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Why psychiatry can't afford to be neurophobic

  • Ed Bullmore (a1), Paul Fletcher (a1) and Peter B. Jones (a1)

The original vision of psychiatry was as a medicine – or physic – of the mind. If psychiatry aspires to be a progressive modern medicine of the mind, it should be fully engaged with the science of the brain. We summarise and rebut three countervailing or ‘neurophobic’ propositions and aim to show that not one provides a compelling argument for neurophobia. We suggest that there are several ways in which psychiatry could organise itself professionally to better advance and communicate the theoretical and therapeutic potential of a brain-based medicine of the mind.

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Corresponding author
Correspondence: Ed Bullmore, University of Cambridge, Department of Psychiatry, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK. Email:
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Declaration of interest

E.B. is employed half-time by the University of Cambridge and half-time by GlaxoSmithKline (GSK), and he holds shares in GSK and the Brain Resource Company.

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1 Craddock, N, Antebi, D, Attenburrow, M-J, Bailey, A, Carson, A, Cowen, P, et al. Wake-up call for British psychiatry. Br J Psychiatry 2008; 193: 69.
2 Johnstone, EC, Crow, TJ, Frith, CD, Husband, J, Kreel, L. Cerebral ventricular size and cognitive impairment in chronic schizophrenia. Lancet 1976; 2: 924–6.
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6 Ellison-Wright, I, Glahn, DC, Laird, AR, Thelen, SM, Bullmore, E. The anatomy of first-episode and chronic schizophrenia: an anatomical likelihood estimation meta-analysis. Am J Psychiatry 2008; 165: 1015–23.
7 Lawrie, SM, McIntosh, AM, Hall, J, Owens, DG, Johnstone, EC. Brain structure and function changes during the development of schizophrenia: the evidence from studies of subjects at increased genetic risk. Schizophr Bull 2008; 34: 330–40.
8 Salisbury, DF, Kuroki, N, Kasai, K, Shenton, ME, McCarley, RW. Progressive and inter-related functional and structural evidence of post-onset brain reduction in schizophrenia. Arch Gen Psychiatry 2007; 64: 521–9.
9 Stephan, KE, Baldeweg, T, Friston, KJ. Synaptic plasticity and dysconnection in schizophrenia. Biol Psychiatry 2006; 59: 929–39.
10 Tan, HY, Callicott, JH, Weinberger, DR. Dysfunctional and compensatory prefrontal cortical systems, genes and the pathogenesis of schizophrenia. Cereb Cortex 2007; 17: 7181.
11 Gonzalez-Burgos, G, Lewis, DA. GABA neurons and the mechanisms of network osciallations: implications for understanding cortical dysfunction in schizophrenia. Schizophr Bull 2008; 34: 944–61.
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The British Journal of Psychiatry
  • ISSN: 0007-1250
  • EISSN: 1472-1465
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Why psychiatry can't afford to be neurophobic

  • Ed Bullmore (a1), Paul Fletcher (a1) and Peter B. Jones (a1)
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Medical Science

Ian P Burges Watson, psychiatrist (retired)
03 June 2009

Medical Science

The recent paper by Bullmore et al (1) is a timely follow-up to the ‘Wake up call’ of Craddock et al (2) who warned against the practical problems of the “creeping devaluaton of medicine”. As Bullmore et al point out, ignorance of the physical basis of a disease has generally led to social stigmatisationof patients with that disease. This is especially true of posttraumatic stress disorder where servicemen particularly continue to be stigmatised by ongoing controversy. This is not helped by the difficulty of reaching a diagnosis,a situation aggravated by ignorance of the physical basis of the disorder.

The bedrock of medical science is biology and the advent of a biopsychosocial approach has blurred the boundaries of what is properly biological psychological and social. The professional turf war is highlighted by the combinations commonly used which offer a non-medical perspective e.g. psychosocial, psychobiology, psychophysiology, psychoneuroendocrinology and sociobiology suggesting the primacy of psychology and sociology. Thus Yule (3) takes a firm psychosocial approach

to PTSD, an approach shared by many contributors to the British Journal of

Psychiatry. Ben Shephard (4), a British historian, clearly sees this as the current authoritative perspective.

