Tuesday 30 June 2015

Sense of Agency and Delusions of Alien Control

This is the fifth and final post in a series of posts on the papers published in an issue of Avant on Delusions. Here Glenn Carruthers (pictured above) summarises his paper 'Difficulties for Extending Wegner and Colleagues' Model of the Sense of Agency to Deficits in Delusions of Alien Control'.

One of Christopher Frith's (e.g. 1992) ideas that has really taken hold is that part of the problem in delusions of alien control is a deficit in the sense of agency. Given that the sense of agency is the feeling that one controls one's actions we can see how a deficit in this feeling could lead to people saying things like:

When I reach my hand for the comb it is my hand and arm which move, and my fingers pick up the pen, but I don’t control them… I sit there watching them move, and they are quite independent, what they do is nothing to do with me… I am just a puppet who is manipulated by cosmic strings. When the strings are pulled my body moves and I cannot prevent it. (Mellor 1970: 18)

Perhaps part of the reason such patients think someone is controlling them is that they do not have this normal sense of agency. To investigate this further we would like to know how the sense of agency is elicited and why it is deficient in these cases. There have been a bunch of hypotheses developed to explain this. Here I will focus on one which was developed by Daniel Wegner and his collaborators (Wegner et al 2004; Wegner and Wheatley 1999).

Wegner and colleagues' hypothesised that the sense of agency is elicited when a subject (unconsciously) infers that one or other of their mental states (e.g. an intention) caused their action. This is called the inference to apparent mental state causation and it occurs automatically when three principles are met:

Priority: The mental state occurs at an appropriate time prior to the action.

Consistency: The mental state is consistent with the action (e.g. the intention specifies the action that actually occurred).

Exclusivity: The mental state is the only plausible cause of the action.

Monday 29 June 2015

All that glitters...

This week Emily T. Troscianko, Knowledge Exchange Fellow at the Oxford Research Centre in the Humanities, and member of the Medieval and Modern Languages Faculty at the University of Oxford, writes about anorexia for our series of accounts by experts-by-experience. Emily (pictured above) also contributes to Psychology Today with a blog called A Hunger Artist.

If there’s any mental illness that offers the sufferer an illusion of having it all, it’s anorexia. The twin towers of that disingenuous promise are thinness and control, bedfellows familiar from pop psychology and the diet industry. No other mental illness gets under observers’ skins (incomprehension, fear, anger, envy) quite like anorexia, and that’s because none other is quite so physical. And it’s in the interplay between the mental and the physical that the hollowness of anorexia’s illusions gets exposed.

In the early days, the heady ‘hunger high’ gets you hooked, the admiring comments about your weight loss keep you hooked, and very soon starvation has kicked in, and then all its profound psychological effects, and all the tenacious feedback loops between the physical and the psychological, make it extremely hard to get unhooked. Take hunger, for example – a powerful nexus of some of the central paradoxes of anorexia. It’s extremely rare for anorexia to involve a consistent absence of hunger. In the vast majority of cases, hunger is an achingly constant companion, and the moments of endorphin-fuelled exhilaration grow rapidly rarer.

Hunger is the thing to be denied – to yourself and to other people (no thanks, I’ve already eaten). Hunger is why you starve yourself – what higher proof of control than shutting your ears to that screaming bodily need, day after day? But hunger always risks stopping you starving yourself – the closer you get to total control, the closer you get to its opposite, in this case bingeing. Hunger is why eating is the most important thing in your day, to be controlled to perfection and indulged in with ecstasy. Hunger distracts you from other pain, and is the ultimate distraction from anything more meaningful. And because so often denied and debarred, and because of the stomach shrinkage and digestive lethargy that come from denying it often enough, hunger deserts you and nausea attacks at the critical moments when you really want to try, and try to want, to eat: on your brother’s birthday, in exam season, when you embark on recovery.

Thursday 25 June 2015

Valuing Health Conference

On 4th June I attended some talks at the Valuing Health Conference at University College London (see picture above), where the themes of Dan Hausman’s book, Valuing Health (Oxford University Press, 2015) were discussed. The event was organised by Jo Wolff and James Wilson. The intended audience was philosophers, economists, and also healthcare policy makers.

