Pinball Wizards and the Doomed Project of Psychiatric Diagnosis

Philip Thomas, MD

The imminent publication of DSM-5 (due to appear in May) is a call to action for those concerned about the role of diagnosis in psychiatry. A number of campaigns are afoot, including the Committee to Boycott the DSM-5 (see established by Jack Carney, although some are concerned that the committee advocates the use of the ICD in parts of the world where remuneration depends on the use of diagnostic codings. There is also an International DSM-5 Response Committee coordinated by a group of clinical psychologists, and which is in the early stages of coordinating a public campaign to coincide with the launch of DSM-5.

Although its position on the ICD is not yet clear, it’s hard to imagine that the criticisms raised about DSM-5 won’t also apply to the ICD. One of the principal concerns is that both lack any sort of scientific basis. The changes to the DSM also raise the deeply worrying prospect of widespread medicalisation of human variation and yet more neocolonialism by pharma. In this article I want to go back to basics, and ask what is the problem with scientific research in psychiatry? I will do this by examining psychiatric diagnosis in two ways. First, I will examine the failure of research to establish empirical evidence to support the scientific validity of diagnostic categories like ‘schizophrenia’; second, to consider through philosophical arguments why this failure has arisen.

Validity and the Natural Sciences

The DSM claims to be a scientific system of classification. The validity of any system of scientific classification is the extent to which it can be shown to reflect the real world. A good example is Mendeleev’s classification of the chemical elements in the Periodic Table. He noticed that if he arranged the elements according to their atomic numbers, a pattern, or periodicity, was observed so that every eighth member of the series shared roughly similar physical properties. For example, the metal lithium is a light, highly reactive element with the atomic number 3. It shares these properties with the metals sodium (atomic number 11) and potassium (19). Ordering all the known elements at the time into groups based on atomic number, he noticed that there were gaps. His predictions about the properties of these elements were subsequently found to be highly accurate when the missing elements were discovered later on. Furthermore, we now understand why Mendeleev’s system of classification was so precise. It reflected fundamental natural laws concerning atomic structure and the physical properties of matter. Bill Fulford and colleagues (2006) point out that such a rigorous definition of validity is beyond the ability of medical science, which is forced to rely on watered-down concepts of validity, such as construct validity and predictive validity. In empirical terms, both are highly problematic as far as psychiatric diagnosis is concerned.

Predictive Validity

This concerns the extent to which a diagnosis predicts a specific course and outcome for a particular diagnosis. Included in this is a specific response to treatment or other therapeutic interventions. This is a matter of vital importance in psychiatry, where the diagnosis of schizophrenia, if you accept Kraepelin’s view of the condition, is associated with poor outcome and ‘deterioration’ in social and psychological function. The late Robert Kendell (formerly Professor of Psychiatry in Edinburgh University, and an international authority on the problems of classification and diagnosis in psychiatry) drew attention to the importance of predictive validity in psychiatry nearly forty years ago. Diagnostic concepts stand or fall by their clinical value in terms of their accuracy in predicting prognosis and therapeutic response, not because of what validity might tell us about the relationships between the symptoms of a disease and the disease process (Kendell, 1975). This is yet another example of how validity has been watered down in psychiatry compared with other branches of medicine. Is there any evidence that the diagnosis of ‘schizophrenia’ predicts poor outcome?

In his original study, Kraepelin (1913) reported that only 13% of his patients suffering from dementia praecox recovered. The results of four long-term outcome studies of over 1,200 people diagnosed with schizophrenia followed up for between 21 to 32 years challenge this, with recovery rates between 49% to 68% (Bleuler, 1978; Huber, 1979; Ciompi, 1980; Harding, 1987).  In broad terms 50% or more of people with the diagnosis make a significant recovery. Other work confirms that people who are given a diagnosis of schizophrenia have a wide range of outcomes, throwing doubt on the view that the condition has a poor prognosis. The work of Strauss and Carpenter (1974a, 1974b, 1977) in the USA shows that social factors such as work status and social contacts, not illness or diagnostic features, are the best predictors of outcome, along with family environment (Leff and colleagues, 1983).

Cultural factors are important too. Richard Warner (1985) uses results from the international pilot study of schizophrenia to show that the outcome of the condition in non-Western cultures is much better than in the Western world. Recent work confirms this. Kua et al (2003) found that two thirds of their patients in Singapore had a good or fair outcome at twenty years. In Madras, Thara et al (2004) found that only five out of their sixty-one subjects followed up over twenty years had been continuously ill. More than three quarters were in employment. Taken overall the results of these studies indicate that the predictive validity of the diagnosis of schizophrenia is very poor. There is simply no evidence that the diagnosis of ‘schizophrenia’ predicts uniformly poor outcome.

Construct Validity

Setting aside the limitations of predictive validity, the crux of claims for the scientific basis of psychiatric diagnosis is construct validity. There are different definitions of construct validity, but in broad terms it concerns the extent to which a diagnosis is related to an underlying theory about the cause of a disease and (what follows is key) the extent to which there is empirical evidence to support this relationship. Construct validity is at the heart of scientific medicine, because the validity of a diagnosis stands or falls by the extent to which the symptoms of the diagnosis can be tied to an underlying causal pathological mechanism. In psychiatry this has proved impossible to achieve, and we will see that there are philosophical reasons for this. Since 1970 there have been four major articles in the psychiatric literature dealing with the issue of construct validity; Robins and Guze (1970), Kendler (1980), Andreasen (1995) and Kendell and Jablensky (2003). These papers are high on aspiration but low on realisation. 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, this indicates that they have a biological basis. Despite this, fifty years of research has revealed no evidence of a genetic basis for the condition (see for example Jay Joseph’s excellent blog at ) Forty years on from Robins and Guze, what empirical evidence is there that disordered brain function is causally related a psychiatric diagnosis like ‘schizophrenia’?

Early studies failed to establish the construct validity of the diagnosis of schizophrenia (see Kendler’s 1980 overview). Bentall and Jackson (1988) point out that the problem with earlier work was that it failed to take into account the effects of years of toxic and dangerous physical treatment and institutionalisation that patients with the diagnosis experienced. There is growing evidence that physical treatments such as neuroleptic drugs and ECT bring about physical changes in brain structure and function that lead to chronicity. Furthermore, many of the studies were correlational in nature and it is not possible to establish a causal link between the physical ‘abnormality’ under investigation and the diagnosis. Much the same criticism applies to the studies of structural brain changes in people with schizophrenia.

