Introduction from The Clearing
We are delighted to publish this important paper, Madness, Science and the Crisis in Psychiatry by Phil Thomas. His sober, and sobering, analysis of the crisis in psychiatry is both illuminating and necessarily thought provoking for all of us. It touches deeply on our common humanity.
The paper is also highly relevant in the light of the controversy that has broken out with the publication of the DSM 5. The reaction in the US of the National Mental Health Institute to DSM 5 – dismissing it by insisting that only neuroscience has the capacity to diagnose mental illness – is in itself profoundly symptomatic of psychiatry’s deep on-going crises.
Underlying the public face of this crisis there is something much less well known : the growing number of studies in the developed world which show how shockingly poor the outcomes are for those given pharmacological treatment for their madness. In using this word we are following the survivors of psychiatry movement who use it to describe states of extreme distress and disturbance. The evidence is mounting that people have much better outcomes in their life and in their health when they avoid taking medication for their experience of madness. Yes, read that sentence again and then read the paper.
But interestingly enough, the crisis in psychiatry is also attracting research and exposure in other academic fields. At Stanford University Tanya Luhrmann, a psychological anthropologist, has undertaken extensive research with women experiencing madness on the street. She argues in her paper ‘Beyond the Brain’ in the Wilson Quarterly that the biomedical paradigm is breaking down: “It is now clear that the simple biomedical approach to serious psychiatric illnesses has failed in turn. At least, the bold dream that these maladies would be understood as brain disorders with clearly identifiable genetic causes and clear, targeted pharmacological interventions (what some researchers call the bio-bio-bio model, for brain lesion, genetic cause, and pharmacological cure) has faded into the mist.”
Here in the UK, Ian McGilchrist’s scholarly book on the Right Brain/Left Brain question, The Master and His Emissary made a huge impact on publication. Now he has joined forces with the Director of Royal Society of the Arts’ Social Brain Centre, Dr Jonathan Rowson to write a paper titled Divided Brain, Divided World. Their paper starts: “The notion that we are rational individuals who respond to information by making decisions consciously, consistently and independently is, at best, a very partial account of who we are. A wide body of scientific knowledge is now telling us what many have long intuitively sensed – humans are a fundamentally social species, formed through and for social interaction, and most of our behaviour is habitual”.
There is in all this also a significant challenge to psychoanalysis, particularly in its historic British formation. For it is reasonable to argue that the British variant of psychoanalysis contains several strands that have historically become entangled with biomedical notions of what humanity is, and what underlies experiences of extreme distress and disturbance . What comes to mind is Freud’s over reliance on the mechanics of drive theory, the Kleinian insistence on envy and hatred in infancy, Kernberg’s argument that underlying all borderline conditions is an excess of aggression, and the language of treatment, scientific meetings, and technique.
This critique is also valid in relation to the current enthusiasm for a marriage between psychoanalysis and neuroscience.
But perhaps the influence of this old paradigm is more widespread and insidious than the more obvious examples mentioned above. Could it be that the biomedical model of distress and disturbance also offers to psychotherapists (of all persuasions) certain comforts and defences. Chief among these we think, might be that such a paradigm offers a life line, a safety harness, a soothing brew, to the raw, actual, alive encounter between two human beings when extreme feelings, extreme states of mind are in the room. How helpful, how safe it can then feel to reach for a diagnosis from the DSM or from one of its psychoanalytic equivalents.
When in the presence of biomedical thinking, we are in danger of losing sight of what the core of our profession is, and how powerful human connection can be. Phil Thomas’s paper is a cogent marshalling of research and thought that calls into profound question the ties between biomedical positions and our therapeutic work with others.
