Abstract
This paper contrasts an interactionist account of delusional misidentification with more traditional one- and two-stage models. Unlike the unidirectional nature of these more traditional models, in which the aetiology of the disorder is said to “progress” from a neurological disruption via an anomalous experience to a delusional belief, the interactionist account posits the interaction of top-down and bottom-up processes to better explain the maintenance of the delusional belief. In addition, it places a greater emphasis on the patient’s underlying phenomenal experience in accounting for the specificity of the delusional content. The role played by patient phenomenology is examined in light of Ratcliffe’s recent phenomenological account. Similarities and differences are discussed. The paper concludes that a purely phenomenological account is unable to differentiate between non-delusional patient groups, who have what appear to be equivalent phenomenal experiences to patients suffering from delusional misidentification but without the delusional belief, and delusional groups, something the interactionist model is able to do.
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Notes
I acknowledge that, with regard to the DSM-IVR classification, the Cotard delusion is not classified as a form of delusional misidentification; nevertheless, I include it under the umbrella term used here for two reasons. First, it is often discussed in relation to other disorders that are classified as forms of delusional misidentification (such as the Capgras and Frégoli delusions): discussion often centring on the varying degrees of similarity the Cotard delusion shares with these other disorders in terms of aetiology, phenomenology and applicability of explanatory models (see Devinsky 2009; Ellis et al. 1994; Marková and Berrios 1994; Weinstein 1994; Young et al. 1994). Second, and more importantly, it is my contention that misplaced being is a form of misidentification that results from a conflict in recognition. When misplaced being occurs in conjunction with delusional beliefs, then the patient undergoes a form of delusional misidentification (of self, in the case of the Cotard delusion), irrespective of any lack of established clinical classification to that effect.
Cognitive models of delusional misidentification are typically concerned with the nature of the cognitive deficit/bias that produces the delusional belief. Such models have little to say about disruption that occurs at the neurological level; consequently, this disruption is not a feature of the model itself but, rather, is presumed to occur (I thank the anonymous reviewer for drawing my attention to this point). Nevertheless, even if not a feature of the model itself, some form of neurological disturbance must be acknowledged implicitly by the aforementioned presumption, leaving the original elements (1–3) valid.
The problem of specificity would also have to be overcome if conjecturing that the delusional belief is the result of a disruption in subpersonal processes that cause directly the delusional belief, thereby by-passing the need for any anomalous experience (I thank the anonymous reviewer for this suggestion). It is not clear how the specificity of the delusional content can stem from a disruption in one’s subpersonal processing, however. What specific area of the brain could be damaged, or what level of neurochemical imbalance could produce subpersonal processing anomalies that target one’s wife or loved ones, specifically, to the effect that they are believed to be impostors (for example)? Surely, this would be on par with positing that damage to Broca’s areas (or somewhere similar) could lead to one not being able to use language effectively when directed towards one’s family but which, nevertheless functioned perfectly well on all other occasions
Although this is a testable hypothesis, to the best of my knowledge, no studies have been carried out to measure the SCR of Frégoli patients.
Young (1999) notes that there have been reports of Capgras patients who claim to perceive differences in the impostor. However, when pressed on what exactly these differences are, they have difficulty pointing them out.
This would help explain why some Cotard patients claim not to be dead but to be immortal or to have been resurrected. These claims are also compatible with a state of being one has never encountered before and is therefore unfamiliar with (Young, under review).
Here, absence of physical recognition should not be understood as necessarily meaning failure of physical recognition. When in the presence of strangers, one would not expect to physically recognise them, and in fact, one may even recognise that they are physically unfamiliar.
Adapted from Young (2010).
The word “tartling”, we are told by Cleary and Specker, has its roots in the Scottish language.
JR presented with damage to the left hemisphere (the lateral temporo-occipital junction).
However, Rapcsak et al. (1999) did report that their patient might claim not to have available further information about the (misrecognised) individual, or extrapolate further and compound the mistake.
Staton et al. (1982) in a not too dissimilar way implicate disruption in the memory process—between stored representations and new perceptions—in their explanation of delusional misidentification.
Estrangement is defined by the Oxford pocket dictionary as a turning away, in terms of feeling or affection, of one person from another (a definition compatible with a loss of appropriate emotional orienting evident in the Capgras patient, I suggest).
Based on Bayes’ theorem: Incoming information is interpreted in light of prior expectation (taken from Corlett et al. 2009, p. 516).
Or it may be extended to incorporate other delusional states—see Startup et al. (2009) for a discussion on delusions of reference.
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Young, G. Beliefs, experiences and misplaced being: an interactionist account of delusional misidentification. Phenom Cogn Sci 10, 195–215 (2011). https://doi.org/10.1007/s11097-010-9168-9
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DOI: https://doi.org/10.1007/s11097-010-9168-9