This is a response to Max Coltheart's contribution to the blog, posted on behalf of Phil Corlett.
Thanks Max.
I suppose if a two-factor explanation of polythematic delusions is an open question, then an aberrant prediction error explanation of monothematic delusions is likewise open.
I think our theories have more in common than perhaps we are allowing with this debate and our apparent disagreement. I think we are talking about different levels of explanation (Marr, 1977). My implementational and algorithmic explanations may be overlapping with your computational one, but it seems you disagree. This is curious and unfortunate, since prediction error is at the heart of both of our explanations.
We make our prediction error case using behavioral and functional imaging data – if people with monothematic delusions were to show aberrant prediction error signals that correlate with delusion severity (as we showed in endogenous and pharmacological settings as well as in healthy individuals with odd beliefs), I would be inclined to favor an aberrant prediction error explanation (Corlett et al., 2010). I suspect they might. Which is to say, I think aberrant prediction error can account for monothematic delusions.
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| Phil Corlett |
Thanks Max.
I suppose if a two-factor explanation of polythematic delusions is an open question, then an aberrant prediction error explanation of monothematic delusions is likewise open.
I think our theories have more in common than perhaps we are allowing with this debate and our apparent disagreement. I think we are talking about different levels of explanation (Marr, 1977). My implementational and algorithmic explanations may be overlapping with your computational one, but it seems you disagree. This is curious and unfortunate, since prediction error is at the heart of both of our explanations.
We make our prediction error case using behavioral and functional imaging data – if people with monothematic delusions were to show aberrant prediction error signals that correlate with delusion severity (as we showed in endogenous and pharmacological settings as well as in healthy individuals with odd beliefs), I would be inclined to favor an aberrant prediction error explanation (Corlett et al., 2010). I suspect they might. Which is to say, I think aberrant prediction error can account for monothematic delusions.
More troubling (to me at least) is the paucity of data from these monothematic delusional subjects with regards to the key predictions of two-factor theory. For example, there are some data on the skin conductance responses of Capgras sufferers to familiar faces (they support the notion that familiarity responses are reduced (Ellis et al., 1997)). To my knowledge though, no one has shown excessive familiarity in Fregoli delusion (the belief that strangers are your family members in disguise) nor have the predicted global deficits in skin conductance response in Cotard delusion (the belief that one is dead) been reported. In the absence of these data, are we to consider 2-factor accounts applicable only to Capgras?
Some further thoughts on polythematic delusions.
Thanks for introducing the distinction. As the apparent originator of the term, perhaps you can clarify some points for me?
It seems to me that your definition and examples of polythematic delusions conflates the number of beliefs (poly – many beliefs) with bizarreness (Cermolacce et al., 2010). Are all polythematic delusions bizarre by your definition? I ask because I am still not clear on what I would predict with regards a general belief evaluation deficit (Factor 2). I personally would predict a deficit in evaluating all beliefs, which might lead to the endorsement of numerous odd beliefs. This is the case when one considers healthy people with unusual ideas – they entertain numerous strange beliefs across numerous domains (some of which contradict one another (Pechey and Halligan, 2012)), I would consider this a belief evaluation dysfunction. In your extensive interactions with patients with monothematic delusions have you ever seen anything like this?
Since we are discussing challenging topics, what is the 2-factor stance on autochthonous delusions – beliefs that apparently arise completely de novo? Do these speak to the sub-personal nature of the 2-factors (Dennett, 1969)?
Now to respond to your responses: As I suggest above, I think we might be talking about different levels of explanation but we are essentially talking about the same things. As I suggested in my initial response, I feel that prediction error may be the implementation of Factors 1 and 2 – it signals that the parameters of our current model are inadequate and need to be updated (within model prediction error, factor 1) and it signals that the current model is inadequate and needs to be replaced (prediction error over models, your factor 2).
When you responded to Lisa’s question about prediction error, you suggested that we (myself, Paul Fletcher, Chris Frith) were wrong, that we thought there was a failure in prediction error and that the prediction error in 2-factor theory was intact/appropriate.
I think this is where some confusion arose.
Do you agree that our theories might have more in common than we are appreciating?
I suppose the only thing you might take issue with is that I think prediction error dysfunctions at the levels of factor 1 and factor 2 may be related to one another. I feel that perception and belief ought not be strictly separated and that perception might involve belief, or as Helmholz called it unconscious inference (Helmholtz, 1878/1971), a point that you allowed for but did not feel relevant to delusions. For me, this is critical, since aberrant prediction errors can arise from various junctures (e.g. a failure of top-down belief-based prediction, excessive bottom-up sensation).
In the spirit of our discussion though, I should like to finish with a respectful disagreement: I believe you suggested the third factor – generation of candidate explanations – not me. This arose when I raised the peculiar temporality of the factors: the brain regions mediating factors 1 and 2presumably get damaged simultaneously, but people wake up from their coma, see their spouse, lack familiarity, update to the imposter belief and then never update again. You suggested a third factor, candidate genesis, about which I sought clarification (e.g. is there anyone in whom this process is disrupted?). I don’t think this answered my original concern though; if belief evaluation is damaged at the same time as factor 1, why would the new imposter belief be formed? Why do they update their belief this one final time? I’m afraid I still don’t understand.
References
Cermolacce M, Sass L, Parnas J (2010) What is bizarre in bizarre delusions? A critical review. Schizophrenia Bull 36:667-679.
Corlett PR, Taylor JR, Wang XJ, Fletcher PC, Krystal JH (2010) Toward a neurobiology of delusions. Prog Neurobiol.
Dennett DC (1969) Content and Consciousness. London: Routledge and Kegan Paul.
Ellis HD, Young AW, Quayle AH, De Pauw KW (1997) Reduced autonomic responses to faces in Capgras delusion. Proc Biol Sci 264:1085-1092.
Helmholtz H, von. (1878/1971) The Facts of Perception. In: Selected Writings of Herman von Helmholtz (Kahl R, ed): Weslyan University Press.
Marr D, Poggio, T. (1977) From understanding computation to understanding neural circuitry. Neurosciences Res Prog Bull 204:301-328.
Pechey R, Halligan P (2012) Using co-occurrence to evaluate belief coherence in a large non clinical sample. PLoS One 7:e48446.