Users of psychedelic drugs often report that their sense of being a self or ‘I’ distinct from the rest of the world has diminished or altogether dissolved. Neuroscientific study of such ‘ego dissolution’ experiences offers a window onto the nature of self-awareness. We argue that ego dissolution is best explained by an account that explains self-awareness as resulting from the integrated functioning of hierarchical predictive models which posit the existence of a stable and unchanging entity to which representations are bound. Combining recent work on the ‘integrative self' and the phenomenon of self-binding with predictive processing principles yields an explanation of ego dissolution according to which self-representation is a useful Cartesian fiction: an ultimately false representation of a simple and enduring substance to which attributes are bound which serves to integrate and unify cognitive processing across levels and domains. The self-model is not a mere narrative posit, as some have suggested; it has a more robust and ubiquitous cognitive function than that. But this does not mean, as others have claimed, that the self-model has the right attributes to qualify as a self. It performs some of the right kinds of functions, but it is not the right kind of entity. Ego dissolution experiences reveal that the self-model plays an important binding function in cognitive processing, but the self does not exist.

Twenty years ago, Baron-Cohen and colleagues argued that autistic performance on false belief tests was explained by a deficit in metarepresentation. Subsequent research moved from the view that the mind has a domain-general capacity for metarepresentation to the view that the mind has a domain-specific mechanism for metarepresentation of mental states per se, i.e., the theory of mind mechanism (ToMM). We argue that 20 years of data collection in lesion patients and children with autism supports a more parsimonious view closer to that of the 1985 paper. Lower-level domain-specific mechanisms--e.g., tracking gaze, joint attention--interacting with higher-level domain-general mechanisms for metarepresentation, recursion, and executive function can account for observed patterns of deficits in both autism and neurological patients. The performance of children with autism or orbitofrontal patients on ToM tests can be explained more parsimoniously by their deficits in lower-level domain-specific mechanisms for processing social information. Without proper inputs, the intact capacity for metarepresentation by itself cannot make correct ToM inferences. Children with autism have no impairment in false photograph tests because their metarepresentational capacity is intact and they have no impairment in inputs required for such tests. TPJ patients have equivalent deficits on ToM and non-ToM metarepresentational tasks, consistent with a failure in domain-general processing. If deficits on ToM tasks can result from deficits in low-level input systems or in higher-level domain-general capacities, postulating a separate ToM mechanism may have been an unnecessary theoretical move.

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Cognitive neuropsychiatry (CN) is the explanation of psychiatric disorder by the methods of cognitive neuropsychology. Within CN there are, broadly speaking, two approaches to delusion. The first uses a one-stage model, in which delusions are explained as rationalizations of anomalous experiences via reasoning strategies that are not, in themselves, abnormal. Two-stage models invoke additional hypotheses about abnormalities of reasoning. In this paper, I examine what appears to be a very strong argument, developed within CN, in favor of a two-stage explanation of the difference in content between the Capgras and Cotard delusions. That explanation treats them as alternative rationalizations of essentially the same phenomenology. I show, however, that once we distinguish the phenomenology (and the neuroetiology), a one-stage model is adequate. In the final section I make some more general remarks on the one- and two-stage models.