This is a response to Phil Corlett's contribution to the blog, posted on behalf of Max Coltheart.
I thank Phil for his illuminating questions about my post, and will attempt to answer them, in Q&A format (Q is Phil, A is me).
Q: Are you aligning prediction error with Factor 1 or Factor 2? It seems Factor 1, but I wanted to check – particularly since you align Factor 2 with the functioning of right dorsolateral prefrontal cortex, which, as you know, we’ve implicated in prediction error signaling with our functional imaging studies.
A: In our account, what generates prediction error is Factor 1: for example, in Capgras delusion, the prediction is that an autonomic response will occur when the face of one’s spouse is seem, but that prediction is in error, since the predicted response does not occur. But detection of this prediction error would only occur if the system that detects such errors is intact. And the job of this system is to generate hypotheses to account for these errors: a delusional hypothesis would not occur unless this function of the prediction-error system were also intact. Our understanding of your model is that there is something wrong with the prediction-error system in people with delusions. As for right dorsolateral prefrontal cortex, we associate Factor 2 with this region, believing that damage to the region results in impairment of the belief evaluation system.
Q: Are you implying that we believe delusions form in the absence of prediction error?
A: Our understanding of your model is that it argues that there is something wrong with the prediction-error system itself in people with delusions. As indicated above, on our account this system needs to be functioning normally for delusions to occur. What’s abnormal is not this system, but input to this system: Factor 1 causes this input to be abnormal in one way or another.
Q: According to your model, you would need to wake up from your coma, have the experience of unfamiliarity for your wife, update your belief appropriately (using the normally functioning prediction error signal) then hold fast to your belief. To form the delusion based on the odd experience, wouldn’t you need belief evaluation to be working normally?
A: No, because we distinguish between candidate-belief formation and belief evaluation. Candidate beliefs are formed using abductive inference in response to unusual experiences (as James and Maher proposed) and we share with those two the view that the process of candidate-belief formation is intact in deluded people. After candidate-beliefs have been generated, these then need to be evaluated, and it is this separate belief-evaluation process which is impaired in deluded people: that impairment is Factor 2 on our model, and the impairment is perhaps associated with damage to right dorsolateral prefrontal cortex.
Q: Why are monothematic delusions so circumscribed: wouldn’t you expect someone with an impaired belief evaluation system to be delusional about many things?
A: We offer an answer to this in Coltheart (2007, pp.1056-1057) and Coltheart, Langdon and McKay (2011, pp. 18-19). Briefly, the answer is: there is evidence from studies of people with monothematic delusions that the belief evaluation system is damaged but not entirely abolished. The system will fail to reject a belief only when there is persistent and strong evidence favouring this particular belief. In monothematic delusion there is only one belief of this kind (the belief that Factor 1 prompts).
Q: Would you agree that your model does not allow for any top-down influence of belief on perception?
A: Our model does not deny that there are such influences. But what is the relevance of such influences to monothematic delusion? Are there any facts about monothematic delusion that need such top-down influences to explain them? I don’t know of any.
Q: What is the factor 1 in confabulation e.g. when a patient who had been a lawyer refers to the hospital’s doctors and nurses as judges and barristers?
A: Metcalf, Langdon, and Coltheart (2007) and Turner & Coltheart (2010) have explicitly applied the two-factor model of delusion formation to confabulation. They suggested that the first factor in confabulation is a retrieval impairment resulting in disrupted search and selection of memories from the autobiographical store. When combined with a second factor, an impairment thatprevents accurate evaluation of the retrieved memories, confabulations are produced.
References:
Coltheart, M. (2007). The 33rd Bartlett Lecture: Cognitive neuropsychiatry and delusional belief. Quarterly Journal of Experimental Psychology, 60, 1041-1062.
Coltheart, M., Langdon, R. & McKay, R.T. (2011). Delusional belief. Annual Review of Psychology, 62, 271-298.
Metcalf, K., Langdon, R., & Coltheart, M. (2007). Models of confabulation: A critical review and a new framework. Cognitive Neuropsychology, 24, 23-47.