The conference started with a brief overview of the arguments in the book, presented by Dan Hausman (University of Wisconsin). There are two basic problems the book was meant to address: (1) we need to be able to compare health improvements brought by different policies; (2) we need to know what to do with the information (e.g., maximise health). Thus, the book provides answers to the following questions: How do we assign values to health states? How do we assess policies on the basis of those values? What role should people play in assigning values to policies? The discussion raises further questions about the relationship between health and wellbeing (the notion of wellbeing is clarified in chapter 6 of the book, and the distinction between wellbeing and the value of health is examined in chapter 10).

Tuesday 23 June 2015

Amending the Revisionist Model of the Capgras Delusion

This is the fourth in a series of posts on the papers published in an issue of Avant on Delusions. Here Garry Young summarises his paper 'Amending the Revisionist Model of the Capgras Delusion: A Further Argument for the Role of Patient Experience in Delusional Belief Formation'.

I currently work as a senior lecturer in psychology at Nottingham Trent University, although my postgraduate studies were in philosophy. My research interests cover three distinct areas. First, I am interested in embodied cognition, particularly the relationship between consciousness and procedural knowledge (knowing how to do something, rather than knowledge of facts). I have argued, using cases of visual pathology (e.g. blindsight and visual agnosia), that a form of knowledge-how (knowing how to do something) can occur in the absence of conscious accompaniment. 

I am also interested in the ethics underlying the virtual enactment of real-world taboos, such as murder or physical/sexual assault, particularly in the context of video games. Finally, and more pertinent to what we are discussing here, I am interested in the experiences of patient suffering from specific types of delusion, such as the Cotard and Capgras delusions.

In 'Amending the Revisionist Model of the Capgras Delusion: A Further Argument for the Role of Patient Experience in Delusional Belief Formation', I challenge recent attempts to account for the Capgras delusion (the belief that a wife or husband, some family member or significant other, is an impostor) in the absence of an explanatory role for patient experience. 

In particular, I argue that a recent revisionist model proposed by Max Coltheart and colleagues is partly incorrect and therefore in need revision. I challenge two important (revisionist) claims made by Coltheart and colleagues (2010): (1) that a fully-formed belief enters consciousness (such as 'This person is not my wife, she is an imposter'), and (2) that this is the first conscious delusion-related event.

Thursday 18 June 2015

Conference on Psychiatry and Society (2)

On 12th May 2015 in London I attended the "Psychiatry and Society" conference organised by the Psychiatry Section of the Royal Society of Medicine. Here I will summarise the talks I heard in sessions 2 and 3, emphasising those themes that have already been discussed in the blog. (If interested in session 1 of the conference, I reported on it last week).

Session 2: Genetics, Neuroscience and Mental Disorder

Neuroscientist Pamela Sklar asked "How may genetics change our understanding of mental illness?" and she focused on schizophrenia as a "mystery", that is a disorder that is both inherited and very common. Thousands of DNA alleles are involved in the risk of developing schizophrenia and bipolar disorder. The difficulty in identifying the genetic bases of such disorders made some people think that research in this area was doomed to failure. But both for bipolar disorder and for schizophrenia some regions that increase risk have been discovered so there is reason for optimism. One very controversial issue is whether genetic risk factors are shared or split among diseases. There is significant more overlap than one would think by following the DSM or the ICD (examples: bipolar and schizophrenia, schizophrenia and autism). Progress in this area will help distinguish between successful and unsuccessful pharmacological treatment, and implies a rejection of current diagnostic categories.

Psychiatrist and psychiatry researcher Robin Murray discussed Pamela's paper and commented on the large study showing which regions are involved in the genetic risks for schizophrenia, welcoming the day we will stop talking about schizophrenia and start using terms that better reflect the advances in genetics and neuroscience. Latest results in neuroscience suggests that there is no one gene responsible for schizophrenia and that schizophrenia is not a categorical concept. Rather, we need to adopt a dimensional view of schizophrenia because this is supported by current research (in other words, we all have some risk of developing schizophrenia).

Risk of psychosis seems to be increased by: (1) childhood adversities; (2) adverse life events; (3) abuse of cannabis and drug abuse; (4) migration and ethnicity.

Neuroscientist and psychiatrist Steven Hyman (pictured above) asked: "How may neuroscience change our understanding of mental disorder?" and focused on the challenges we face because of the inaccessibility of the brain in life and because of the inadequacy of animal modelling. We need to better understand the brain as "this magnificent machine produced by evolution" and recognise the collision between biological science and the subjective, lived experience of people.