Andreasen’s (1995) editorial in the American Journal of Psychiatry conceded 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). Nancy Andreasen was writing at the mid-point of the ‘decade of the brain’, and was immersed in a range of neuroscientific studies using the latest brain imaging technologies to map the ‘broken brain’. Her editorial refers to ‘unstable genes’, the maturation of the frontal cortex in autism, and evidence from brain potential studies of an auditory sensory memory deficit in schizophrenia, all of which pointed to what she called a ‘second programme’ for the validation of psychiatric diagnoses. This involved careful clinical descriptions (neo-Kraepelinism) tied to external validators including studies based in molecular genetics, neurochemistry, neuroanatomy, neurophysiology and neuro-imaging. These technologies are, she argued, capable of ‘…prob[ing] beneath…surface features and seek to identify actual neural or genetic mechanisms’ (162).

Twenty years since Andreasen’s panegyric where does the validation of the diagnosis of schizophrenia stand? Anckarsäter (2010) used the Robins and Guze 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 diagnostic category in psychiatry, neither is there any evidence to support the view that these categories have specific outcomes and responses to treatment (predictive validity). He summarises the situation as follows:

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.

(Anckarsäter, 2010:61-62)

Although the literature abounds with studies claiming to find differences in the brains of those with a diagnosis of schizophrenia and those not so diagnosed, the results of replication studies either fail to confirm initial findings, or are inconclusive. Even the most recent NICE guidelines on the treatment of schizophrenia (the UK clinical practice guidelines) 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)

Biological research has failed to reveal a point of discontinuity between people with the diagnosis of schizophrenia, and those without. Psychiatric diagnoses like schizophrenia simply 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.

(Kendell and Jablensky, 2003:10)

This is because unlike somatic medicine, psychiatric diagnoses are almost exclusively descriptive and based in symptoms rather than aetiology. A negative interpretation of this is that psychiatry is ‘scientifically primitive’. Until the seventeenth century diagnosis in somatic medicine was almost entirely descriptive, consisting of syndromes as Kendell (1975) pointed out. In psychiatry twenty-first century technology is being wasted in attempts to solve a nineteenth century problem based on seventeenth century assumptions about the brain-mind relationship. Despite this, those involved in neuroscience research in psychiatry still maintain, as did Robins and Guze over forty years ago, and Andreasen twenty years ago, that it is only a matter of time before science will lift the veil that hides the biological basis of madness. The key question is whether any form of technology will ever be capable of establishing the validity of any system of classification in psychiatry.

The problem of body-mind dualism

The idea that there could be such a thing as a casual biological fault or mechanism underlying a psychiatric diagnosis is the keystone of scientific validity in psychiatric diagnoses, but the idea that this fault could be revealed by technology is based in a flawed and reductionist set of assumptions about the relationship between brain and mind. Let us take as an example the latest brain imaging technologies. Until quite recently it was not possible to study the part of the body most closely tied to mental states, the brain. Scientific studies of psychiatric diagnoses relied on indirect observations of brain function, through skull X-rays or examination of the cerebrospinal fluid that bathes the brain and spinal cord.

This changed with the introduction of new imaging technologies, first computerised tomographic (CT) scans then nuclear magnetic resonance (NMR) scans, making it possible to examine the brain in much greater detail. It is even possible through regional cerebral blood flow (rCBF) and fMRI (functional magnetic resonance) imaging to examine brain activity more or less in real time.  For example, studies have investigated if there are differences in the patterns of brain activity when people hear voices. A recent study by van Lutterveld and colleagues (2013) appears to show that activity in several areas of the brain is associated specifically with the experience of hearing voices, and this activity is not related to non-specific brain activity associated with the methodology specific to the research study (i.e. stimulus detection and motor response).

This raises a fundamental problem. How can we know that there is a link between a specific pattern of brain activity and a mental state like hearing the voice of James T. Kirk? This in essence is the problem of body-mind dualism. Such research assumes that the observed brain events cause the mental states. How can we be certain that that is the case?

On the face of it this is a very attractive proposition. The new generation of brain imaging technologies, what my colleague the Dutch psychiatrist Dirk Corstens calls the ‘pinball’ view of the brain, assumes that brain events cause mental events. This is a neat and apposite metaphor worth thinking through. When we play a pinball machine we know that the purpose of the game is to manipulate the ball to trigger the switches and relays that increase the score. We do this through physical actions that include using the paddles and tilting the table. Coincidentally, some of these switches and relays operate lights in different parts of the display and trigger off electronic sound effects. The lights are incidental to the purpose of the game. The only purpose they serve is to enhance our enjoyment. We do not need to know how these processes occur. We do not need to know anything about the machine’s wiring diagram if we are to play the game successfully.

But we do not hold the belief that these incidental properties, the lights, cause my physical manipulation of the paddles as I play the game. In truth most people would consider me mad to hold such a belief. The ultimate cause of all these physical aspect of the game, paddle, table tilting, lights and sounds, is my intention to play the game and beat the other player. Note that this brings us back to the issue of intentional causality that I raised in my last blog about narrative psychiatry.

The tacit assumption in all brain imaging studies is that brain activity causes the experience of hearing voices. This is equivalent to saying that the flashing lights in the pinball machine cause the game. Brain imaging studies, indeed all scientific investigations of the experiences of madness assume that there is only one form of causality, and this operates only in one direction. Brain events are a priori, and mental events are secondary, in other words only non-intentional causality matters.

This is an example of the epiphenomalist position made famous by Thomas Huxley in 1874 who said that mind (in relation to brain) is of no more significance than the whistle of a steam engine. It disregards the possibility that intentional mental states can lead to similar or identical patterns of brain activity. This is what McGuire and colleagues (1995) found in a rCBF study that examined patterns of brain activation in three tasks; a control situation in which subjects were asked to read silently from a list of words; an ‘inner speech’ task in which they had to recite mentally a sentence ending in a given word; and an auditory verbal imagery task, similar to the second task, but in which they were told to imagine the sentences being read by an unknown neutral voice. They found that mental state events, in this case intentional mental state events representing inner speech, produce brain events. This makes it difficult to sustain the simplistic notion of causal determinism, that brain events only lead to mental events.

