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Young and colleagues (e.g. Young, A. W., & Leafhead, K. M. (1996). Betwixt life and death: case studies of the Cotard delusion. In P. W. Halligan & J. C. Marshall (Eds.), Method in madness: Case studies in cognitive neuropsychiatry. Mahway, NJ: Lawrence Erlbaum Associates.) have suggested that cases of the Cotard delusion (the belief that one is dead) result when a particular perceptual anomaly (caused by a disruption to the affective component of visual recognition) occurs in the context of an internalising attributional style. This hypothesis has not previously been tested directly. We report here an investigation of attributional style in a 24-year-old woman with Cotard delusion (“LU”). LU’s attributional style (and that of ten healthy control participants) was assessed using the Internal, Personal and Situational Attributions Questionnaire (Kinderman, P., & Bentall, R. P. (1996). A new measure of causal locus: the internal, personal and situational attributions questionnaire. Personality and Individual Differences, 20(2), 261–264.). LU showed a significantly greater proportion of internalising attributions than the control group, both overall and for negative events specifically. The results obtained thus support an association of Cotard delusion with an internalising attributional style, and are therefore consistent with the account of Young and colleagues. The potential brain basis of Cotard delusion is discussed.

Few pathologies of the self are as profound and striking as those reported in cases of Cotard syndrome, which can involve the belief that one is dead. The assertions of some patients with this delusion come close to violating the famous Cartesian dictum cogito ergo sum. Descartes explored the limits of radical scepticism and concluded that whereas one could certainly doubt the evidence of one’s senses, it was not possible to doubt one’s existence. Yet some Cotard patients maintain that they are dead or that they do not exist ( Young & Leafhead, 1996). The classic reports of this condition were published by the psychiatrist Jules Cotard (e.g. Cotard, 1882), who described a clinical state that he termed délire des négations. The French eponym délire de Cotard was later adopted, and translated into English as Cotard’s syndrome ( Berrios & Luque, 1995a). Although this latter designation is often identified with the belief that one is dead, Cotard himself did not regard that belief as an essential defining feature of the condition he described ( Berrios and Luque, 1995b and Young and Leafhead, 1996). Young and Leafhead’s analysis of Cotard’s (1882) cases revealed a series of commonly occurring features and symptoms, including self-deprecatory delusions, suicidal ideation, 1 feelings of guilt, and denial of body parts. Young and Leafhead’s subsequent comparison of three patients with the belief that they had in fact died revealed a consistent combination of additional symptoms including depressed mood, abnormal feelings, depersonalisation and derealisation, and evidence of face-processing impairments. More exotic concurrent symptoms have been reported elsewhere, including hydrophobia ( Nejad, 2002) and lycanthropy ( Nejad & Toofani, 2005). The issue of whether the Cotard phenomenon is best conceptualised as a psychiatric symptom or a discrete syndrome is yet to be resolved ( Silva et al., 2000 and Young and Leafhead, 1996). For present purposes we shall equate the term “Cotard delusion” with the belief that one is dead. According to Gardner-Thorpe and Pearn (2004), the Cotard delusion usually presents in the context of schizophrenia or bipolar disorder, although it may also occur subsequent to organic insult. Temporo-parietal lesions of the non-dominant hemisphere are particularly implicated in cases of Cotard delusion associated with cerebral trauma. A patient described by Young, Robertson, Hellawell, de Pauw, and Pentland (1992) provides an example of this presentation. For months following a motorcycle accident, the patient was convinced that he was dead. Computerised tomography (CT) scans showed contusions affecting temporo-parietal areas of the right hemisphere as well as some bilateral damage to the frontal lobe. A variety of authors have suggested that the most comprehensive explanation of monothematic delusions such as the Cotard delusion will implicate contributing factors at two levels—the experiential and the inferential (see for e.g. Davies et al., 2001, Ellis and Young, 1990, McKay et al., 2005b, Wright et al., 1993, Young and de Pauw, 2002 and Young et al., 1994; c.f. Gerrans, 2000 and Gerrans, 2002). Such two-factor explanations incorporate an empiricist perspective on delusion formation ( Campbell, 2001), in that they implicate unusual perceptual experiences (caused by a spectrum of neuropsychological abnormalities) as a first factor in delusion formation (see also Maher, 1992, Maher, 1999 and Maher and Ross, 1984). Anomalous perceptual experiences are not thought to be sufficient for the development of delusions, however, because there exist individuals with such experiences who do not develop delusory beliefs about them ( Langdon & Coltheart, 2000). Two-factor models thus invoke an additional explanatory factor or set of factors, to account for how perceptual anomalies lead to the adoption of delusional beliefs. Young and colleagues (e.g. Wright et al., 1993, Young, 2000, Young and Leafhead, 1996 and Young et al., 1994) have proposed