Interview with Max Coltheart: Delusion Formation (Part 1)

Max Coltheart

While visiting the ARC Centre of Excellence in Cognition and its Disorders at Macquarie University, I interviewed Max Coltheart, Professor of Cognitive Science, on the topic of delusion formation.

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 delusions—about eight or nine of them—proposing a first factor, showing that that’s 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 ‘normal range’, 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 can’t deny that, and so it’s not very parsimonious, with that evidence, to appeal to it sometimes being individual differences. Then you’re saying that there are two different kinds of second factors. There’s one that’s down to brain damage, and there’s one that’s down to individual differences. The two problems with that is that it’s not parsimonious and there’s no evidence that any patients like this have a second factor that’s pre-morbidly present and down to individual differences. Now that doesn’t 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 can’t 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 you’re looking for brain damage that couldn’t be the source of the first factor in Capgras then it’s 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 don’t know of any cases where a really good scan has been done without finding that but there are plenty of cases where it just wasn’t done. So we’re left up in the air as far as whether it’s 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 we’d proposed that, then the next case of Capgras after we’d published this, had a tiny little stroke in right dorsolateral prefrontal cortex, so that adds up to me being fairly convinced that you’ll 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 it’s wrong and even though evidence is produced to show that it’s 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 I’ve ever been able to do is to get the delusion to sort of waver a bit but never to go away, you can’t persuade a person with a delusion that their belief is wrong.

ES-B: I’m 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 don’t understand the motivation for it because it’s 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 it’s always right hemisphere damage, show me an example that isn’t. And so you then have to develop this pre-morbid individual differences notion so as to say here’s how I can identify who pre-morbidly has the second factor so if they had the first factor that would be delusional. And so you’d have to say what tests would we use to identify such people? Now we’re not going to be lucky enough for them to go on and have a stroke, nevertheless I think that’s the way to think about it. So, that means you’ve got to flesh out the pre-morbid individual differences concept. I don’t think there’s any doubt that there is this range of individual differences in what you might call credulity, I just don’t see any reason to believe that it’s implicated in delusion.