There is an absurdity at the heart of the assumption that brain events cause the experience of hearing voices that needs further explication. Let us say, just for the sake of argument, that when specific areas of my brain light up, or are activated, I hear the voice of James T. Kirk telling me that I am the next Klingon Emperor. These events may be seen to take place in my brain, but the voice I hear is a content of consciousness in my mind. This raises the question of how brain and mind interact. How is it possible for physical processes in my brain to give raise to unique and specific contents of my consciousness? This question arises as one consequence of the distinction between body and mind introduced by the French philosopher Renee Descartes in the seventeenth century. Why he found it necessary to make this distinction isn’t relevant here (if you want, you can find more details in Bracken and Thomas, 2005), but Descartes located his solution to the problem of brain-mind interaction in the pineal gland. He believed this was the site in the brain where it all came together, sensation, imagination, memory, bodily movement and action.

The problems this raises are set out by the philosopher Daniel Dennett (1991) who likens the role of the pineal gland in Descartes’ theory to a theatre. In this theatre “I”, the subject, sit, watch and listen as the brain activity that represents my experience of the voice of James T. Kirk is presented before me. This, however, still fails to address the question, how do I become aware of and experience this specific brain activity as the voice of James T. Kirk, and not a different hallucinatory voice saying something else. The ‘theatre’ metaphor also fails to account for how, in the same subject, activity in the same areas of the brain give rise to voices with quite different content. One way around this is to postulate that my mind must have an inner ‘centrum’ where this brain activity is presented yet again before another observer.

This is plainly ridiculous because we run into an endless regress, an infinite array of Babushka dolls nested inside each other, spiralling  away to infinity. Of course at one level brain events bear a relationship to the contents of consciousness, but this arguably is at a level beyond neuroscience, and in any case it is not of necessity a causal relationship. Neuroimaging studies fail to account for two things, the precise way in which brain and mind interact, and the specificity of individual experience. Free will and autonomy (not that these are unproblematic) are swept aside in the pinball game that clinical neuroscience has become.

The latest generation of brain imaging studies deal with this problem by denial. They fail to acknowledge the complexity of the problematic relationship between brain and experience, preferring instead naive materialism and reductionism.  I have not encountered a single study that has engaged in a serious discussion of this problem (if anyone can direct me to one that does so convincingly, I’d be very grateful). They fail to engage with the specificity problem by limiting any concern with the content of voices to those aspects that are only necessary to make a diagnosis of schizophrenia.

It is possible to extend this argument more generally to any scientific attempt to set out a causal basis for the experiences of madness through diagnostic categories, and thus the validity of these categories. This is why fifty years of study and investigation, and huge sums of money spent across the Western world on neuroscientific research institutes, on careers and equipment, has failed to establish the validity of a single psychiatric diagnosis. How much more money must be wasted on the doomed project of neuroscience in the service of psychiatric diagnosis?



Anckarsäter, H. (2010) Beyond categorical diagnostics in psychiatry: Scientific and medicolegal implications. International Journal of Law and Psychiatry, 33, 59–65.

Andreasen, N. (1995) The Validation of Psychiatric Diagnosis: New Models and Approaches. American Journal of Psychiatry, 152, 161 – 162.

Bentall, R. & Jackson, H. (1988) Abandoning the concept of ‘schizophrenia’: Some implications of validity arguments for psychological research into psychotic phenomena. British Journal of Clinical Psychology. 27, 303 – 324.

Bracken, P. & Thomas, P. (2005) Postpsychiatry: Mental Health in a Postmodern World. Oxford, Oxford University Press (see especially Chapter Four, pp. 105 – 138)

Bleuler, M. (1978). The schizophrenic disorders: Long-term patient and family studies. New Haven, Yale University Press.

Ciompi, L (1980) The natural history of schizophrenia in the long term. British Journal of Psychiatry, 136, 413-420.

Dennett, D. (1991) Consciousness Explained. London, Allen Lane.

Harding, C. M., G. W. Brooks, et al. (1987). The Vermont longitudinal study of persons with severe mental illness: I. Methodology, study sample, and overall status 32 years later. American Journal of Psychiatry 144(6): 718-726.

Huber, G., G. Gross, et al. (1975). A long-term follow-up study of schizophrenia: Psychiatric course of illness and prognosis. Acta Psychiatrica Scandinavica 52: 49-57.

Kendell, R. (1975) The Role of Diagnosis in Psychiatry. Blackwell Scientific Publications, Oxford.

Kendell, R. & Jablensky, A. (2003) Distinguishing Between the Validity and Utility of Psychiatric Diagnoses. American Journal of Psychiatry; 160:4–12

Kendler, K. (1980) The Nosological Validity of Paranoia (Simple Delusional Disorder) Archives of General Psychiatry, 37, 699 – 706.

Kraepelin, E. (1913) Psychiatrie, ein Lehrbuch fur Studierende und Artzt (Psychiatry, a textbook for students and practitioners) (8th edition), Vol. 3. Leipzig, Barth.

Kua, J., K. E. Wong, et al. (2003). A 20-year follow-up study on schizophrenia in Singapore. Acta Psychiatrica Scandinavica 108(2): 118-125.

Leff, J., Kuipers, L., Berkowitz, R., Vaughn, C. & Strugeon, C. (1983) Life events, relatives’ expressed emotion and maintenance neuroleptics in schizophrenic relapse. Psychological Medicine, 13, 799 – 806.

McGuire, P., Silbersweig, D.A., Wright, I., Murray, R.M., David, A.S., Frackowiak, R.S.J. & Frith, C.D. (1995) Abnormal monitoring of inner speech: a physiological basis for auditory hallucinations. Lancet, 346, 596 – 600.

National Collaborating Centre for Mental Health (2010) Schizophrenia: The NICE Guidelines on Core Interventions in the Treatment and Management of Schizophrenia in Adults in Primary and Secondary Care. Updated Edition. London, The British Psychological Society and The Royal College of Psychiatrists. Accessed on 17th April 2010 at

Robins, E. & Guze, S. (1970) Establishment of Diagnostic Validity in Psychiatric Illness: Its Application to Schizophrenia. American Journal of Psychiatry, 126, 983 – 987.

Strauss, J. & Carpenter, W. (1974a) The prediction of outcome in schizophrenia: II. Relationships between predictor and outcome variables. Archives of General Psychiatry, 31, 37 – 42.

Strauss, J. & Carpenter, W. (1974b) Characteristic symptoms and outcome in schizophrenia. Archives of General Psychiatry, 30, 429 – 434.

Strauss, J. & Carpenter, W. (1977) Prediciton of outcome in schizophrenia. III. Five year outcome and its predictors. Archives of General Psychiatry, 34, 159 – 163.

