1 Introduction

In Le Délire de Négation (1897), Jules Séglas considers depersonalization to be an essential step in the development of the Cotard delusion[1] (CD; as cited in Debruyne 2009; Gerrans 2002), and prima facie the two states share a number of characteristics: Patients suffering from the former feel as if they are dead or do not exist, whereas those who suffer from the latter sincerely believe and experience this state. However, the central characteristics of these disorders are distinct. Patients describe the experience of depersonalization as follows:

It's really weird. It's sort of like I'm here, but I'm really not here and that I kind of stepped out of myself, like a ghost... I feel really light, you know. I feel kind of empty and light, like I'm going to float away... Sometimes I really look at myself that way... It's kind of a cold eerie feeling. I'm just totally numbed by it. (Cited in Steinberg 1995)

The emotional part of my brain is dead. My feelings are peculiar, I feel dead. Whereas things worried me nothing does now. My husband is there but he is part of the furniture. I don't feel I can worry. All my emotions are blunted. (Shorvon 1946, p. 783)

As illustrated in these subjective descriptions, depersonalization is characterized by a loss of the sense of presence (Critchley 2005) or an increased “sense of detachment”—the “[e]xperience of unreality, detachment, or being an outside observer with respect to one's thoughts, feelings, sensations, body, or actions” (American Psychiatric Association 2013, p. 302). On the other hand, in the Cotard delusion (CD), mental autobiographies are acutely distorted—in such a way that patients are convinced that they are dead or that they do not exist:

An 88-year-old man with mild cognitive impairment was admitted to our hospital for treatment of a severe depressive episode. He was convinced that he was dead and felt very anxious because he was not yet buried. This delusion caused extreme suffering and made outpatient treatment impossible. (Debruyne et al. 2009, p. 197)

Researchers in the field of delusion studies have debated the way in which anomalous experience leads to false belief. In this commentary I am interested in the following questions: What cognitive architecture could, in principle, explain CD in terms of its development from depersonalization, and what exactly are the underlying differences between patients suffering from the Cotard delusion and those suffering from depersonalization disorder (DPD) but free from the Cotard delusion?

In his target paper, Gerrans explores the cognitive structure of self-awareness—the “awareness of being a unified persisting entity” (this collection, p. 2). To explain the emergence of self-awareness and its loss in DPD and CD, he provides an account that integrates the appraisal theory of emotion, the simulation model of memory and prospection, and the hierarchical predictive coding model. First, based on the appraisal theory, Gerrans shows that the activation of the anterior insular cortex (AIC) allows an organism to experience the emotional significance of a relevant state by experiencing appraisal. According to Gerrans, these reflexive processes are what sustain the self from moment to moment: “An organism that can use that affective information in the process is a self” (this collection, p. 8). Second, the integration of affective processing and simulated episodes allows the organism to experience itself as a persisting entity overtime (see more below). Last, he endorses the predictive coding framework, according to which the human mind can be accounted for by the principle of predictive error minimization. Perception, for instance, is realized by the operation of both top-down prediction and bottom-up predictive error. If the general theoretical model is correct, it will not only apply to perception, but also to affective processing (ibid., p. 9). Gerrans (this collection) applies this framework to explain the phenomenon of depersonalization and CD: Depersonalization occurs due to a failure to attribute emotional relevance to bodily states, which results from hypoactivity of the AIC. The prediction error from the mismatch between the predicted and the actual activation level of the AIC would lead to allocation of attention, the function of which, according to the predictive coding framework, is to disambiguate signals. If the prediction error cannot be cancelled and attention cannot be diverted, increased attention brings about anxiety in DPD and CD, which is “an adaptive mechanism that primes the organism cognitively and physiologically to solve uncertainty” (ibid., p. 11). This is reflected in the patients’ subjective reports concerning the loss of awareness of their bodies. This integrated theory provides an explanation of depersonalization as well as of how self-awareness is constructed through the interaction of different forms of cognitive processing.

In Gerrans’ account, the simulation system allows the organism “to simulate temporally distant experiences by rehearsing some of the same perceptual and emotional mechanisms activated by the simulated situation” (ibid., p. 6), such that the affective associations result in integrated episodes of experience that lead to the feeling of persisting over time. I argue (1) that the simulation model should not be thought of as independent from other memory systems: without memory systems at lower levels—semantic and procedural memory systems—the simulated episodes cannot be constructed (section 2); and (2), that by considering the role of memory under the predictive coding framework, the simulation model not only plays a role in simulating temporally-distant episodes but also contributes to the knowledge required for the creation of predictive models in the present (section 3). On such a view of the simulation model, delusion can be explained and I will suggest (3) two factors contributing to the development of CD from depersonalization: the compromised decontextualized supervision system and the expectation of high precision from interoceptive signals (section 4); that is, only if these two factors are present in a depersonalized subject may CD develop.