There is no psychobacteriology or psychochemistry (there is little of

immediate relevance to claim) but there is psychogenetics although it is recognized that the further back genetics is traced the less significant are both psychology and sociology (5).This is not to deny the importance of psychology and sociology in understanding human behaviour and the presentation and management of much illness but there is an evolutionary history involving biology, physiology and neuroendocrinology that demonstrate well established patterns of relationship long before psychology or sociology had any relevance. Relationships involved in our psychosocial world occur in the context of these much older relationships.

Not so long ago animal studies were only considered relevant if a social environment, or life style, equivalent with that experienced by humans, was demonstrable and, in the minds of many, that still appears to be the case.Likewise the fear of reductionism is raised as an argument rather than whether concepts are useful and valid. The advances in brain chemistry should by now have encouraged a review of these positions. It is suggested that humans do not possess uniquely different neurochemical mechanisms and the control cascades are arguably similar across a very wide range of species.

Sociobiology is widely regarded as one of the controversies of the 20th and 21st centuries and posttraumatic stress disorder is clearly another. While criterion creep has maintained (and probably increased) the controversy, the essential value of the diagnosis was the ‘official recognition’ of a diagnosis that attributed a psychiatric condition to an environmental cause. Does it matter that not everybody experiencing even extreme stress seems to suffer

posttraumatic stress disorder and does it matter that, as it is currently defined, it is not the only condition an individual may suffer as a resultof such stress? It would still make sense if it was considered the most serious of the adjustment disorders. It is a problem, but no disgrace, that the diagnosis of PTSD is not set in concrete. As Bullmore et al say, “it is much more likely that we will need to develop more complex accounts, involving the interactions between multiple genes each of minor effect, post-translational and epigenetic factors, and the differential impact of environmental stressors depending on individual genetic susceptibility”.

The whole gamut of responses to threat and challenge, ‘normal’ and pathological (morbidity and mortality) have demonstrably similar responsesin the animal world – inviting a conclusion that genetic and environmental factors are involved. While True & Pitman (6) almost apologise for suggesting a genetic component in PTSD, a “prototypical environmentally caused disorder”, Uher (7) argues that, in disease, “the interacting effects of genetic and environmental factors are the rule rather than the exception”.

From the most minor to the most severe life threatening stress, animals as well as humans have developed mechanisms for coping and when these fail (and even sometimes when they are dramatically successful) there are demonstrable consequences. The evolutionary history of these mechanisms must be expressed in humans suggesting a very complex gene-environment picture in response to all stressors.

No other psychiatric disorder has a more obvious evolution. (It has been suggested in the past that manic-depression/bipolar may be connected with hibernation but the connection, attractive as it is, has nothing like the wide association of morbidity and mortality in the animal world resulting from excessive stress).

So what prevents this schema being widely embraced and appropriately investigated?Probable reasons may be:1. Political drives - to cut costs and appease a wide range of right wing interests including religious and military conservatives.2. Interprofessional rivalries. – particularly with our psychologist colleagues who are now very numerous and outvoting psychiatrists in their interest in

PTSD.3. Skepticism of some psychiatrists – perhaps related to suspicion of psychologists.4. Perhaps that some psychiatrists see PTSD as not really a serious mental


Professor Max Hamilton once said to one of us, in the company of two other academics (an American and an Australian), that PTSD, with reactive anxiety and depression, could happily be handed over to psychologists.Zohar et al (8) suggest “the disorder requires deeper understanding and consensus among professionals,” and since the disorder is a psychiatric diagnosis, that consensus needs to be achieved among psychiatrists.Is there any reason why we should not acknowledge the useful help of psychologists in the treatment of the disorder while forging a closer liaison with biologists in understanding the disease process?