Madness, Science and the Crisis in Psychiatry
by Phil Thomas
Psychiatry is in crisis; at a turning point. For one hundred and fifty years it has been engaged in a fruitless search for the biological basis of madness[i]. Evidence of this crisis is to be found in the National Institute of Mental Health’s (NIMH) decision not to use the American Psychiatric Association’s DSM-5 published on 18th May 2013. It can also be found in the highly critical responses to DSM-5 of organisations as diverse as the Hearing Voices Network[ii], Mental Health Europe[iii], and the Critical Psychiatry Network. This is no guild dispute between clinical psychologists and psychiatrists. Four editorials or special articles published by the British Journal of Psychiatry over the last five years (Craddock et al, 2008; Bullmore et al, 2009; Oyebode & Humphreys, 2011; Bracken et al, 2012) have acknowledged that psychiatry is in crisis. These articles offer different analyses of the crisis, and different solutions, but the fact is that scientific research has failed to reveal the causes of madness, and confidence in the quality of the scientific evidence used to justify the treatment of people with psychiatric diagnoses has been seriously undermined.
Despite this the search for the causes of madness will continue through the BRAIN Initiative (Brain Research through Advancing Innovative Neurotechnologies) and Human Brain Project [iv] – both launched this year. The rise of neuroscience is generating a view of humanity and its consciousness couched solely in biological terms. Our most deeply felt and meaningful experiences are reduced to the passage of sodium and potassium ions in and out of brain cells. I defy anyone who sees the tears falling from my eyes as I listen to Sophie and Octavian’s ecstatic duet at the end of Strauss’s Der Rosenkavalier to persuade me that this is so. The tapestry of experiences out of which our consciousness is woven, how others relate to us, whether they love and care about us or hate and reject us, whether they nurture and support us or abuse and oppress us, all these aspects of being human are based in brain processes. This is a brain in a tank, a brain ruptured from the immediacy of the world as we experience it, and the things in it that matter for us. It is impossible to fathom their relevance to our experience of the world. Neuroscience is incapable of delivering a full account of the embodied and encultured complexity of human consciousness (Tallis, 2011).
What does science have to say about our consciousness? More to the point, what has it contributed to the way that psychiatric knowledge is used in relation to madness? I will start this essay by showing that science has brought us no closer to understanding madness and distress. An important consequence of this is that there is no evidence that technological interventions based in scientific theories about madness are effective. In fact it is the human aspects (or non-specific factors) of care – human relationships, trust, hope, and the placebo effect[v] – that are effective. The conclusion to be drawn is that the technological paradigm in psychiatry is in crisis. Technological psychiatry, in the guise of evidence-based practice, towers over the landscape of mental health work, and for this reason the crisis has implications for all who work in the field of mental health. To understand why, I will set out two problems raised by scientific studies of consciousness, interiority and determinism, that ultimately lie beneath psychiatric and mental health practice. These direct our attention away from the importance of contexts and human agency in understanding madness. I will end by posing a number of questions that arise from this analysis with the purpose of encouraging further debate and discussion.
The Failure of the Technological Paradigm
With a few notable exceptions, some varieties of psychoanalysis and existentialism (Laing, 1960[vi]) and some schools of social psychiatry), psychiatry has almost exclusively seen madness through a scientific lens. This orientation, or the technological paradigm (Thomas, Bracken & Timimi, 2013), has yielded valuable insights into the nature of diseases of the brain in neurology, as well as dieases of the heart, liver and kidneys. These insights, driven by developments from the human genome project, are revolutionising our understanding and treatment of diseases like cancer. In psychiatry, the technological paradigm is the dominant paradigm, what Thomas Kuhn (1962) called ‘normal science’. It maintains that the principles of scientific thought and study that have been so successful in other fields of medicine can be applied to problems with our thoughts, feelings and relationships. What was once biological psychiatry has been taken over by neuroscience, cognitive science and molecular genetics. The paradigm makes the following assumptions (Bracken et al: 2012):
1. Madness arises from faulty mechanisms or processes involving specific [vii] abnormal physiological or psychological events occurring within the individual.
2. These mechanisms or processes can be modelled in causal terms. They are not context-dependent.
3. Technological interventions are specific and instrumental, and can be designed and studied independently of non-specific factors (relationships, contexts and values).
However, scientific evidence simply fails to support these assumptions. What evidence is there that psychiatric diagnoses like schizophrenia are caused by specific disturbances in brain function? This question concerns the issue of the validity of psychiatric diagnosis.
