Thursday, 23 October 2014

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.

Tuesday, 21 October 2014

PERFECT Launch (3): Depression and its Benefits

Magdalena Antrobus
My research focuses on epistemic and pragmatic benefits of imperfect cognitions found in the clinical population. More specifically I am interested in acquiring answers related to the question of the possible positive sides of mental disorders.

It is commonly known that mental illness constitutes a source of profound harm. It relates to individual suffering, distorts one’s cognitive, emotional and behavioural processes, and sometimes leads to severe impairment. However, the results of more recent psychological studies indicate that psychiatric disorders might be linked to particular benefits as well as causing pain.

There has been a well-researched relationship between bipolar disorder and creativity. It is believed that certain clinical symptoms brought by the illness, for example thought speed or openness for new experiences, may contribute to enhanced creativity (see for instance Ghaemi, 2011; Andreasen, 2005; Jamison, 1996). (For more details see my interview with Greg Currie.) If that were true, we would have the grounds to believe that bipolar disorder brings certain epistemic benefits. At the same time the illness may cause cognitive impairments in other areas of functioning, for example it may affect memory, sleep and concentration. The idea that pragmatic or psychological harm may coexist with the benefits of an epistemic kind is relatively new in psychiatry, thus researching it seems very exciting.

Thursday, 16 October 2014

Interview with Martin Davies: Delusions (Part 3)


Martin Davies
This is the third part of an interview with Professor Martin Davies on delusions. (Although this part can be read independently of the previous two, you may want to read also the first and second part of the interview if you haven't done so already!)


LB: In the first stage of our project PERFECT we are going to ask whether delusions can have pragmatic and epistemic benefits. You and your collaborators have noticed how anosognosia (denial of illness), despite initially interfering with rehabilitation, can then lead to lower anxiety and protect from negative emotions (Aimola Davies et al., 2009). Can you think of other examples of delusions having a positive psychological impact? 

MKD: Let me begin by reviewing the findings that you mentioned in your question. Some researchers distinguish denial of illness from anosognosia and use the ‘denial’ terminology for cases with a ‘psychological’ rather than neurological aetiology. In our paper, we referred to a theoretical review by Kortte and Wegener (2004), who found support for both adaptive and maladaptive effects of denial of illness across a range of rehabilitation populations.

They proposed two distinctions to explain these different effects: (i) subtypes of denial and (ii) different time points from symptom identification to hospitalisation and rehabilitation. On (i), they suggested that the effect of avoidance of illness-related information is more likely to be maladaptive while a positive reinterpretation of the illness experience was more likely to be adaptive. On (ii), and focusing now on Kortte and Wegener’s discussion of denial of heart disease, denial at the stage of symptom (self-)identification has obvious negative consequences and long-term denial (particularly, of the avoidance type) after discharge from hospital has been linked with poorer compliance with medication regimes and a failure to heed medical advice about risk factors. However, denial (particularly, of the positive reinterpretation type) during the hospitalisation stage appears to be associated with more positive effects, such as protection from negative emotional states and reduced medical complications.

Tuesday, 14 October 2014

PERFECT Launch (2): Biological Function and Formation of Delusions

Our project logo.
My research so far has been on belief, and this is an area I will continue to focus on. I am interested in researching two main areas: first, how best to think about delusional beliefs when we look to the biological function of belief, and second, accounts of delusion formation.

In my PhD I defended a biological account of belief according to which our mechanisms of belief-production have (at least) two biological functions proper to them. The first is the function to produce true beliefs, and the second is the function to produce useful beliefs. When I say ‘useful’, I do not mean useful an approximation to truth, but rather useful with respect to facilitating the effective functioning of the believer. I was mainly concerned with explaining the connection between belief and truth, and so much of the work was done by appeal to the function of producing true beliefs. However, towards the end of my thesis, I gestured towards the kind of explanatory work which might be done by appeal to the function of producing useful belief.

In terms of future research I am very keen to think about how much work the functional account of belief I developed in my doctoral work can do when we look to pathological belief in the clinical population, specifically, delusional belief. I think there are several questions to ask about delusional belief in the context of my account. Firstly, what is the biological proper function of delusional belief?

Friday, 10 October 2014

Schizophrenia and Logic


Mental Health Awareness Weeks logo
Today, 10th October 2014, is World Mental Health Day. This year it is dedicated to living with schizophrenia. On this important occasion, Gareth Owen kindly agreed to discuss his fascinating work on schizophrenia and logic. Gareth is Clinical Senior Lecturer at the Institute of Psychiatry, Psychology and Neuroscience, King's College London.

People with schizophrenia do worse than others on many tasks. Indeed a global conclusion in the psychology of schizophrenia is that people with this disorder have somewhat lower IQ than those without – a conclusion that makes schizophrenia seem a disorder of cognition like dementia or learning disability. But this is an incomplete perspective. The phenomenology of schizophrenia also points in the direction of representational overactivity (1). Additionally, delusions, which people with schizophrenia often exhibit, are not explained by failures of formal inference such as inability to reason with modus ponens or modus tollens or inability to adhere to Bayesian updating norms. That is striking when one considers that delusion and illogically are often assumed to be the same.

Thursday, 9 October 2014

Interview with Martin Davies: Delusions (Part 2)

Martin Davies
This is the second part of an interview with Professor Martin Davies on delusions. You can read the first part of the interview here.


LB: Presentations of the two-factor account of delusion formation usually begin with two questions. The first question is about where the content of the delusion came from and the second is about the adoption or persistence of the belief. The two factors are supposed to provide answers to these two questions. But it sounds as if you are distinguishing a question about adoption from a question about persistence (or maintenance). If there are more than two questions to be answered, will an explanation of a delusion have to appeal to more than two factors?

MKD: Thank you for raising this issue of the relationship between questions and factors. It is quite important for understanding the two-factor framework. Questions about the aetiology of a delusion can be multiplied and, correspondingly, explanations of a delusion can be increasingly detailed, appealing to more than two ‘factors’ in the ordinary sense of that term. But, crucially, factors in the sense relevant to the two-factor framework are not just elements in an explanation. They are, specifically, pathologies or departures from normality, such as neuropsychological deficits.

You are right to say that I want to distinguish between a question about adoption of the delusional belief and a question about the belief’s persistence. If we are going to say something substantive about the nature of the second factor then we need to be clear about the role of the second factor. Where, in the total story of the aetiology of a delusion, does it figure? So, along with the first question about the source of the delusional idea or hypothesis, there should be the adoption question, ‘Why is the delusional hypothesis adopted as a belief?’, and the persistence question, ‘Why does that belief, once adopted, persist; why is it not subsequently rejected?’.