1. Bullmore E, Fletcher P, Jones PB. Why psychiatry can’t afford to be neurophobic. Br J Psychiatry 2009; 194; pp 293-295.

2. Craddock N, Antebi D, Attenburrow M-J & Bailey A, Carson A, Cowen P. A Wake up call for British Psychiatry. Br J Psychiatry 2008; 193(1): pp 6-9.

3. Yule W. Post-Traumatic Stress Disorders Concepts and Therapy.Chichester: John Wiley and Sons, 1999.

4. Shephard B. A War of Nerves. London: Jonathon Cape, 2000.

5. Cantor C, Price J. Evolution and post-traumatic stress disorder. (Letter).Aust.N.Z.J.Psychiatry 2007; 41:770-771.

6. True WR, Pitman RK. Genetics and posttraumatic stress disorder. In

Posttraumatic stress disorder: a comprehensive text (eds PA Saigh & JD Bremner), pp144-159. Boston: Allyn and Bacon, 1999.

7. Uher R. Forum: the case for gene-environment interactions in psychiatry.Current Opinion in Psychiatry 2008; 21(4): pp 318-321.

8. Zohar J, Juven-Wetzler A, Myer V, Fostick L. Post-traumatic stressdisorder: facts and fiction. Current Opinion in Psychiatry 2008; 21(1):74-77.

Declaration of interest: None

I Paddy Burges Watson MD MRCPsychResearch Fellow, University of Taswmania

Adrian J Bradley Bsc (Hons) PhD LLB.Sen .Lecturer School of Biomedical SciencesThe University of Queensland

Correspondence: P Burges Watson, PO Box 5, Kettering, Tasmania, Australia 7155.

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Psychiatry and "Neurophilia" in Developing Countries

Prof K.A.L.A. Kuruppuarachchi MD,FRCPsych(UK), Professor of Psychiatry
03 June 2009

Why psychiatry can’t afford to be neurophobic by Bullmore, Fletcher and Jones (BJP, 2009) raises several important issues related to understanding the aetiology, course and the management of psychiatric illnesses.Obviously the “Mind- Body” dichotomy is going to be a continuous debate for a considerable period of time as the exact causation of mental illnesses is not clear.It is note worthy that the psychoanalytic theories to understand the symptoms, aetiology course of the illness and the therapeutic approaches were developed when the understanding of the neuro-chemical/neuro-endocrinological basis of the psychiatric disorders were inthe infantile stage. The “Biological Concept” of psychiatry has been debated and narrow and erroneous interpretation of biological psychiatry has been discussed(Kingdon & Young , 2007). It is interesting to note that the general pattern of the symptoms, courseof the illness and the treatment outcome in many psychiatric ailments suchas schizophrenia, bipolar affective disorder , major depressive disorder ,delusional disorders, autism , epileptic psychoses and even obsessive compulsive disorder are similar in many parts of the world despite the patients are from different socio-cultural backgrounds. So much so many clinicians use the same standard diagnostic criteria in clinical practice and in research work. However the culture can shape/colour the symptom pattern to some extent. Even though the cross-cultural factors are important in understanding and management of psychiatric ailments, the concept of culture – bound psychiatric disorders has been debated .The initial research evidence for better prognosis for schizophrenia in developing countries has been questioned (Cohen A. et al, 2008) Catatonic symptoms secondary to organic causes such as viral encephalitis are seen in countries like Sri Lanka (Kuruppuarachchi & Rajakaruna , 1999). Dramatic response of severe depressive symptoms/disorder to electro-convulsive therapy( which is still widely practiced in our countries) is also in favour of neurochemical basis for psychiatric illnesses. Neurobiological explanations in the causation and therapeutic interventions in aggression and violence have been highlighted (Siever, 2008). However the contribution of psychological and socio-cultural factors inthe understanding of the aetiology , maintenance of the illness and the therapeutic interventions in psychiatric disorders should not be under estimated.As suggested in the article the medical curricular (both undergraduate andpostgraduate) should be strengthened with regard to this important area.We feel that the psychiatrists in different sub specialties across the globe may work hand in hand to improve the understanding of this importantarea which will eventually benefit the patients all over the world.