Thara, R. (2004). Twenty-Year Course of Schizophrenia: The Madras Longitudinal Study. Canadian Journal of Psychiatry 49(8): 564-569.

van Lutterveld, R., et al., (2013) The influence of stimulus detection on activation patterns during auditory hallucinations, Schizophrenia Research,

Warner, R. (1985) Recovery from Schizophenia: Psychiatry and Political Economy. London, Routledge and Kegan Paul.

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  1. Behind *each* and *every* DSM psychiatric diagnosis there is a root cause (or causes):

    1) Underlying *physical* condition(s).
    2) An *emotional* response to stress or trauma
    3) A spiritual* opportunity for growth.

    There are no true psychiatric illnesses as definded by the DSM.
    There never have been.
    There never will be.

    Duane Sherry, M.S.

  2. excellent: the psychiatrist as rainbow chaser, except the rainbows have rather nasty effects on those who get diagnosis.

    This article challenges the basis of psychiatry and everyone who has ever had a psychiatric diagnosis. This is potentailly really useful in deconstrucing diagnosis and listing the attempts to justify them.

  3. Excellent article. I agree with you the medical foundations of psychiatry are not well established, and many common assumptions don’t stand serious scrutiny.

    Following your reasoning (which I totally share), there is still one immediate open question remaining once we have rejected the medical validity of ICD or DSM: what kind of (likely non-medical) criteria, or classifications could be used today to determine or prioritize who is entitled to public help and resources, and to account for how those resources (be it counseling, social work, hospital or other respite centers) are used.

    I wish we would live in a world of such prosperity that just asking would be a sufficient criteria to obtain help, but in our real world, managing scarcity of resources (human or otherwise) is a reality, and that requires guidelines and criteria to do it fairly. And removing any kind of public role in providing help to people in difficult situations does not seem a viable option to me either.

    • The ideas that Lucy Johnston outlined in a series of articles on this site are on alternative to pshychniatic classifictaions. This is called Formulation:

      An assesement of how limiting a persons distress is to their ability to take part in society and what they might need to restore a reasonable level of functioning could be used to justify funds for the relevent help. Dr’s and social workers make these kinds of assessments all the time ( a wheel chair for Mrs Jones, a hip operation for Mr Smith, a supply of insulin for Jonny and vitamin tablets for Janey).

      In certain circumstances this happens already. In the uk you might be on a waiting list for therapy anything up to two years in certain areas but if you are very seriously distressed you will be forced to go into hospital. This is not quite the same as rationing due to need as hospital might be more harmful than helpful, but you get the idea. Access to services has some relation to need already, even if that need is assessed in a squiffy way and no matter how good or bad the service.

      The other point you riase is about prosperity/scarcity. I don’t think this is about prosperity/scarcity. We live in a world where the divide between the rich and poor is getting ever wider. As the old song goes: it the same the whole world over (or those where neo-liberal capitasm has reached), it’s the poor wot gets the pain (or ritalin, prozac and dipixol) and the rich wot gets the pleasure (or private therapists) aint it all a bleedin shame?

      The poor are more subject to “mental illness” that the rich. Some say that psyhciatry’s function is to cover up the social causes of distress, including poverty. So a nice diagnosis, which makes absolutely no mention of social factors lets the rich off the hook in thier contribution to mental distress (poverty, homelessness, the banking crisis….)

    • “Fear is Not a Mental Disorder: Or What is Really Wrong With the DSM”
      Stanley, Here is one solution to replace the DSM.
      I am a practicing clinical psychologist who for years has believed that the DSM is inaccurate and misleading in fundamental ways and could even be considered harmful to clients. I believe, as many do, that the time is right to completely re-conceptualize diagnostic strategies from the ground up, with the goal of developing a replacement for the DSM. The mythology of the DSM has for decades hindered therapeutic treatment of clients, and generally complicated what are very simple, understandable concepts that underlie human behavior.
      I have written an essay that takes a broad, philosophical look at concerns about the DSM. I present a powerful and concise new theoretical framework to use when diagnosing human behavioral and emotional distresses. This new paradigm is explained in depth in my book Pack Leader Psychology. This paradigm offers numerous benefits not found in the DSM, corrects many of the theoretical errors in the DSM, and provides an effective diagnostic and therapeutic solution.
      Quite simply, Pack Leader Psychology is based on this concept: The majority of “mental disorders” that people experience are due to the primal fear response. Fear is not a disorder, but a normal, adaptive human reaction.
      Pack Leader Psychology is based on indisputable facts, not the unscientific, confusing, and complex “system” of “diagnostics” of the DSM. Most important, the Pack Leader Psychology model brings numerous benefits to clients, whom we in the psychology profession are ethically bound to protect and help. Where the DSM pathologizes human behaviors as illnesses and disorders, Pack Leader Psychology offers an innovative paradigm that explains these behaviors as normal, natural responses to perceived or real threats and fears. Pack Leader Psychology is a more positive, optimistic, and straightforward framework that strips away harmful, judgmental labels and de-stigmatizes “mental illness” in a profound and fundamental way.
      I would love to hear feedback on my essay and book. Learn more at

  4. The title of this and the evocation of “Pinball Wizard” from “Tommy” invites mention of the only exception I can think of in terms of the DSM’s tendency to expand diagnoses: the contractions in diagnostic criteria for conditions largely shown to be caused by products marketed by industries which sponsor DSM panel members. In the latest DSM, the autism diagnosis is split up in such a way that it pushes the bulk of those with the diagnosis off into newly concocted diagnostic categories, like “Social Communication Disorder”– which is already being hooked up with corresponding on-patent or soon-to-be-patented drugs.

    Anyone over 35 who’s set foot in a school which doesn’t have the resources to ship its disabled students out of sight to institutional schools can see for themselves that not only is autism more prevalent than it used to be, not only aren’t “most” on some vaguely definable “high functioning” end of the spectrum, the rate of autism is far higher than the currently pronounced 1 in 88. Is it any wonder that the strongest environmental evidence points to pharmaceutical products– both psychopharm drugs and vaccines– and the fuel industry?

    Not that this exception disproves the rule of fake DSM diagnostics or undercuts the point of this post. Autism is probably the only case where industry is driven to actually hide the increase in rate (while more quietly crowing about the promised increase in drug sales from an epidemic out of the other side of their mouths: ). But I don’t think it’s the only case of false turf-grabbing, just the most obvious one. Mixed within more “grab bag” diagnoses like “ADHD” and “OCD,” etc., are probably clinical cases of actual medical environmental conditions such as moderate lead poisoning and so forth.