Cognition, emotion, decision-making, and behavioural control are "emergent properties of neural circuits" and at the moment we can only rely on indirect observation to link activity in the brain with cognitive and emotional behaviours. That partially explains why it is difficult to predict whether adolescents with behavioural difficulties will develop schizophrenia and why understanding the reward system is not sufficient to solve the problem of addiction. Ultimately, people with mental disorders need to be seen both as objects and subjects: the loss of agency and the loss of control characterise their predicament and cause significant distress that cannot be dismissed.

Psychiatrist George Szmukler (in the picture above) discussed Hyman's talk and started with a question: "What does it mean to ask a patient to wait a long time before neuroscience can provide some answers to their questions?" Szmukler argues that people with mental illness need to participate in research and become advocates for it. They need to be involved and to understand, with some training, what success in neuroscientific research requires.

Patients need to collaborate actively and be asked what they think the risks are from an ethical perspective in these studies. The best outcome, he said, is to reduce stigma and at the same time offer hope for treatment. This helps people come on board. But it is not easy, due to the hypothesis that psychotic medication decreases the chances of recovery long term even if it is effective in the short term. This hypothesis seems to be supported by some data suggesting that disability in people with mental illness has increased in the last 50 years. At the moment, there is no other data that can be used to assess this hypothesis, and that is why patient participation is so fundamental to future research.

Session 3: Implications for Diagnosis in Psychiatry

Social scientist Nikolas Rose (pictured above) asked: "What should count as a psychiatric diagnosis?"and expressed some scepticism about the the capacity that neuroscience might have to affect clinical practice. The starting point is to establish what the object of diagnosis is. The crisis of psychiatric diagnosis highlighted by criticism of the DSM comes from the attempt to categorically divide conditions, specify for each a set of criteria, and propose unique aetiology, prognosis and treatment. The problem is that no biomarkers can be associated with DSM categories and the list of criteria identified are behavioural.

A break from the DSM was made by Insel who launched the RDoC as an alternative, but one thing that did not change is that the approach is to look at the causes of mental illness within the person's body, and in particular the brain. Even if RDoC is primarily an aspiration for research, the goal is to achieve "precision medicine for mental disorders". One worry is that this approach does not take into account the circumstances of the individuals who experience mental health issues, and these can differ widely across diagnostic categories, independent of whether these categories are based merely on symptoms or on biomarkers. Instead, we need to start with the patient's complaint.

Psychiatrist and researcher in psychiatry Simon Wessely (in the picture above) responded to Nikolas by observing that it has always been claimed that psychiatry is in a crisis, but that the "perpetual crisis of diagnosis" is overestimated and exaggerated. We are not losing the essence of psychiatry or the social dimension of psychiatry which are still at the core of the clinical encounter.

Actually, Simon argued that the social dimension is something that attracts people to clinical practice and won't be made irrelevant by neuroscience or the RDoC. Diagnosis presents challenges but is an important part of education for psychiatrists and it captures overlaps among mental health issues that are important and useful.

Tuesday 16 June 2015

Bayesian Inference, Predictive Coding and Delusions

This is our third of a series of posts in the papers published in an issue of Avant on Delusions. Here Rick Adams summarises his paper (co-written with Harriet R. Brown and Karl J. Friston) 'Bayesian Inference, Predictive Coding and Delusions'.

I am in training to become a psychiatrist. I have also recently completed a PhD at UCL under Prof Karl Friston , a renowned computational neuroscientist. I am part of a new field known as Computational Psychiatry (CP). CP tries to explain how various phenomena in psychiatry could be understood in terms of brain computations (see also Corlett and Fletcher 2014, Montague et al., 2012, and Adams et al. forthcoming in JNNP).

One phenomenon that ought to be amenable to a computational understanding is the formation of both ‘normal’ beliefs (i.e. beliefs which are generally agreed to be reasonable) and delusions.

There are strong theoretical reasons to suppose that we (and other organisms) form beliefs in a Bayesian way. Thomas Bayes was an 18th century mathematician who tackled ‘inverse’ probability problems. ‘Direct’ probability is the probability of some data given their causes, e.g. a fair coin toss resulting in a ‘head’. Inverse probability is the opposite, e.g. the probability of a coin being fair, given a particular distribution of heads and tails. Bayes showed how to calculate the likely causes of data given the data and pre-existing beliefs (called ‘priors’) about the existence of those causes.

This inverse (now known as Bayesian) probability problem confronts all organisms with sensory systems: they collect sensory data and wish to infer the causes of those data. Sensory data are often extremely complex and noisy, and in this case appropriate prior beliefs are required to interpret them. ‘Beliefs’ used in this sense refer to probability distributions, not folk psychological statements.