The problem of validity
Validity is at the heart of the claim for the scientific basis of all diagnoses in medicine. This concerns the extent to which there is evidence that people with a given diagnosis differ biologically from those who do not have the condition. The validity of a diagnosis stands or falls depending upon whether it can be tied to an underlying causal pathological mechanism. In psychiatry this has proved impossible to achieve. Since 1970, there have been four major papers in the psychiatric literature dealing with this issue; Robins and Guze (1970), Kendler (1980), Andreasen (1995) and Kendell and Jablensky (2003)[viii]. These papers are high on aspiration but low on evidence. Robins and Guze’s (1970) highly influential paper on the validity of psychiatric diagnoses refers to laboratory studies, including chemical, physiological, radiological and anatomical findings, as well as psychological tests, and family studies of the inheritance of psychiatric disorders. They assert that since psychiatric illnesses like schizophrenia run in families, they must have a biological basis, yet there is no evidence for this (see Chapter Six of Mary Boyle’s,1990, seminal Schizophrenia: A scientific delusion? and more recently Jay Joseph’s, 2003, The Gene Illusion, and for an equally pessimistic geneticist’s view, Goldman, 2011)
Kendler’s (1980) overview confirmed that early biological studies failed to establish the construct validity of schizophrenia. Nancy Andreasen’s (1995) American Journal of Psychiatry editorial promises future riches through molecular genetics, neurochemistry, neuroanatomy, neurophysiology and neuro-imaging, but she concedes that the long-hoped-for laboratory tests anticipated by Robins and Guze (1970) had not materialised; ‘…we still lack definitive diagnostic tests equivalent to the measurement of blood sugar for diabetes or the ECG for myocardial infarction’ (Andreasen, 1995:161). It is worth noting that she was writing at the mid-point of the ‘Decade of the Brain’, and was up to her neck in brain studies of schizophrenia, with the latest generation of imaging technologies to map the ‘broken brain’. Fifteen years on, has neuroscience delivered the promised riches?
Anckarsäter (2010) used the Robins and Guze (1970) criteria for validity to assess meta-analyses and review papers for neurobiological markers and treatment effects in major psychiatric disorders. Apart from conditions like Huntington’s Chorea, which has an established basis in molecular genetics (and which is arguably a neurological condition), no laboratory marker has been found to support the construct validity of any psychiatric diagnosis. Neither is there any evidence to support the view that they have specific outcomes and responses to treatment. He writes:
Despite the obvious lack of empirical support for today’s diagnostic models, it is not without a sense of heresy one has to conclude that most, if not all, of the mental disorders known today, i.e. the categories that have structured both the psychiatric praxis and the research into their prevalences, patterns of distributions, “comorbidities”, and aetiologies, simply do not exist as such.
Although the literature abounds with studies claiming to have found differences in the brains of those with a diagnosis of schizophrenia and those who do not, replication studies either fail to confirm initial findings, or are inconclusive. Even the most recent NICE guidelines on the treatment of schizophrenia acknowledge the lack of evidence for a biological basis for schizophrenia:
The possible causes of schizophrenia are not well understood. Research has attempted to determine the causal role of biological, psychological and social factors. The evidence does not point to any single cause. Increasingly, it is thought that schizophrenia and related psychoses result instead from a complex interaction of multiple factors.
(National Collaborating Centre for Mental Health, 2010:22)
Neuroscience has failed to demonstrate that people who have the diagnosis of schizophrenia are biologically different from those who don’t. Psychiatric diagnoses do not carve nature at the joint. Kendell and Jablensky (2003) acknowledge that since Robins and Guze’s (1970) paper, the validation of the diagnosis of schizophrenia remains unresolved, either in terms of its symptom profile, or its genetic (and thus biological) basis. They note that an ‘… air of disenchantment…’ is apparent ‘…in the light of the failures of the revolutionary new nosology [classification] provided by DSM-III and its successors to lead to major insights into the aetiology of any of the main syndromes.’ (Kendell & Jablensky, 2003:7) They conclude that psychiatry is two hundred years behind other branches of medicine because it can only define most of its conditions in terms of syndromes (i.e. groups of symptoms that tend to occur together).