    Thomas Szasz once wrote something to the effect that if every diagnosis in the DSM had a biological basis, psychiatry would have been absorbed into the field of neurology ages ago. Mostly this statement is taken as an argument– which I think is mostly correct– that the vast majority of diagnoses have no biological basis. But it could also be taken as a caveat that industry is in a turf war to label little understood (or hugely denied) environmental conditions with druggable voodoo psychiatric labels. After all, Prozac and Ritalin do zilch for lead poisoning– other than increasing the porosity of the blood brain barrier and ensuring more lead will get to the brain. They defend their turf by launching legal wars against labs and clinicians that test for sequestered heavy metals– metal levels already absorbed deeply into bone and tissue– since lead levels won’t show up in blood tests if the gap between last exposure and testing is too great.

    Patients and parents of children who view autism and certain less definable conditions like OCD and some cases of so-called “ADHD” as environmental are far less likely to drug their children with neurotoxic medications and this stands as a threat to the pharmaceutical industry’s growing “Halliburton” construct as well as threatening big polluters which share board members with Big Pharma.

  5. Outstanding article; thank you Philip. I’m so glad that you bring up ephiphenomenalism which, as you say, underlies much of what is wrong with psychiatry. I remember talking to a psychiatrist (and a university professor to boot) and being shocked by the extent to which he was not aware of this basic problem in the conception of the relationship mind-brain; “we don’t really used the word ‘mind’ in our profession” was his response.
    I think the problem is compounded by an almost superstitious belief that brain morphology does not change throughout adult life, or that if it does this change is controlled by genes rather than caused by experience. I suppose the alternative makes people nervous because they misinterpret it as advocating ‘mind over matter’. I hope research into neuroplasticity is moving things in the right direction but, again, many people seem to regard neuroplasticity as a dirty word.

    Thank you again for this article. I think it is fundamental to raise awareness of the philosophical assumptions underpinning psychiatry.

  6. “The latest generation of brain imaging studies deal with this problem by denial. They fail to acknowledge the complexity of the problematic relationship between brain and experience, preferring instead naive materialism and reductionism. I have not encountered a single study that has engaged in a serious discussion of this problem (if anyone can direct me to one that does so convincingly, I’d be very grateful).”

    I can’t direct you to a study, but instead to a book about the paradigm shift taking place, away from our left-brained “objectified & logical” understanding of our “explicit” self, towards a more valid “sense” of our right-brained “implicit” self, and its capacity to heal the kind of traumatic experiences which can lead one to hearing voices. Please consider;


    A. Schore has described how the emotion-processing limbic circuits of the infant’s developing right brain, which are dominant for the emotional sense of self, are influenced by implicit intersubjective affective transactions embedded in the attachment relationship with the mother (Schore, 1994, 2005). Implicit processing underlies the quick and automatic handling of nonverbal affective cues in infancy, and “is repetitive, automatic, provides quick categorization and decision-making, and operates outside the realm of focal attention and verbalized experience” (Lyons-Ruth 1999, p. 576). Trevarthen (1990) described how prosodic vocalizations, coordinated visual eye-to-eye messages, and tactile and body gestures, serve as channels of communicative signals in the proto dialogues between infant and mother, which induce instant emotional effects. Bowlby (1969) also described “facial expression, posture, and tone of voice” as the essential vehicles of attachment communications between the emerging self and the primary object (Schore, 2001a).

    The dyadic implicit processing of these nonverbal attachment communications are the product of the operations of the infant’s right hemisphere interacting with the mother’s right hemisphere. Attachment experiences are thus imprinted in an internal working model that encodes strategies of affect regulation acting at implicit nonconscious levels. Neuroscientists have documented that visual input to the right (and not left) hemisphere during infancy is essential for the development of the capacity to efficiently process information from faces (Le Grand, Lucci, Mazzatenta, & Tommasi, 2003). These findings support earlier speculations in the psychoanalytic literature that “The most significant relevant basic interactions between mother and child usually lie in the visual area: the child’s bodily display is responded to by the gleam in the mother’s eye” (Kohut, 1971, p. 117); that early mental representations are specifically visually oriented (Giovacchini, 1981); and that historical visual imagery is derivative of events of early phases of development (Anthi, 1983).

    It is important to note that these early experiences may be regulated or dysregulated, imprinting either secure or insecure attachments. Watt (2003, p. 109) observes, “If children grow up with dominant experiences of separation, distress, fear and rage, then they will go down a bad pathogenic developmental pathway, and it’s not just a bad psychological pathway but a bad neurological pathway.” This is due to the fact that during early critical periods organized and disorganized insecure attachment histories are “affectively burnt in” the infant’s rapidly developing right brain (Schore, 2001a, 2003a). These stressful relational experiences are encoded in unconscious internal working models in the right, and not left, brain. In a study of hemispheric lateralization of avoidant attachment, Cohen and Shaver (2004) conclude, “Emotional negativity and withdrawal motivation have been connected in psychophysiological studies with the right frontal lobe of the brain” (p. 801), and that avoidant individuals show “a right hemisphere advantage for processing negative emotion and attachment-related words” (p. 807).

    It is now accepted that the “non-verbal, prerational stream of expression that binds the infant to its parent continues throughout life to be a primary medium of intuitively felt affective-relational communication between persons” (Orlinsky & Howard, 1986, p. 343).

    Most relational transactions rely heavily on a substrate of affective cues that give an evaluative valence or direction to each relational communication. These occur at an implicit level of rapid cueing and response that occurs too rapidly for simultaneous verbal transaction and conscious reflection. (pp. 91– 92)  

    Scaer (2005) describes essential implicit communications embedded within the therapist– client relationship:   Many features of social interaction are nonverbal, consisting of subtle variations of facial expression that set the tone for the content of the interaction. Body postures and movement patterns of the therapist … also may reflect emotions such as disapproval, support, humor, and fear. Tone and volume of voice, patterns and speed of verbal communication, and eye contact also contain elements of subliminal communication and contribute to the unconscious establishment of a safe, healing environment. (pp. 167– 168)

    A fundamental question of treatment is how we work with what is being communicated but not symbolized with words. In discussing subsymbolic processing, Bucci (2002) observes, “We recognize changes in emotional states of others based on perception of subtle shifts in their facial expression or posture, and recognize changes in our own states based on somatic or kinesthetic experience” (p. 194). These implicit communications are expressed within the therapeutic alliance between the client’s and therapist’s right brain systems.  