Thursday 11 June 2015

Conference on Psychiatry and Society (1)

On 12th May 2015 in London I attended the "Psychiatry and Society" conference organised by the Psychiatry Section of the Royal Society of Medicine. Here I will summarise the talks I heard in session 1, emphasising those themes that are close to our blog readers' hearts.

Session 1: Genetics and Neuroscience of Mind, Self and Behaviour

Neuroscientist Jean-Pierre Changeux (pictured above) kicked off the conference with a presentation entitled: "What neuroscience can tell us about mind and behaviour?" He presented the brain as a very complex physico-chemical system about which we know a lot already but not everything. This is because the brain is the product of the integration of different types of evolution occurred in millions of years (evolution of species in terms of variability of genome, ontogenetic development in terms of variability of connections, evolution of thought in terms of variability of spontaneous activity and synaptic efficacies, and social and cultural evolution in terms of variability of synaptic efficacies and extra cerebral memories).

The differences in the forms of evolution that interest the brain and the levels of analysis are reflected in different brain disorders. There are single gene ones (such as microcephaly) but conditions such as autism do not involve just one gene, rather more than 500 predisposition genes. In such cases, one can't say: "one gene, one brain". In some other disorders, due to brain lesions, one can lose the capacity to read (alexia) without losing the capacity to write (agraphia) which shows post-natal selection of cultural circuits. In the case of pathological gambling and other cases of loss of control, automatic behaviour prevails over controlled behaviour and paralimbic abnormalities are detected. In sociopathy and other disorders affecting interactions with other people we find problems with the patterns of connections underlying conventional and ethical norms.

Next, philosopher Jonathan Glover (in the picture above) spoke about "Neuroscience, agency and responsibility". He argued that there is a paradox in psychiatry. One the one hand, for many disorders such as addiction, recovery seems to depend on agency. On the other hand, neuroscience tells us that agency does not work in the way we think, and that the will itself may be an illusion. So it is important to understand the role of neuroscience in understanding agency and responsibility. One important question is whether we are responsible for what we do when we are compelled to act or behave in that way. What makes some action something irresistible as opposed to something that was not resisted? Another important question is what impact ability and motivation have on action.

Tuesday 9 June 2015

The Causal Role Argument Against Doxasticism About Delusions

This is the second in a series of posts on the papers published in an issue of Avant on Delusions. Here Kengo Miyazono summarises his paper (co-written with Lisa Bortolotti) 'The Causal Role Argument Against Doxasticism About Delusions'.

Doxasticism about delusion is the claim that delusions are beliefs. Delusions are usually regarded as beliefs in psychiatry. For instance, in the DSM-5 delusion is defined as a 'false belief based on incorrect inference about external reality that is firmly held despite what almost everyone else believes and despite what constitutes incontrovertible and obvious proof or evidence to the contrary' (American Psychiatric Association 2013: 819). Moreover, cognitive scientists working on theories of delusion formation assume that the mechanisms responsible for the formation of delusions are also the mechanisms responsible for the formation of beliefs (Coltheart 2007; Corlett et al. 2010).

However, doxasticism is not very popular among philosophers. Greg Currie and colleagues (Currie 2000; Currie and Jureidini 2001) argue that delusions are not beliefs but imaginings. Andy Egan (2009) thinks that they are 'bimaginations' (i.e., they are the states with some belief-like features and some imagination-like features). Eric Schwitzgebel (2012) suggests that they are 'in-between beliefs' (i.e., they are not beliefs, but not non-beliefs). Jakob Hohwy and colleagues (Hohwy and Rosenberg 2005; Hohwy and Rajan 2012) propose that they are perceptual inferences.

The main philosophical argument against doxasticism is what we call 'the argument from causal role'. The argument goes as follows.
Argument from Causal Role

(P1) Many delusions fail to play belief-roles.
(P2) A mental state is a belief only if it plays belief-roles.
(C) Therefore, many delusions are not beliefs.

Here, 'belief-roles' refers to the distinctively belief-like causal roles. Premise (2) is entailed by functionalistic theories of belief, including representational functionalism and dispositional functionalism. Eric Schwitzgebel (2012) calls them 'token-functionalisms'. Premise (1) is supported by clinical observations. It is commonly assumed that playing belief-roles includes being more or less sensitive to evidence, being more or less coherent with other beliefs and guiding action in relevant circumstances. What clinical observations often reveal is that delusions lack these features.