…most contemporary psychiatric disorders, even those such as schizophrenia that have a pedigree stretching back to the nineteenth century, cannot yet be described as valid disease categories.
It is worth stressing the provenance of this text. The late Robert Kendell, formerly Professor of Psychiatry at Edinburgh University, was a leading international authority on the role of diagnosis in psychiatry, and was thus very well placed to express his opinions about its shortcomings. I should declare an interest here. In the early 1980s, I worked with Professor Kendell, when I was a lecturer in Edinburgh, on the use of linguistic analysis as a diagnostic aid in schizophrenia. Needless to say, we didn’t have a great deal of success (see Fraser et al, 1986). I should also point out that I spent a week in Nancy Andreasen’s department in the University of Iowa in 1986, where I was trained in the use of her clinical rating scales for thought disorder and negative symptoms. Despite the failure of scientific research to establish the validity of psychiatric diagnoses, those currently involved in neuroscience research in psychiatry still maintain, as did Andreasen twenty years ago, that it is only a matter of time before neuroscience will lift the veil of madness (Bullmore et al, 2009).
If you want further proof of the crisis in psychiatry over the scientific status of diagnosis, you need look no further than the National Institute of Mental Health’s (NIMH) decision at the end of April 2013 not to use the American Psychiatric Association’s DSM-5 due to be published towards the end of May 2013. In a blog dated 29th April 2013 (http://www.nimh.nih.gov/about/director/2013/transforming-diagnosis.shtml) the Director of NIMH, Thomas Insel, makes it clear that the reason NIMH has opted for its own Research Diagnostic Criteria (RDoC) is because they believe psychiatric patients deserve something better than DSM-5. Psychiatric diagnoses, he correctly points out, are symptom-based, and by implication lack validity. He clearly has his eye on some of the $100 million pledged by President Obama for the BRAIN initiative on 2nd April this year ( http://www.whitehouse.gov/infographics/brain-initiative), in his quest for the neuro-validity of psychiatric disorders[ix].
The problem of the effectiveness of technological interventions
If scientific psychiatry has failed to find the cause of schizophrenia or depression, then it should come as no surprise to discover that it has failed to confirm the effectiveness of treatments based in (unproven) scientific theories of madness. Science in the guise of evidence-based medicine investigates the efficacy and effectiveness of different medical treatments and therapy. In theory, double-blind randomised controlled trials (RCTs) reduce the influence of non-specific factors on outcome like the placebo effect and therapist variables, which get in the way of assessing the effectiveness of the specific elements of treatment or therapy[x]. Meta-analyses pool data from many such studies, so that we can know with even higher degrees of certainty what is effective. A recent paper in the British Journal of Psychiatry, co-authored by thirty members of the Royal College of Psychiatrists (Bracken et al, 2012) draws attention to the growing evidence from evidence-based medicine that fails to support the technological paradigm in psychiatry. In fact it demonstrates the importance of the human elements of care in helping people to recover from conditions like depression and schizophrenia.
We (Bracken et al, 2012) examined twelve meta-analyses of drug treatments and psychotherapy for depression. For drug treatment, differences in outcome between active drug and placebo groups are minimal (Andrews, 2001; Kirsch & Saperstein, 1998; Kirsch et al, 2008). Even in the most severely depressed people, where active treatment-placebo differences are reported as clinically significant, these differences are small, and may be due to the reduced responsiveness of very depressed people to placebo rather than the fact they respond better to active treatment. Similar findings emerge for different forms of psychotherapy. Advocates of CBT argue that it is effective because it specifically rectifies faulty cognitions that are believed to cause depression. Several studies have shown that most of these ‘specific’ elements can be dispensed with without adversely affecting outcome (e.g. Jacobson et al, 1996; Longmore & Worrell, 2007). More generally, there is overwhelming evidence that non-specific factors such as the quality of the therapeutic alliance as seen by the person receiving therapy have a more potent effect on therapy outcome than specific therapeutic elements (Wampold, 2001; Castonguay & Beutler, 2005; Stiles et al, 2008).