    Human beings rely extensively on nonverbal channels of communication in their day-to-day emotional as well as interpersonal exchanges. The verbal channel, language, is a relatively poor medium for expressing the quality, intensity and nuancing of emotion and affect in different social situations … the face is thought to have primacy in signaling affective information. (Mandal & Ambady, 2004, p. 23)

    In the developmental attachment context, right brain– to– right brain auditory prosodic communications also act as an essential vehicle of implicit communications within the therapeutic relationship. The right hemisphere is important in the processing of the “music” behind our words. When listening to speech, we rely upon a range of cues on which to base our inference as to the communicative intent of others. To interpret the meaning of speech, how something is said is as important as what is actually said. Prosody conveys different shades of meaning by means of variations in stress and pitch— irrespective of the words and grammatical construction (Mitchell, Elliott, Barry, Crittenden, & Woodruff, 2003). These data support suggestions that the preverbal elements of language— intonation, tone, force, and rhythm— stir up reactions derived from the early mother– child relationships (Greenson, 1978).

    During heightened affective moments, these right brain dialogues between the relational unconscious of both the patient and the therapist (like the attachment communications of the infant and mother) are examples of “primary process communication” (Dorpat, 2001). According to this author, “The primary process system analyzes, regulates, and communicates an individual’s relations with the environment”:  

    [A] ffective and object-relational information is transmitted predominantly by primary process communication. Nonverbal communication includes body movements (kinesics), posture, gesture, facial expression, voice inflection, and the sequence, rhythm, and pitch of the spoken words. (Dorpat, 2001, p. 451)

    It is important to stress that all of these implicit nonconscious right brain– mind– body nonverbal communications are bidirectional and thereby intersubjective (see Schore 2003b for a right hemisphere– to– right hemisphere model of projective identification, a fundamental process of implicit communication within the therapeutic alliance). Meares (2005) describes,   Not only is the therapist being unconsciously influenced by a series of slight and, in some cases, subliminal signals, so also is the patient. Details of the therapist’s posture, gaze, tone of voice, even respiration, are recorded and processed. A sophisticated therapist may use this processing in a beneficial way, potentiating a change in the patient’s state without, or in addition to, the use of words. (p. 124)  

    Implicit right brain– to– right brain intersubjective transactions lie at the core of the therapeutic relationship. They mediate what Sander (1992) calls “moments of meeting” between patient and therapist. Current neurobiological data suggest that “While the left hemisphere mediates most linguistic behaviors, the right hemisphere is important for broader aspects of communication” (van Lancker & Cummings, 1999). In light of this, A. Schore (2003b) has proposed that just as the left brain communicates its states to other left brains via conscious linguistic behaviors, so the right brain nonverbally communicates its unconscious states to other right brains that are tuned to receive these communications. Regulation theory thus describes how implicit systems of the therapist interact with implicit systems of the patient; psychotherapy is not the “talking” but the “communicating” cure.

    The neuroscience literature holds that “The left hemisphere is more involved in the foreground-analytic (conscious) processing of information, whereas the right hemisphere is more involved in the background-holistic (subconscious) processing of information” (Prodan, Orbelo, Testa, & Ross, 2001, p. 211). Indeed, the right hemisphere uses an expansive attention mechanism that focuses on global features, whereas the left uses a restricted mode that focuses on local detail (Derryberry & Tucker, 1994). In contrast to the left hemisphere’s activation of “narrow semantic fields,” the right hemisphere’s “coarse semantic coding is useful for noting and integrating distantly related semantic information” (Beeman, 1998), a function that allows for the process of free association. Bucci (1993) has described free association as following the tracks of nonverbal schemata by loosening the hold of the verbal system on the associative process and giving the nonverbal mode the chance to drive the representational and expressive systems, that is, by shifting dominance from a left to a right hemispheric state. These nonverbal affective and thereby mind– body communications are expressions of the right brain, which is centrally involved in the analysis of direct kinesthetic information received by the subject from his own body, an essential implicit process. This hemisphere, and not the linguistic, analytic left, contains the most comprehensive and integrated map of the body state available to the brain (Damasio, 1994). The therapist’s right hemisphere allows him or her to know the patient “from the inside out” (This was my DIY self-therapy challenge, to understand my fearful emotional dysfunction form the inside-out.)”

    Excerpts from “The Science of the Art of Psychotherapy” by Allan N. Schore,.

    IMO hearing voices and the experience of psychosis is “thermodynamic” in nature, a product of the primary processes of organism in its need of “survival.” As Stephen Porges suggests hearing voices is most likely generated by our evolved mammalian fear of predator’s, yet of coarse in our love affair with the mind’s “cognitive constructs” we tend to deny the reality of evolution and power of its negative sensations within the body. Perhaps this is why we tend to shy away from our own reality, in our myopic focus on brain research alone.

    In my attempts to come to terms with the subconscious nature of my psychotic experience and its attachment dynamics, I’ve had to break the golden rule and speak out about the unspeakable nature of family attachments and the generational transmission of the “implicit self.”

    “The Butterfly Effect & Generational Nature of Affect-Regulation?
    So how does this notion of generational emotionality lead to a child who comes to suffer a major mental illnesses like bipolar disorder? In my opinion, the hidden factor in the generational process is internal “sensitivity,” a sensitivity of the organism’s complex feedback systems which cannot be observed. A constitutional sensitivity conditioned, in my case, by my genetic inheritance and my birth experience and circumstantial neglect. A sensitivity maintained by my subsequent experience of coping with the “transmission of affect,” in my family’s generational style of affect-regulation. Please consider the forward to Allan N Schore’s complex, yet brilliant book “Affect Regulation & The Origins of The Self.”

    “In his work on “shame” Dr. Schore brought to our attention the unusual importance of a particular stage of infancy, 10-12 to 16-18 months, the practicing sub-phases of separation and individuation, a period of heightened activation of the sympathetic aspects of the autonomic nervous system, and the need for the mother to attune properly to the infant’s excitement at that time. Failure to do so results in the premature activation of excessive shame to counterbalance the now-found-to-be-dangerous excitement of the early practicing period.

    Thus he postulated that in the early practicing sub-phase normal excitement evolves and has to be properly attuned. Then, in the later aspects of practicing, the parasympathetic system comes into play becoming a normal neurobehavioral “antagonist” to its predecessor so as to mediate and regulate its expression.

