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Max Coltheart |
ES-B: According to the one-factor account of delusion formation, we need only appeal to an anomalous experience to explain why a subject comes to hold a delusional belief, it is only the kinds of experiences subjects with delusions have which sets them apart from the non-delusional population. What do you think is wrong with this account?
MC: Whenever you identify an anomalous experience that you think is the cause of a delusion, you can always find patients who have that experience but are not deluded. We have done that systematically. We just go through a whole lot of different monothematic delusionsāabout eight or nine of themāproposing a first factor, showing that thatās a plausible source of the content of the belief and for each of those first factors showing that there are patients that have that first factor who are not delusional. And so I think that rules out a one-factor explanation for all of those monothematic delusions.
ES-B: Could the one-factor approach appeal to individual differences here? If the belief formation mechanisms of patients with delusions operate within what we might call the ānormal rangeā, this might allow for a range of possibilities regarding forming beliefs upon certain experiences. What is wrong with that kind of line?
MC: Well, first of all you have to decide whether there are at least some cases where the second factor is due to brain damage, and I think you canāt deny that, and so itās not very parsimonious, with that evidence, to appeal to it sometimes being individual differences. Then youāre saying that there are two different kinds of second factors. Thereās one thatās down to brain damage, and thereās one thatās down to individual differences. The two problems with that is that itās not parsimonious and thereās no evidence that any patients like this have a second factor thatās pre-morbidly present and down to individual differences. Now that doesnāt rule out this theory, you can never completely rule out a theory, just, why say it? The only reason to say it would be if you denied that the second factor was ever due to brain damage, and you canāt do that.
ES-B: Is it the case that with the Capgras delusion the kind of brain damage which gives rise to or constitutes the second factor is present in all and only Capgras patients?
MC: One problem with that is that if youāre looking for brain damage that couldnāt be the source of the first factor in Capgras then itās nothing to do with the autonomic nervous system, certainly many patients have been reported having right frontal damage, even specifically right dorsolateral prefrontal cortex damage, so there are plenty of patients where that has been observed. I donāt know of any cases where a really good scan has been done without finding that but there are plenty of cases where it just wasnāt done. So weāre left up in the air as far as whether itās true for all the patients, but all the patients who have been properly scanned that I know of have pre-frontal cortex damage. And what interests me is that after weād proposed that, then the next case of Capgras after weād published this, had a tiny little stroke in right dorsolateral prefrontal cortex, so that adds up to me being fairly convinced that youāll always find this in Capgras.
ES-B: In your work you have argued that we need to appeal to a second factor in delusional belief formation to explain why a delusion is maintained in the face of counterevidence, rather than to explain why it is formed at all. Could you say a little more about this?
MC: We like to say that you can understand delusions if you can answer two questions: 1. Where did the delusion come from, that is, why did a belief with this content get formed in the first place? 2. Why does the belief get maintained even though everybody around you is saying that itās wrong and even though evidence is produced to show that itās wrong? One patient I saw in Melbourne with his wife, as long as I was focussing on the evidence that this was actually his wife, his belief would waver. But as soon as I stopped talking about that he just went back to the delusion. So the most Iāve ever been able to do is to get the delusion to sort of waver a bit but never to go away, you canāt persuade a person with a delusion that their belief is wrong.
ES-B: Iām interested in developing a notion of a normal range because I think it might be useful in developing a plausible one-factor account. The normal range would have to rule in a range of rational and irrational beliefs, so what do you think the potential is for developing such a notion, and might it be useful?
MC: I donāt understand the motivation for it because itās not needed. We know that the second factor is at least sometimes right hemisphere damage so the parsimonious way to proceed is to say I think itās always right hemisphere damage, show me an example that isnāt. And so you then have to develop this pre-morbid individual differences notion so as to say hereās how I can identify who pre-morbidly has the second factor so if they had the first factor that would be delusional. And so youād have to say what tests would we use to identify such people? Now weāre not going to be lucky enough for them to go on and have a stroke, nevertheless I think thatās the way to think about it. So, that means youāve got to flesh out the pre-morbid individual differences concept. I donāt think thereās any doubt that there is this range of individual differences in what you might call credulity, I just donāt see any reason to believe that itās implicated in delusion.