The same holds for recovery from schizophrenia. At face value most RCTs suggest that neuroleptics are superior to placebo in the short-term management of the condition. However, as Joanna Moncrieff (2008) points out, most of these studies last only a few weeks, whereas most episodes of schizophrenia last for years. Evidence from the very small number of RCTs that followed up patients for a year or more provide a very different view of the clinical effectiveness of these drugs. Moncrieff identified only three studies since 1967 that followed up acutely psychotic patients for a minimum of one year (May et al, 1981; Rappoport et al, 1978; Schooler et al, 1967). All three found that although active treatment groups improved more rapidly than placebo groups in the early weeks, a year later these differences disappeared. One study (Rappoport et al, 1978) found that only 27% of the placebo group were readmitted after a year, compared with 62% of people on active treatment. Those who were given placebo and remained off active treatment over the follow-up period showed greater clinical improvement and better adjustment in the community compared with active treatment groups. There is growing evidence that people with the diagnosis of schizophrenia, who avoid long-term treatment with neuroleptics, do better (Bola & Mosher, 2003; Lehtinen et al, 2000). The most recent evidence from Martin Harrow’s long-term follow-up studies of people with the diagnosis of schizophrenia in Chicago show that a substantial proportion have better clinical and social outcomes if they remain off neureolptic medication (Harrow et al, 2007) These benefits persist at twenty years (Harrow et al, 2012). This is vitally important given the evidence that the long-term use of neuroelptic drugs is associated with increased risk of cardiovascular disease and diabetes (Casey et al. 2011), and a significant reduction in life expectancy, on average 16 years or more, in people with schizophrenia (Wildgust et al 2010; Chang et al (2011). Finally, there is growing recognition that personally meaningful recovery from serious mental disorder is not necessarily related to the specific treatments that are prescribed (Davidson, 2003). Research also points to the importance of the therapeutic alliance in determining outcomes (Frank & Gunderson, 1990).
Why has the technological paradigm failed?
This should come as no surprise. If there is no biological basis for schizophrenia, then what grounds are there to expect that other than the soul-numbing properties of neuroleptic drugs (which a small number of people may find marginally helpful), these drugs should be effective in treating the condition? This is further evidence that the paradigm has failed. Contrary to those who argue that it’s simply a matter of (yet more) time, and that the investment of (even vaster) sums of money in neuroscience, such research will at some future point reveal the cause of madness, I am deeply sceptical that this will ever happen. In any case, pursuing a narrow neuroscientific agenda in the hope of discovering the cause of madness obscures the moral basis of our relationship to those who experience it. This will become apparent if we examine the first two assumptions of the technological paradigm that I presented earlier. Here they are again: first, madness arises from faulty mechanisms or processes involving specific abnormal physiological events occurring in the individual, and second: these mechanisms can be modelled in causal terms. They are not context-dependent. I will argue that the first of these assumptions hinges on the importance neuroscience attaches to interiority, and the second on the role of determinism and causality in science.
Science and Interiority
A full discussion of interiority is beyond the scope of this essay[xi], but our contemporary preoccupation with the inner world of the mind and its biological basis in the brain begins in the seventeenth century with the philosopher René Descartes. He was preoccupied with the question of certainty; how can we be sure that our inner view of the world is an accurate and truthful one? The answer, claimed Descartes, was by turning away from the world and looking inwards to scrutinise the contents of consciousness without reference to those aspects of the external world that they represent. This turning in made it possible to think of the mind as a ‘thing’ (albeit a very strange sort of thing without physical qualities) that could be studied through science.
The influence of this idea can be traced through most forms of psychology (except behaviourism), psychoanalysis, some forms of phenomenology and more recently cognitive neuroscience. The latter uses a computer metaphor of mind, which sees consciousness as the outcome of information processed by modules in the brain. This has provided the impetus for functional brain imaging studies that claim to reveal the modules that ‘light up’ or are active when we look at a photograph of the person we love (Bartels & Zeki, 2000), the intense emotions we experience when we listen to a piece of music (Salimpoor et al, 2013), or when someone with a diagnosis of schizophrenia hears voices (van Lutterveld et al, 2013). The mind/brain (and the trend in neuroscience is to replace the former with the latter) is the seat of our consciousness and all it contains. Everything about us – our thoughts, emotions and relationships, our madness and distress, our aesthetic preferences, even our religious and spiritual beliefs – can be accounted for by the physical processes that occur in the one and a half kilos of goo contained within our skulls.