    The infant brings inherent, constitutional givens (genotype) to the birth situation, which continue to unfold for a considerable length of time past birth. These genetic endowments are partially open to environmental modification (phenotype) and are also partially closed. To the extent that they are open they are acted upon, modified, completed, and developed in a continuous dialectical interaction with primary caregivers.

    What psychoanalytic theory had speculated upon from its very beginnings now turns out to be truer than had been anticipated. As in chaos theory, which states that there occurs an unusual sensitivity to initial conditions, the role of the mothering person with her offspring, which had been all but neglected in the dawn of psychoanalysis. Nobody then anticipated how dependant the infant’s brain was on the mothers care giving.

    In developmental disorder one thinks of psychopathology, insecure attachments and their neuropsychological consequences, affect dysregulation, the onset of personality disorders, and vulnerability to somatization disorders. Developmental psychopathology, which is rapidly becoming a field unto itself, can certainly be understood in no small measure by the concept of the “failed appointment,” that is, failure, whether by chance, trauma, neglect, or inherent genetic programming, for the key neuronal connections to have been evoked at the proper time by the mother-as-appropriate-self object at the appropriate time.

    One certainly must now view such disorders on the anxiety spectrum, such as the disorders of anxiety, panic, phobia, hypochondria, and such trait-state disorders as borderline personality, the obsessive compulsive disorders, affect dysregulation (the manic-depressive-dysthymic spectrum disorders), schizophrenia, and many others as being deeply rooted in one or another form of a neuro-biologically induced disorder of regulation.

    Joseph Palombo, who works with the neuro-perceptual-cognitive aspects of developmental disorders of childhood, including borderline syndrome, calls attention to the presence in these impaired children of a discrepancy between their private, personal selves and their shared selves in terms of a lack of ease in communication. Put another way, these damaged children seem to sense that there is something neurodevelopmentally wrong with them, and they feel a deep sense of shame about themselves as a result.”

    “The concept of the “failed appointment,” that is, failure, whether by chance.” A concept of chance, otherwise known to chaos theory as “the butterfly effect.” Or as this forward to Schore’s book points out. “As in chaos theory, which states that there occurs an unusual sensitivity to initial conditions,” the post-natal maturing of our brain-nervous systems, is subject to the Universal law of chaos, as our complex biological systems develop orders of stability, dependant on enviromental conditions. Who would have thought that chaos theory could explain human personality and mental illness? Framed in these terms, would an understanding of this reality of affect/emotional development, soothe the subconscious reactions of shame avoidance in my own family-of-origin, just as much as the concept of a brain disease does? Or am I just blaming and shaming my Mom & Dad? And what is that curious term in my sub-heading Subconscious, reactions to “the transmission of affect?” Please consider;

    “In a time when the popularity of genetic explanations for social behavior is increasing, the transmission of affect is a conceptual oddity. If transmission takes place and has effects on behavior, it is not genes that determine social life; it is the socially induced affect that changes our biology. The transmission of affect is not understood or studied because of the distance between the concept of transmission and the reigning modes of biological explanation. No one really knows how it happens, which may explain the reluctance to acknowledge its existence. But this reluctance, historically is only recent. The transmission of affect was once common knowledge; the concept faded from the history of scientific explanation as the individual, especially the biologically determined individual, came to the fore.

    We think that the ideas or thoughts of a given subject has, are socially constructed, dependant on cultures, times, and social groups within them. Indeed, after Karl Marx, Karl Mannheim, Michel Foucault, and any social thinker worthy of the epithet “social,” it is difficult to think anything else. But if we accept that our thoughts are not entirely independent, we are peculiarly resistant to the idea that our emotions are not altogether our own. The taken-for-grantedness of the emotionally self-contained subject is a bastion of Eurocentrism in critical thinking, the belief in the superiority of one’s own worldview over that of other cultures. The idea that progress is a modernist and Western myth are nonetheless blind to the way that non-Western as well as premodern, preindustrial cultures assume that the person is not “affectively” contained.
    Notions of the transmission of affect are suspect as non-white and colonial cultures are suspect.

    But the denial is not reasonable. The denial of transmission leads to inconsistencies in theories and therapies of the subjective state. All reputable schools of psychological theory assume that the subject is energetically and affectively self-contained. At the same time, psychologists working in clinics experience affective transmission. There are many psychological clinicians ( especially the followers of Melanie Klein) who believe they experience the affects of their clients directly.”

    Best wishes to all,

    David Bates.

  7. Dr Thomas – Thank you for a concise and insightful piece.

    Some thoughts:

    I think when you say “scientific,” you should say something like “conventional medical.” We usually assume that “hard” data like that revealed by autopsy, microscopes or modern imaging is required for science. But science is defined more by method than by the object of observation.

    Really, all we ever have to go on is phenomenological data – the “hard science” phenomena we study are just constructs we infer from phenomenological data. And it is possible to apply the scientific method to our own phenomenological data. To be “scientific” about how we think, feel and act, we do not necessarily have to observe the inner workings of the human body at all.

    Paris Williams, in his book – is it Re-Thinking Madness? – refers to psychosis as a “placeholder” – not a real “thing” that can be defined once and for all. It is a blank that in different eras, cultures, groups and even individuals, fill in differently. Williams also sees psychosis not as an “illness” or even an affliction, but as a process some of us go through in the course of working out serious issues in our lives. It seems the most horrendous aspects of that process largely come from the fact that those around the “psychotic” person are unprepared to provide the nurturing, supportive environment needed to move through the process to a resolution.

    With all the medical and psychiatric attempts to define “madness,” one common element exists, and it is the reason for the failure of medical diagnosis: We define others as “mad” when we get scared, overwhelmed and hopeless about our ability to deal with them. When we feel helplessly out of our comfort zones and see no end to it – we pathologies “them,” saying “it’s genetic” or something of the kind.

    NOT doing this is key to Open Dialogue’s success. They see psychosis as a client’s response to difficult experiences that their social environment doesn’t allow them to process; the key to Open Dialogue is the therapists’ “tolerance of uncertainty” – not flipping out when the client and family system flip out. By not diagnosing, not pathologizing or correcting client or family; by setting an atmosphere where nobody is judged and everyone is heard, by making it safe for client, family and support system to re-examine the experience of psychosis, over 80% of clients actually recover.

    Open Dialogue values the phenomenological and virtually eliminates conventional diagnosis. After the most effective sessions, people often can’t analyze exactly what worked – they just know they shared an experience in which client, family and therapist all changed.