Turner, M., & Coltheart, M. (2010). Confabulation and delusion: A common monitoring framework. Cognitive Neuropsychiatry, 15, 346-376.
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| Max Coltheart |
Q: Are you aligning prediction error with Factor 1 or Factor 2? It seems Factor 1, but I wanted to check – particularly since you align Factor 2 with the functioning of right dorsolateral prefrontal cortex, which, as you know, we’ve implicated in prediction error signaling with our functional imaging studies.
A: In our account, what generates prediction error is Factor 1: for example, in Capgras delusion, the prediction is that an autonomic response will occur when the face of one’s spouse is seem, but that prediction is in error, since the predicted response does not occur. But detection of this prediction error would only occur if the system that detects such errors is intact. And the job of this system is to generate hypotheses to account for these errors: a delusional hypothesis would not occur unless this function of the prediction-error system were also intact. Our understanding of your model is that there is something wrong with the prediction-error system in people with delusions. As for right dorsolateral prefrontal cortex, we associate Factor 2 with this region, believing that damage to the region results in impairment of the belief evaluation system.
Q: Are you implying that we believe delusions form in the absence of prediction error?
A: Our understanding of your model is that it argues that there is something wrong with the prediction-error system itself in people with delusions. As indicated above, on our account this system needs to be functioning normally for delusions to occur. What’s abnormal is not this system, but input to this system: Factor 1 causes this input to be abnormal in one way or another.
Q: According to your model, you would need to wake up from your coma, have the experience of unfamiliarity for your wife, update your belief appropriately (using the normally functioning prediction error signal) then hold fast to your belief. To form the delusion based on the odd experience, wouldn’t you need belief evaluation to be working normally?
A: No, because we distinguish between candidate-belief formation and belief evaluation. Candidate beliefs are formed using abductive inference in response to unusual experiences (as James and Maher proposed) and we share with those two the view that the process of candidate-belief formation is intact in deluded people. After candidate-beliefs have been generated, these then need to be evaluated, and it is this separate belief-evaluation process which is impaired in deluded people: that impairment is Factor 2 on our model, and the impairment is perhaps associated with damage to right dorsolateral prefrontal cortex.
Q: Why are monothematic delusions so circumscribed: wouldn’t you expect someone with an impaired belief evaluation system to be delusional about many things?
A: We offer an answer to this in Coltheart (2007, pp.1056-1057) and Coltheart, Langdon and McKay (2011, pp. 18-19). Briefly, the answer is: there is evidence from studies of people with monothematic delusions that the belief evaluation system is damaged but not entirely abolished. The system will fail to reject a belief only when there is persistent and strong evidence favouring this particular belief. In monothematic delusion there is only one belief of this kind (the belief that Factor 1 prompts).
Q: Would you agree that your model does not allow for any top-down influence of belief on perception?
A: Our model does not deny that there are such influences. But what is the relevance of such influences to monothematic delusion? Are there any facts about monothematic delusion that need such top-down influences to explain them? I don’t know of any.
Q: What is the factor 1 in confabulation e.g. when a patient who had been a lawyer refers to the hospital’s doctors and nurses as judges and barristers?
A: Metcalf, Langdon, and Coltheart (2007) and Turner & Coltheart (2010) have explicitly applied the two-factor model of delusion formation to confabulation. They suggested that the first factor in confabulation is a retrieval impairment resulting in disrupted search and selection of memories from the autobiographical store. When combined with a second factor, an impairment thatprevents accurate evaluation of the retrieved memories, confabulations are produced.
References:
Coltheart, M. (2007). The 33rd Bartlett Lecture: Cognitive neuropsychiatry and delusional belief. Quarterly Journal of Experimental Psychology, 60, 1041-1062.
Coltheart, M., Langdon, R. & McKay, R.T. (2011). Delusional belief. Annual Review of Psychology, 62, 271-298.
Metcalf, K., Langdon, R., & Coltheart, M. (2007). Models of confabulation: A critical review and a new framework. Cognitive Neuropsychology, 24, 23-47.
Turner, M., & Coltheart, M. (2010). Confabulation and delusion: A common monitoring framework. Cognitive Neuropsychiatry, 15, 346-376.