There is, however, an important consequence of interiority. It overlooks the fact that consciousness, the content of our mental worlds, is tied to what goes on outside our heads. The neuroscientist and philosopher Alva Noë (2009) argues that we are wrong to assume that consciousness can be accounted for in terms of brain activity alone. The brain is a necessary condition for consciousness, but it isn’t a sufficient condition. If we are to understand consciousness, we have to understand how we respond to the world we find ourselves in, how we act, respond and behave, especially to the others around us. In other words, consciousness is something we do. We do not passively experience consciousness as a result of causal processes the brain.
This has a number of implications. In philosophical terms it draws attention to the importance of intentionality. The thoughts, images, emotions and images that crowd our consciousness are not solitary fragments created by the physical processes in our brains, severed from external referents. They are about things, usually, not always, things in the world outside, but especially things that matter to us. This leads to the next point. Insofar as consciousness is concerned with the world we find ourselves in, it is also concerned with the way the world stands out for us as meaningful in our attempt to understand it and find our way around it physically though our bodies[xii], emotionally and interpersonally. For this reason, it is important we are aware that our preoccupation with interiority has the consequence that we disregard the importance of the world in understanding consciousness. Consciousness without a world is life without meaning. ‘World’ here refers not just to the physical world of objects, landscapes, heavens and universe, but our diverse historical, cultural and political contexts. ‘Historical’ includes group and personal narratives. Neuroscience writes all this out of the frame, creating a dangerous delusion, fraught with moral peril, that we can explain madness without reference to these contexts. I will return to the moral peril shortly.
Science and Determinism
Determinism is the view that all events in the natural world are effects. The provenance of this belief is ancient, but its rise to prominence in science can be traced back to Isaac Newton, whose work in the second half of the seventeenth century (The Mathematical Principles of Natural Philosophy) set out the laws of motion and gravitation. This made it possible to describe and predict the motion of celestial bodies. In science, determinism is linked to the idea that there are fundamental laws of nature that make it possible to predict the occurrence of an event if we can provide a full account of the physical circumstances immediately preceding it. Its most extreme manifestation in physics is the theory of everything, which holds that if we have a full account of all known physical phenomena and could link these together, we could in theory predict the outcome of any experiment ever carried out.
Determinism has important consequences for our understanding of ourselves. A current theme in some areas of neuroscience and neurophilosophy runs as follows. Our mental states have physical consequences. For example, I was so enraged by a politician I heard being interviewed on the radio that I kicked the kitchen door in anger, bruised my toe and scraped the paint. If we hold the belief that our mental states can bring about changes in the physical world (the swelling and bruising of my left big toe, a scuff mark on the door) then it must follow that mental states in turn are physical events. In other words, mental states are caused by physical events in my brain – the exchange of sodium and potassium ions across the axon membrane and so forth. This, as Raymond Tallies (2011) argues, gives rise to a causal ancestry of consciousness that passes way beyond the boundaries of what you would consider to be you:
You – your brain, your mind, your consciousness – are wired into the universe. And the wiring does not simply connect you to your body, or even your immediate environment; it goes all the way back to the initial conditions of the universe. In short, you are stitched into a seamless flow of material events subject to the laws of nature. Your actions cannot in any way be exempt from these laws. You are just a little byway in the boundless causal nexus that is the material world.