    So, my working assumption is that: people encounter distress in their lives; sometimes they can’t resolve it within their social support network, and it causes problems for them and those around them; if it becomes bad enough for long enough, people get scared feel helpless, and attribute the problem to one or more person’s “mental illness’; if the social system can be helped to calm down and communicate in new ways, the problem can be resolved.

    Conclusion – looking for “madness” within an individual’s brain doesn’t work, because the “diagnosis” that he/she is “mad” is a group phenomenon rooted in human relationships and communication – not (with rare and identifiable disease exceptions) within the individual client or his/her brain.

  8. There is great need for a more nuanced, less black & white understanding of the actual nature of so-called mental illness, yet can we expect to see such a nuanced understanding emerge when we overwhelmingly in denial about our individual sense of nuance?

    Please consider more from Allan N Schore and the kind of understanding which seeks a truly holistic awareness, beyond the simple needs of self-empowerment and our business as usual social politics. A business as usual game, which is largely based on a “left-brained” and false-sense-of-self.

    ““Research suggests that sensitivity and flexibility in the administration of therapeutic interventions produces better outcomes than rigid application of … principles” (p. 278). Sensitivity has, of course, been well studied in the developmental attachment literature, wherein researchers observe that maternal sensitivity cultivates synchronous, reciprocal, and jointly satisfying mother– infant interactions, which in turn foster the development of a secure attachment relationship.

    The dictionary definition of sensitivity is “susceptible to the attitudes, feelings, or circumstances of others; registering very slight differences or changes of emotion” (American Heritage Dictionary). In discussing “the art of psychotherapy,” Bugental (1987) stresses the importance of the sensitive clinician’s ability to “learn to experience finer and finer distinctions or nuances.”

    (This is the essence of human nuance, which is rarely found in the thought, spoken or written word, which “autonomically seeks to “cover-up“ the raw energies of the body. As Damasio points out “A mind is so closely shaped by the body and destined to serve it that only one mind could possibly arise in it. No body, never mind.” _Antonio Damasio, “The Feeling of What Happens.”_D Bates)

    Bugental states, “The primary instrument brought to the support of the client’s therapeutic efforts is the therapist’s trained, practiced, and disciplined sensitivity. In many ways, this sensitivity is akin to a musical instrument which must be carefully prepared, maintained, tuned, and protected” (p. 222). The clinician’s capacity for intersubjective communication depends upon her “being open to intuitive sensing of what is happening in the back of the patient’s words and, often, back of his conscious awareness” (p. 11). This clinical sensitivity to even low levels of nonverbal attachment communications allows for the clinician’s involvement in a wider array of co-created, affectively charged intersubjective fields.

    These clinical principles apply especially to working in enactments with patients with a history of relational attachment trauma and pathological dissociation (Ginot, 2009; Schore, 2007). Such work implies a profound commitment by both participants in the therapeutic dyad and a deep emotional involvement on the part of the therapist (Tutte, 2004). An attachment-based clinical approach highlights the unconscious nonverbal affective factors more than the conscious verbal cognitive factors as the essential change process of psychotherapy. Thus, at the most essential level, the intersubjective work of psychotherapy is not defined by what the therapist does for the patient, or says to the patient (left brain focus). Rather, the key mechanism is how to be with the patient, especially during affectively stressful moments (right brain focus). Bowlby stated that attachment behavior was based on the need for safety and a secure base. We have demonstrated that attachment is more than this; it is the essential matrix for creating a right brain self that can regulate its own internal states and external relationships. Attachment intersubjectivity allows psychic structure to be built and shaped into a unique human being. Regulation theory enhances and deepens the field’s bio-psycho-social-cultural perspective.


    An explosion of developmental and neurobiological research has added substantially to the theoretical understanding of the 110 years since Freud (1895/ 1966) first published his Project for a Scientific Psychology (Schore, 1997). Having been grounded in drive, ego, object relations, self psychology, and relational psychology through the 1980s, the addition of attachment theory has moved psychodynamic clinicians’ sensibilities into an awareness of real experience and a keen focus on early development as the root of all. Then, beginning in the 1990s, the advances in neuroscience, added to the temperament research, the biological component in our biopsychosocial frame, have provided a remarkable underpinning and expansion of all the pertinent developmental psychoanalytic theoretical concepts that came before. Using this knowledge on a daily basis, finding new understandings in clinical assessments, shaping therapeutic interventions from relevant theory, and providing a unique awareness of the adaptive nonconscious functions of the implicit self are some of the profound results of this theoretical integration.

    The intersubjective process of developing a *true-self* that can enter into meaningful relationships shows us how the internal world is structured on a psychophysiological base, which takes into account the unique genetic endowment of the particular infant in interaction with his or her relational environment. In a recent overview, Glass (2008) concludes, “Recent research in brain imaging, molecular biology, and neurogenetics has shown that psychotherapy changes brain function and structure. Such studies have shown that psychotherapy affects regional cerebral blood flow, neurotransmitter metabolism, gene expression, and persistent modifications in synaptic plasticity” (p. 1589). Tucker (1992) observes, “the baby brain must begin participating effectively in the process of social information transmission that offers entry into the culture” (p. 79). He asserts that social interaction that promotes brain differentiation is the mechanism for teaching “the epigenetic patterns of culture” (p. 122), and that successful social development requires a high degree of skill in negotiating emotional communication, “much of which is nonverbal” (p. 80). Tucker concludes that such emotional information engages “specialized neural networks in humans, within the right hemisphere” (p. 80). This conceptualization clearly suggests an important and unique role for clinical social work in infant mental health and optimal right brain development, particularly for attachment programs aimed at prevention and early intervention.

    Excerpts from “The Science of the Art of Psychotherapy” by Allan N. Schore,.

    Best wishes to all,

    David Bates.

  9. Great use of the term ‘Pinball Wizards’!

    Thanks for the great article and the stellar list of references!

    I am increasingly astounded that the DSM is even still going to be published. It is so clearly illegitimate…useless for much of anything beyond confusing people about the human condition and causing great harm.

    Does the APA have no shame?

  10. My original psychiatrist admitted he’d diagnosed me wrongly but later he sent letters refuting such saying he was legally protecting himself. I went to other psychiatrists who said I was fine, in no way was I mentally ill but the original diagnosis is out there in open hospital charts and physicians office records.

    I’ve already experienced the abruptness by any physician who has access to the diagnosis. How can one psychiatrist’s diagnosis continue to do such damage?

    My psychiatric diagnosis was wrong and so what do I do to protect myself from this??