that the Cotard delusion results from a similar anomalous perceptual experience to that putatively involved in the Capgras delusion (see Ellis, Whitley, & Luaute, 1994). Patients with the Capgras delusion believe that a loved one has been replaced by a physically identical impostor. Two independent studies have demonstrated that Capgras patients fail to show the normal pattern of autonomic discrimination (as indexed by skin-conductance response) between familiar and unfamiliar faces (Ellis et al., 1997 and Hirstein and Ramachandran, 1997). Whereas control participants showed significantly greater skin-conductance responses to familiar faces, for Capgras patients familiar and unfamiliar faces engendered skin-conductance responses of equivalent magnitude. On the basis of such results, Capgras patients are thought to have damage to neural pathways underpinning the emotional component of face recognition (Ellis and Young, 1990, Langdon and Coltheart, 2000 and Stone and Young, 1997). The ensuing discordance between experiences of the way someone “looks” and the way they “feel” is thought to underpin the impostor delusions of these patients. The spirit of this formulation dates back to the original paper by Capgras and Reboul-Lachaux (see Ellis et al., 1994), and later to Derombies, who “suggested that the syndrome results from simultaneous intellectual recognition and affectively engendered non-recognition of faces”. (1935, cited in Enoch & Trethowan, 1991; p. 13). Following Cotard himself (see Young & Leafhead, 1996), Young and colleagues have suggested that disruptions to the affective component of visual recognition may occur in Cotard cases as well as in Capgras cases. However, whereas Capgras patients interpret the resultant experiences in accordance with a paranoid, projective attributional style (see Kinderman and Bentall, 1997 and Lyon et al., 1994), Cotard patients interpret them in accordance with a depressive, introjective attributional style (see Peterson et al., 1982 and Seligman et al., 1979). In other words, whereas Capgras patients make an external attribution (“that woman is not my wife but rather a physically identical impostor”), Cotard patients attribute the cause of the anomalous experiences to themselves (“that woman looks like my wife but doesn’t ‘feel’ like her—it must be because I’m dead”). Young and colleagues thus hypothesise that cases of Cotard delusion result when a particular perceptual anomaly (caused by a disruption to the affective component of visual recognition) occurs in the context of an internalising attributional style. This hypothesis has yet to be tested directly (Fig. 1). Full-size image (19 K) Fig. 1. The Young et al. explanation of the Cotard and Capgras delusions. Figure options An alternative, single factor proposal is that whereas Capgras patients have a circumscribed disconnection syndrome, involving disruption to pathways underpinning the emotional component of face recognition, Cotard patients have a more global disconnection of all sensory areas from the limbic system, “leading to a complete lack of emotional contact with the world” ( Ramachandran & Blakeslee, 1998; p. 167; see also Gerrans, 2000 and Gerrans, 2002). Under this latter proposal one would not expect Cotard patients to display a marked internalising attributional style ( Fig. 2). Full-size image (17 K) Fig. 2. The Ramachandran and Blakeslee explanation of the Cotard and Capgras delusions. Figure options We report here an investigation of attributional style in a 24-year-old woman with Cotard delusion. The results obtained support an association of Cotard delusion with an internalising attributional style, and are thus consistent with the account of Young and colleagues.

The two IPSAQ indices and the DASS depression score are shown in Table 3 for LU and for the control group. In each case LU’s score was compared to the control group using Crawford and Howell’s (1998) modified t-test (one-tailed). LU was found to have a greater internalising bias than the control participants, in that she showed a significantly greater proportion of internalising attributions, both overall and for negative events specifically, than the control group. She also reported a higher level of depression than the control group, although the difference was only borderline-significant. Table 3. IPSAQ indices and DASS depression scores for patient LU and the healthy control participants (ranges in parentheses) Patient LU Control means (ranges) Statistics IPSAQ indices IB 0.69 0.42 (0.28–0.59) t[9] = 2.67, p = .013 IBN 0.88 0.39 (0.19–0.75) t[9] = 2.92, p = .009 DASS depression 20 7.90 (0–21) t[9] = 1.76, p = .056 Table options In view of the established connection between depression and internalising attributions on the one hand (Peterson et al., 1982, Seligman et al., 1979 and Sweeney et al., 1986), and depression and Cotard’s syndrome on the other (Berrios and Luque, 1995a, Enoch and Trethowan, 1991 and Young and Leafhead, 1996), it is possible that both LU’s nihilistic delusions and her evident internalising bias are consequences of her depression. However, it should be noted here that her DASS depression score places her in only the Moderate range for depression. Moreover, the self-reported depression of one of the ten control participants was greater than LU’s, yet this participant was clearly not delusional and her internalising indices were comparable to the control group mean (in fact numerically lower; IB = .38, IBN = .31).