In this neuroscientific view of consciousness, free will is an illusion. Our experience of agency is an illusion, a post hoc rubber-stamping of physical events that have already taken place in our brains before we experience them. All the contents of our consciousness, our beliefs, intentions, desires and actions are nothing more than the outcome of physical processes in the brain. We could in principle predict all these aspects of our consciousness if we had a full understanding of all the natural laws governing the physical events in our brain, and its initial state (Minority Report eat your heart out!). This is absurd. One way around this is the recognition that there are different types of causality; non-intentional and intentional (Bolton and Hill, 1996). Non-intentional causality concerns events in the physical world that follow natural laws. Intentional causality concerns human agency. For example, we know that the reason that day follows night is because of the natural laws that govern the rotation of the earth. We can explain how this happens through the laws of physics. As an example of non-intentional causality, it has nothing to do with human intentions or actions. On the other hand, last night I set my alarm clock because I had to get up early this morning to catch a train. I didn’t want to be late. The reason I carried out this action is understandable through my intention to be present at a meeting I wanted to attend. The psychotherapist Jeremy Holmes (2000) points out that intentional causality underlies our understanding of human agency in narrative. It enables us to see ourselves and others as having the freedom to make decisions, and thus act as moral beings through the choices we make. Being human means having agency, and thus having to face and make choices and decisions to do things, or not to do things. This lies at the heart of our lives as moral beings. The decisions we make have implications for others as well as ourselves; some good, some bad.
Science in Context
By now you may think that I am anti-science. I am not. I am opposed to scientism, the belief that science is ultimately capable of answering all human problems. Some forms of science have made valuable contributions to our understanding of madness. For example, recent scientific research has opened up perspectives on madness that force us to consider the moral basis of our engagement with people who suffer madness and distress. John Read and colleagues (2005) have reviewed the relationship between child abuse, psychosis and schizophrenia. Although the diagnosis of post-traumatic stress disorder (PTSD) has drawn attention to the importance of trauma in a wide range of psychiatric disorders, the main focus of this work has been on non-psychotic conditions. Relatively little attention has been paid to the role of trauma in ‘schizophrenia’. They found clear evidence of a link between childhood abuse and schizophrenia in the scientific studies they reviewed, and a particularly strong relationship between childhood abuse and hearing voices across diagnostic boundaries. They also found a strong relationship between abuse and delusional beliefs. Some studies indicated that the content of delusions and voices in people with a history of childhood sexual abuse was related to the abuse, with references to ‘evil’ or ‘the devil’.
They (Read et al, 2009) also identified eleven epidemiological studies that investigated the relationship between psychosis and childhood adversity in the general population. Ten found significant associations between childhood ill-treatment and psychosis. The evidence indicates that the relationship between psychosis, schizophrenia and childhood abuse and neglect is at least as strong as it is for more common psychiatric conditions. Large-scale population studies suggest that the link may be a causal one – that the more severe and persistent the abuse, and the more varied it is, the stronger the relationship with adult psychosis. Abuse takes many forms, including the racial abuse, or racially motivated attacks and discrimination regularly experienced by people from BME communities. Not surprisingly, similar relationships have emerged in epidemiological research into the impact of racism and the mental health of people from BME communities. Karlsen et al (2005) examined the impact of racism on the mental health of different ethnic groups in England. African-Caribbean people were most likely to report racial harassment, followed by Pakistanis and Indians. The risk of psychosis was significantly associated with the experience of verbal racial abuse, physical assaults and work-place discrimination. Experiences of racial abuse (verbal or physical) doubled the risk of psychosis compared with those who had no such experiences. In Holland, Janssen et al (2003) carried out a longitudinal study of nearly 6,000 people. In people from BME communities the rate of delusional beliefs in people who reported one instance of discrimination (0.9%) was nearly twice as high as the rate in those who reported none. In addition, 2.7% of those who experienced discrimination in more than one domain showed evidence of delusional beliefs (but not hallucinations).
A turn to neuroscience will see psychiatry enter an intellectual and moral cul-de-sac. It will shut itself off, away from the world of human contexts, of oppression and abuse that epidemiological science has revealed to be an important feature of madness. It will isolate itself in a world remote from the concerns of ordinary people who suffer injustice and inequality. Neuroscientific psychiatry will steal the words from the mouths of the mad. What point is there in speaking the truth about madness if that truth is erased by countless, invisible physical events in the molecules and atoms of our brains? In the introduction to History of Madness Michel Foucault wrote:
‘There is no common language: or rather, it no longer exists; the constitution of madness as mental illness, at the end of the eighteenth century, bears witness to a rupture in dialogue, gives the separation as already enacted, and expels from the memory all those imperfect words, of no fixed syntax, spoken falteringly, in which the exchange between madness and reason was carried out. The language of psychiatry, which is a monologue by reason about madness, could only have come into existence in such a silence.’
