions) and those arising in the normal course of that system's operations (e.g., beliefs based on incomplete or inaccurate information). The former are instances of biological dysfunction or pathology, reflecting “culpable” limitations of evolutionary design. Although the latter category includes undesirable (but tolerable) by-products of “forgivably” limited design, our quarry is a contentious subclass of this category: misbeliefs best conceived as design features. Such misbeliefs, unlike occasional lucky falsehoods, would have been systematically adaptive in the evolutionary past. Such misbeliefs, furthermore, would not be reducible to judicious – but doxastically1noncommittal – action policies. Finally, such misbeliefs would have been adaptive in themselves, constituting more than mere by-products of adaptively biased misbelief-producing systems. We explore a range of potential candidates for evolved misbelief, and conclude that, of those surveyed, onlypositive illusionsmeet our criteria. (shrink)

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

In this paper I explore the nature of confabulatory explanations of action guided by implicit bias. I claim that such explanations can have significant epistemic benefits in spite of their obvious epistemic costs, and that such benefits are not otherwise obtainable by the subject at the time at which the explanation is offered. I start by outlining the kinds of cases I have in mind, before characterising the phenomenon of confabulation by focusing on a few common features. Then I introduce (...) the notion of epistemic innocence to capture the epistemic status of those cognitions which have both obvious epistemic faults and some significant epistemic benefit. A cognition is epistemically innocent if it delivers some epistemic benefit to the subject which would not be attainable otherwise because alternative (less epistemically faulty) cognitions that could deliver the same benefit are unavailable to the subject at that time. I ask whether confabulatory explanations of actions guided by implicit bias have epistemic benefits and whether there are genuine alternatives to forming a confabulatory explanation in the circumstances in which subjects confabulate. On the basis of my analysis of confabulatory explanations of actions guided by implicit bias, I argue that such explanations have the potential for epistemic innocence. I conclude that epistemic evaluation of confabulatory explanations of action guided by implicit bias ought to tell a richer story, one which takes into account the context in which the explanation occurs. (shrink)

Patients with right parietal lesions often deny their paralysis , but do they have "tacit" knowledge of their paralysis? I devised three novel tests to explore this. First, the patients were given a choice between a bimanual task vs a unimanual one . They chose the former on 17 of 18 trials and, surprisingly, showed no frustration or learning despite repeated failed attempts. I conclude that they have no tacit knowledge of paralysis . Second, I used a "virtual reality box" (...) to convey the optical illusion to the patient that she was moving her paralyzed left hand up and down to the rhythm of a metronome, and yet she showed no sign of surprise. Third, I irrigated patient BM′s left ear canal with cold water, a procedure that is known to shift that patient′s spatial frame of reference by stimulating the vestibular system. Surprisingly, this allowed her "repressed" memory of paralysis to come to the surface; she said she had been paralyzed continuously for several days. I suggest that the vestibular stimulation produces these remarkable effects by mimicking REM sleep. These patients also emply a whole arsenal of grossly exaggerated Freudian "defense mechanisms" to account for their paralysis. To explain this, I propose that in normal individuals the left hemisphere ordinarily deals with small, local anomalies by trying to impose consistency but, when the anomaly exceeds threshold, an interaction with the right hemisphere forces a "paradigm shift". A failure of this process, in patients with right hemisphere damage, might partially account for anosognosia. Finally, I present a new conceptual framework that may help link several psychological and neurological phenomena such as Freudian defense mechanisms, vestibular stimulation, anosognosia, memory repression, visual illusions, anterograde amnesia, REM sleep, dreaming, and humor. (shrink)

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 ...

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)

Theories of self-deception divide into those that hold that the state is characterized by some kind of synchronic tension or conflict between propositional attitudes and those that deny this. Proponents of the latter like Al Mele claim that their theories are more parsimonious, because they do not require us to postulate any psychological mechanisms beyond those which have been independently verified. But if we can show that there are real cases of motivated believing which are characterized by conflicting propositional attitudes, (...) however, the parsimony argument against incongruent mental state accounts is undermined. I argue that anosognosia presents us with a real-life example of motivated belief together with (sub)-doxastic conflict. (shrink)