Bullmore E, Fletcher P, Jones P.B.(2009) Why psychiatry can’t afford to be neurophobic, The British Journal of Psychiatry , 194, 293-295.

Kingdon D, Young A.H.(2007) Research into putative biological mechanisms of mental disorders has been of no value to clinical psychiatry, The British Journal of Psychiatry , 191, 285-290.

Kuruppuarachchi K.A.L.A., Rajakaruna R.R.(1999) Psychiatry in Sri Lanka , Psychiatric Bulletin , 23, 686-688.

Cohen A, Patel V, Thara R, Gureje O. (2008) Questioning an Axiom: Better Prognosis for Schizophrenia in the Developing World? Schizophrenia Bulletin , 34(2):229-244.

Siever L.J.(2008) Neurobiology of Aggression and Violence, American Journal of Psychiatry , 165, 429-442.
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Conflict of interest: None Declared

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Medical causal explanation and destigmatisation

Dusan Kecmanovic, Consultant psychiatrist and Visiting professor, University of Belgrade
13 May 2009

Bullmore, Fletcher and Jones (2009) presented ‘Proposals for strategic action’ aimed at supporting ‘the future growth of a brain-based medicine of the mind and its psychiatric practitioners’. The goal of the fifth of the five proposed actions is to enhance psychiatrists’ efforts tocommunicate the neuroscientific basis of mental disorders to patients, their families and the general public because ‘greater knowledge of the physical basis of mental illness should have a destigmatising benefit for our patients’. To have such a transforming effect on entrenched social attitudes towards mental illness – that are, as widely known, negative – the new medicine of the mind, the authors state, will need to be communicated more effectively to the public.

In a very recently published paper, Jorm and Oh (2009), on the basis of an analysis of the studies that have been carried out to assess whethermedical or psychosocial causal explanation have a greater influence on thestigma of mental illness, concluded that the findings are consistent: varying (biological versus psychosocial) causal explanation has no effect on social distance from a mentally ill person. And social distance is not only a dimension of the stigma but also one of the measures of how strong the stigma is.

Moreover, the medicalisation of mental disorders does not result in the attenuation or neutralization of negative responses to people with mental illness. It just leads to the expansion of stigma to psychiatry itself. (Guimon, Fischer and Sartorius, 1999)

Thus since the destigmatisation of mentally ill people is beyond the reach of the propagation of either a biological or psychosocial causal explanation, Bullmore, Fletcher and Jones, so as to make their ‘Proposal’ purposeful, should delete its fifth point.

Bullmore E, Fletcher P, Jones PB. Why psychiatry can’t afford to be neurophobic. Br J Psychiatry 2009; 194: 293-295.

Guimon J, Fischer W, Sartorius N. Introduction. In The Image of Madness. The Public and Professional Facing Mental Illness and PsychiatricTreatment (eds J Guimon, W Fischer, N. Sartorius): p. VIII, Karger, 1999.

Jorm A F, Oh E. Desire for social distance from people with mental disorders: a review. Aust NZ J of Psychiatry 2009; 43: 183-200.
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what lies behind this alleged neurophobia?

Hugh M Jones, Consultant Psychiatrist
28 April 2009

The Professors are perhaps unduly pessimistic ( Bullmore et al 2009) about their clinical contemporaries. Agreement is surely general that essentially all mental activity(whether mental illness or merely say thinking about the weather) is realised in the brain somewhere. At issue is what value is added by confirming this assumption in all cases? There is rather impatience that the gadgetry of modern scientific research mightmore interestingly help shape clinical practice.