Perhaps at last we are beginning to grasp the profundity of that silence. I will finish with some questions raised by this analysis. I am not going to attempt to answer them here, although I am deeply preoccupied by them. There will of course be many other questions that I haven’t thought of and that you will have. The purpose of this essay is to raise questions and evoke your responses, which I very much welcome. Here are my questions.
- Given the problems with neuroscience is there a role for any form of science in helping people who experience madness?
- If so, what sort of science?
- What other ways of knowing about human beings might have a role to play in helping people who experience madness?
- Do the first three questions have implications for the future direction of psychiatry and other professional groups working in mental health services?
- What are the implications of this analysis for the moral basis of our work in helping people who experience madness?
- If there is no clear scientific basis for its use, what role is there for medication in helping people who experience madness?
- What role is there for specific forms of therapy in helping people who experience madness, when the scientific evidence indicates that the human, common factors are more important for outcomes than the specific factors?
- What are the implications of this analysis for the legal role of mental health professionals under the Mental Health Act in detaining and forcibly treating people who are mad (whether in hospital or community)?
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[i] Throughout this essay I will use the words madness and distress in preference to schizophrenia and depression. This is because these words carry no causal assumptions. In addition, groups like Mad Pride (see http://madpride.org.uk/index.php ) have reclaimed the words mad and madness as a form of political action that has similarities to the way that gay activists claimed the word gay.
[ii] http://www.hearing-voices.org/about-us/position-statement-on-dsm-5/ accessed on 22nd May 2013
[iii] http://www.mhe-sme.org/news-and-events/mhe-press-releases/dsm5_more_harm_than_good.html accessed 22nf May 2013
[iv] http://www.whitehouse.gov/infographics/brain-initiative and http://www.humanbrainproject.eu accessed 24th April, 2013. Both have much wider (and potentially sinister) ramifications than the elucidation of madness, but inevitably both will be exercised in this area.
[v] The medical anthroplogist Daniel Moerman calls the placebo effect the ‘meaning’ effect (Moerman, 2002). His work reveal the ubiquity of the effect in all fields of medicine.
[vi] The work of the Scottish psychiatrist R. D. Laing is the most notable exception here. In his early work, (Laing, 1960) he challenged the psychopathological view of madness that dominates psychiatry, arguing that it failed to engage with the meaningful nature of the experience. He drew on object-relations theory, and continental philosophy (especially Heidegger and Sartre) to set out a way of understanding the experiences of madness.
[vii] I use the adjective specific to refer to those elements of therapy that are thought to be effective because they rectify the underlying causes that are believed to be specific to the condition being treated. I use the adjective non-specific to refer to those elements of therapy that are believed not to be related to any specific underlying cause, but which, for other reasons, may nevertheless be effective. The placebo effect is an example of this.
[viii] This work is not the jaundiced scrivening of sceptical social constructivists or antipsychiatrists, but that of leading academic psychiatrists who dedicated their careers to the search for the biological basis of madness.
[ix] The problem of course is that neuroscience and neuogenetics make so many flawed assumptions about the neural basis of consciousness that they cannot be taken seriously, and any hope that they will reveal the neural basis of madness is hopelessly unrealistic. For those interested see my blog on Mad in America, http://www.madinamerica.com/2013/05/why-neuroscience-cannot-explain-madness/
[x] Again, the evidence suggests that in psychiatry this is almost impossible to achieve, see Moncrieff et al (2011) for evidence that this is so, and the consequences, which include inflating the apparent effectiveness of active drugs in antidepressant trials.
[xi] Those interested can turn to Bracken & Thomas (2005; 2008).
[xii] There is neither the time nor space here to dwell on the importance of the body in relation to consciousness. This is explored in the first chapter of Alva Noë’s book. Ian Burkitt’s (1999) excellent Bodies of Thought also dwells on the importance of the body for identity and consciousness.