In our new paper 'The Causal Role Argument against Doxasticism about DelusionsLisa and I (pictured above) critically examine the argument from causal role and show that its premises might be resisted.

Thursday 4 June 2015


In this post, Piers Benn presents his book entitled Commitment. Piers (pictured above) is a Visiting Lecturer at Heythrop College, University of London, and Adjunct Professor at Fordham University New York, based at its London Centre. He was a lecturer in philosophy and in medical ethics in previous posts.

The title I chose for my book for the Acumen Press Art of Living series was Commitment (2011) but in many ways it could equally well have been Doubt. Thinking about it afresh after a few years away from it, I can see that it was largely a philosophical attempt to defend various forms of doubt, as a state forced upon us by judicious reasoning rather than desirable in itself. I focused on three main areas where the tension between commitment and doubt felt particularly powerful: love, work and faith.

I wanted to uphold the value of commitment, but only when properly thought through. Commitment can be energising, morally improving and conducive to a deeply satisfying sense of meaning, purpose and value. But there are sometimes good reasons why the temptation to commit oneself should be resisted. I put the point rather grandly, saying that where there is a conflict between the pursuit of truth and the pursuit of happiness, the pursuit of truth should win out.

Tuesday 2 June 2015

From the Internal Lexicon to Delusional Belief

Max Coltheart

This is the first in a series of posts on the papers published in an issue of AVANT on Delusions. Here Max Coltheart summarises his paper  'From the Internal Lexicon to Delusional Belief'.

Ten years ago, in an article on the two-factor theory of delusion, I wrote: 

'Suppose that as we go about everyday life we use an internal model of the world (Gray 1995Sokolov 1963) to continuously predict what we will experience next. These predictions will normally be fulfilled, but occasionally not: occasionally something not predicted by the internal model occurs. That event indicates that there is something wrong with the database of beliefs that the model uses to predict what will happen next in the world. So the database needs to be fixed (by modifying existing beliefs or adopting new ones) so that it becomes compatible with the unexpected event' (Coltheart 2005).

As I emphasize in my Avant article, this is the model of belief formation on which the two-factor theory of delusional belief has been based since its inception (Langdon and Coltheart 2000; Davies et al. 2002). The key point here is that in cases of delusion, the prediction error that leads to the adoption of some new belief – the delusional belief – occurs because of some defect of perceptual or affective processing: this defect is Factor 1 in the two-factor account. For example, people predict that when they encounter a person emotionally close to them – a spouse, for example – a response of the autonomic nervous system will occur (since that is what usually occurs when one encounters such a person). 

If a neuropsychological impairment is suffered which disconnects the face recognition system from the autonomic nervous system, this prediction will fail when the spouse is encountered. That prediction error prompts the idea 'That is not my wife, it is a stranger', since if the encountered person were indeed a stranger that would explain the absence of autonomic response. The belief here is the Capgras delusion. But the absence of autonomic response – Factor 1 - is not sufficient to cause Capgras delusion, since patients with ventromedial frontal damage also lack this autonomic response to familiar faces, yet are not delusional. So, the two-factor theorist argues, a second factor must also be present, a Factor 2, which is an impairment of the normal processes of belief formation – perhaps always associated with specific damage to right dorsolateral prefrontal cortex (Coltheart 2007).

We have proposed this type of analysis for a variety of monothematic delusions. For each delusion, we have:

(a) identified or proposed a particular neuropsychological impairment that would cause a prediction error that prompts the delusional idea;

(b) shown or argued that each impairment has been reported in patients who are not delusional;

(c) and argued that in all of these delusional conditions a Factor 2 which is impaired belief evaluation is also present which is responsible for the delusional idea being adopted as a delusional belief.

Hence two-factor theorists have always held the view that prediction error is a key component in the genesis of delusional belief, whilst arguing that this is not sufficient for the causation of such beliefs: two factors, not one, are necessary. Fletcher and Frith have agreed: 'two deficits are necessary to explain these delusions: a primary deficit (paralysis or memory loss) and a failure to suppress the implausible responses that result from
this deficit. In the case of neurological patients, false beliefs seem to derive from the coincidence of damage in two locations, with the abnormal belief formation associated with damage to the prefrontal cortex' (2009: 50-1).

I know of no account of delusional belief other than the two-factor theory that has been successfully applied to the explanation of such a range of monothematic delusions.