They describe how brain imaging demonstrates changes that emerge during the course of first onset psychosis. These are interpreted as deficits, although current statistics by reducing brain activity to quantitative measures rather enforces such change to be viewed in this linear fashion. Such a view does not fit straightforwardly with current psychopharmacology. Although psychosis is often viewed as a condition of dopaminergic overactivity the weak D2 antagonist clozapine remains superior to other drugs with more robust D2 antagonism activity.

Besides statistical simplicity however this accords with a modern cognitivist account of brain function. Here illness is viewed on a continuum with health with the same brain mechanisms in use albeit workingless well than usual. This contrasts with the psychoanalytic tradition in which abnormal brain function is related to distinct brain mechanisms. Such a dichotomy is essentially that of the empiricist and rationalist traditions within the philosophy of mind.

Although the neuroscience community has pretty much wholescale embraced cognitivism, the clinical Psychiatry community rightly or wronglystill clings to insights derived from psychoanalysis. Is it too much to expect brain science to help us decide between these viewpoints? Although one understands the need to embrace prevailing scientific orthodoxy current statistical methodology doesn’t really allow this to be evaluated in a proper fashion. There is also the danger that in allying itself so closely with modern cognitive psychology ‘scientific’ psychiatry leaves itself at the mercy of any future reversal of fortune similar to what befell psychoanalysis in the 1970’s.

Bullmore E, Fletcher P, Jones PB (2009) Why Psychiatry cant afford tobe neurophobic . British Journal of Psychiatry 194 293-295
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Levels of Analysis in explaining Mental Illness

Carl F Johansson, CT1 Psychiatry
28 April 2009

Bullmore et al (1) argue for psychiatry to continue to develop as a neuroscientific discipline rebutting what they describe as ’neurophobic’ views of mental illness. I share their enthusiasm for further understanding the biological basis of psychological conditions and the article highlights an unhealthy division that continues to cause debate and disagreement in those treating mental illness. It often manifests itself in day to day clinical practice and is expressed as the view of mental illness as ‘psychological’ and those that look for a ‘biological’ explanation. Obviously the two can not be separated – unless clinging to aDescartian dualistic viewpoint one must be optimistic that all mental lifewill eventually be mapped onto a neuronal substrate.

Proponents of both approaches would do well to familiarise themselveswith David Marr (2) , acknowledged as the founder of Computational Neuroscience, and his concept of ‘levels of analysis’ which he applied to his seminal explanations of the visual system’s information processing. Hepointed out that one must be aware of the ‘level’ at which one is trying to explain a problem. Bullmore et al urge us to find explanations to mental functioning at the implementational level involving the biological substrate i.e genes, molecular and cellular interactions creating a complex system. Theories put forward by Beck and Seligman on explaining Depression for example and Clark’s work on Panic Disorder (3)are set a higher level of explanation and do not address the implementation of the processes. For example Clark postulated that it was a catastrophic interpretation of body state that lead to a panic attack. This level of explanation offers a psychological mechanism but does not comment on the biological underpinning of the disorder. This does not mean that Clark’s explanation of panic attacks claims the disorder to be ‘psychological’ rather than ‘biological’. Instead the explanation is set at a computational level and not an implementational level.

To understand that brain-based and psychological explanations are notmutually exclusive but that they offer different levels of explanation will help avoid unnecessary debate. We can no more afford to be ‘neurophobic’ than we can afford to be ‘psychophobic’; understanding at every level is vital in moving psychiatry forward as a discipline of medicine.

Decleration of Interest: None declared


1. Bullmore E, Fletcher P, Jones P. Why psychiatry can’t afford to beneurophobic Br J Psychiatry 2009 194: 293-295

2. Marr D. Vision: A computational investigation into the human representation and processing of visual information W.H Freeman and Co., 1982

3. Clark DM Clark, D. M. (1986). A cognitive approach to panic disorder. Behaviour Research and Therapy, 24, 461–70
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