Failing to self-ascribe thought and motion: Towards a three-factor account of passivity symptoms in schizophrenia

Abstract

This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. There has recently been emphasis put on providing two-factor accounts of monothematic delusions. Such accounts would explain (1) whether a delusional hypothesis (e.g. someone else is inserting thoughts into my mind) can be understood as a prima facie reasonable response to an experience and (2) why such a delusional hypothesis is believed and maintained given its implausibility and evidence against it. I argue that if we are to avoid obfuscating the cognitive mechanisms involved in monothematic delusion formation we should split the first factor (1 above) into two factors: how abnormal experience can give rise to a delusional 'proto-hypothesis' and how a 'proto-hypothesis' in consort with normal experiences and background information, can be developed into a delusional hypothesis. In particular I will argue that a schizophrenic is faced with the unusual requirement of having to identify an introspectively accessible thought as one's own, and that this requirement of identification is the central experiential abnormality of thought insertion, auditory verbal hallucination, and alien control (i.e. passivity symptoms). Additionally, I will consider non-experiential factors which are required for the formation of a delusional hypothesis.

Aberrant Salience Is Related to Dysfunctional Self-Referential Processing in Psychosis

“…We report 3 key findings: first, schizophrenia patients showed increased aberrant salience attribution compared with healthy controls, with individuals with subclinical delusional ideation taking an intermediate position; second, patients displayed decreased activation during selfreferential processing in the vmPFC compared with both healthy controls and individuals with subclinical delusional ideation; third, the activation in this region correlated negatively with aberrant salience in schizophrenia patients. These findings support the relevance of altered self-referential processing 6,7 and aberrant salience attribution in schizophrenia. 2,3…”

“…Our findings provide experimental evidence for the hypothesis of aberrant salience attribution [1][2][3] and dysfunction of the self 1,[6][7][8][9][10][11] in schizophrenia. We demonstrate reduced neural self-referential processing in the vmPFC, the core region of self-relevance coding, which was associated with increased aberrant salience attribution in schizophrenia patients.…”

“…4,5 However, attribution of salience to otherwise irrelevant stimuli does not explain why environmental perceptions are imbued with specific meaning centered around the psychotic person or why his/her thoughts appear to be transmitted from the outside or spoken aloud in the environment. Indeed, this failure to self-ascribe thoughts, 6 as well as aberrant self-relevance attribution to environmental stimuli 6,7 both point to a dysfunction of the self, which can also be observed in transcultural studies of schizophrenia. 8 The concept of schizophrenia includes the notion of a disturbed basic sense of self as a core mechanism specific to schizophrenia.…”

Aberrant Salience, Self-Concept Clarity, and Interview-Rated Psychotic-Like Experiences

“…Most theoretical models of PLEs can be characterized as social-cognitive models, in that they posit a role for the individual interacting with people in the environment to produce PLEs (e.g., Bell, Halligan, & Ellis, 2006; Freeman, 2007; Gray, 2014; Maher, 2003). Two common factors central to nearly all of these models are aberrant salience and self-relevant information processing (Bell et al, 2006; Cicero, Becker, Martin, Docherty, & Kerns, 2013; Freeman, 2007).…”

Schizophrenia and Corollary Discharge: A Neuroscientific Overview and Translational Implications

“…The patient finds oneself subjected to varied stimuli that bring about the classic presentation of formal thought disorder in these patients 8). Symptoms like thought insertion present in schizophrenia are thus postulated to be a result of defective corollary discharge mechanism 64). A study claimed that the lack of ownership of a thought occurs on account of lack of efference copy to the attention bias.…”