Macquarie University ResearchOnline

In their pursuit of adaptively biased misbelief-making systems, McKay & Dennett (M&D) describe a putative doxastic shear-pin system which enables misbeliefs to form in situations of extreme psychological stress. Rather than discussing their argument, I consider how this shear-pin system might combine with both pathological belief-making (“culpable” breakdowns caused by neuropathy) and normal beliefmaking to explain a spectrum of delusions. Textbook definitions of delusions (as, e.g., false beliefs) are inadequate to capture the nature of pathologies that cause delusions (see David 1999; see also McKay & Dennett’s [M&D’s] comment that delusions might sometimes be “serendipitously true” [sect. 1, para. 2]). The three signs that clinicians use to diagnose delusions (incorrigibility, subjective certainty, and incomprehensibility) are better pointers to the nature of these pathologies than are textbook definitions. Incorrigibility refers to the rigid persistence in the face of rational counter-argument. Subjective certainty concerns the quality of self-evident truth with which delusions are espoused. Incomprehensibility can be “sheer” or “contextual” (Langdon & Bayne, in press). The sheer content of some delusions is sufficient as to render them incomprehensible; the belief that one is dead (Cotard delusion) is like this. Mundane delusions, like delusional jealousy, are contextually incomprehensible; patients with these delusions lack the evidence, or lack the irrefutable evidence that would warrant the subjective certainty with which the delusion is espoused (e.g., a patient once vehemently justified her persecutory delusion about a neighbour by referring to the provocative way in which the neighbour had intentionally jingled her keys when walking ahead of the patient). In our original “two-deficit” model, Langdon and Coltheart (2000), we proposed two distinct, concurrent pathologies to explain the incomprehensibility and the incorrigible, subjective certainty of bizarre monothematic delusions. The first breakdown explains why a delusional person generates a fantastic thought with content so beyond the bounds of normal experience. This first break also varies from patient to patient to explain the variable delusional themes. First breaks to sensory/ somatosensory mechanisms were our primary focus; these distort perceptual experience and so explain the sheer incomprehensibility of bizarre delusions. Since many non-delusional people experience distorted perceptions (e.g., phantom-limb sufferers), a second break was proposed to explain the failure to reject the bizarre thought as implausible: the incorrigibility. Current conceptions of this second break vary; see, for example, M&D’s discussion of excessive biases towards either observational adequacy or doxastic conservatism. Langdon and Bayne (in press) propose that the second break in bizarre monothematic delusions is an inability to inhibit a default setting to upload and maintain the content of perceptual experience into belief (see also, Davies et al. 2001). For example, the patient with a mirrored-self misidentification delusion misperceives a stranger in the mirror, misbelieves that there is a stranger in the mirror, and cannot reason as if there only seems to be a stranger in the mirror. It is this inability to inhibit the misperceived reality that explains the self-evident, subjective certainty. In Langdon and Coltheart (2000), although we focused on pathology, we also considered normal belief-making. Normal processes, we suggested, might nuance specific elaborations of a bizarre delusion: One Cotard patient with an internalising attributional bias might believe that God is punishing her for her evil ways, while another Cotard patient with an externalizing bias might believe that evil doctors have stolen her “life essence.” Normal processes might also feature in the generation of mundane delusions by way of expectation-fuelled attentional biases concerning, for example, a straying partner (delusional jealousy) or health concerns (hypochondrial delusions). Even a mundane grandiose delusion, like believing that one is a gifted pianist despite poor playing skills and vocal audience criticism, might begin with the positive illusions that interest M&D. Combinations of pathological and normal belief-making explain: normal beliefs about normal experiences (with no pathological breaks present); normal beliefs about bizarre experiences (with only a first break present, as occurs, e.g., when an aberrant signal of familiarity causes insightful déjà vu); mundane delusions (with only a second break present); and bizarre delusions (with two breaks present). Expanding the framework in this way prompts two questions, though. The first concerns the adoption of the belief. The adoption of a bizarre delusion which has been triggered by some disturbance of sensory/somatosensory processing is relatively straightforward to explain by way of a default to believe our senses, at least initially. The adoption of a mundane delusion is less straightforward to explain; when and why does a worrying or a fantasizing become a convicted believing? The second question concerns the nature of the second break; is it the same in mundane and bizarre delusions? This seems unlikely if the second break in bizarre delusions is an inability to inhibit a default setting to believe what our senses tell us. In a recent review of persecutory delusions, which are often mundane, Langdon et al. (2008) found no compelling evidence for the involvement of right-frontal brain damage; we suspect that brain damage of this type underpins the second break in bizarre delusions. More recently, therefore, we have shifted to a more general, “two-factor” approach (e.g., Coltheart 2007) to ask two questions about each delusion: (1) What generates the Commentary/McKay & Dennett: The evolution of misbelief BEHAVIORAL AND BRAIN SCIENCES (2009) 32:6 527 delusional content in the first place? (2) Having once entertained a particular thought, why does a deluded patient cling to it rather than reject it? Sometimes the answers will be neuropsychological and sometimes they will be motivational. But, even if the aetiology of the second break is sometimes motivational and sometimes neuropsychological, the second break might still be similar at an on-line cognitive level. M&D’s idea of “doxastic shear-pins” is relevant here. If belief-making components shear in situations of extreme psychological stress to permit beliefs that would ordinarily be rejected, I assume that the shearing is localized and constrained by the context. I also assume that the shearing involves some on-line neural/cognitive “short-circuit,” as opposed to a stable neuropsychological impairment. If so, then perhaps we might describe the second break in all delusions, bizarre or mundane, as a “doxastic inhibitory failure”: a failure to “demote” a belief so as to reason about it as if it might not be true. In bizarre monothematic delusions, this failure might only manifest via an inability to inhibit a default tendency to upload and maintain (distorted) perceptual experience into (mis)belief; in mundane motivated delusions this failure might only manifest when the psychological cost of demoting the belief into a “maybe-it’s-not-true” mental space is too great; and in dementing patients with widespread bizarre and/or mundane delusions this failure might reflect more general inhibitory compromise.