Electronic Letters to:
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eLetters: Electronic letters published:
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Why psychiatrists can't afford to be neurophobic: where is the evidence?
- Vivek Datta (7 April 2009)
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I may be neurophobic but at least I don’t have BPD
- Sami Timimi (7 April 2009)
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Neurohawks Fight Back
- Andrew Blewett (7 April 2009)
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Does psychiatry need to address an ideological question?
- S M Singh (17 April 2009)
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Why psychiatry cannot be emotionless
- Daniel McQueen (17 April 2009)
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Levels of Analysis in explaining Mental Illness
- Carl F Johansson (28 April 2009)
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what lies behind this alleged neurophobia?
- Hugh M Jones (28 April 2009)
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Medical causal explanation and destigmatisation
- Dusan Kecmanovic (13 May 2009)
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Medical Science
- Ian P Burges Watson, Adrian J Bradley (3 June 2009)
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Psychiatry and "Neurophilia" in Developing Countries
- Prof K.A.L.A. Kuruppuarachchi MD,FRCPsych(UK) (3 June 2009)
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Vivek Datta, Visiting Research Fellow Division of Psychological Medicine, Institute of Psychiatry, King's College London
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vivek.datta{at}doctors.org.uk Vivek Datta
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Bullmore and colleagues (1) falteringly attempt to challenge 'neurophobic' positions in psychiatry, and then fail to present a persuasive argument for the increasing prominence of the neurosciences in psychiatry. They also contradict themselves in a number of places. For example, they argue that psychiatrists implicitly rely on neuroscience through prescribing drugs, suggesting that psychiatrists would not do so unless they believed that mental disorders were related to abnormal signalling between nerve cells, but later on admit that the true mechanism of action of psychiatric drugs and pathophysiology of mental disorders are unknown, but despite this conclude by advocating for more psychopharmacology in the MRCPsych curriculum. They correctly highlight the false dichotomy between functional and organic disorders. However, they fail to acknowledge that disorders previously conceived as psychiatric, for which a neuropathology has been elucidated are now considered neurological disorders and the preserve of neurologists. Huntington’s disease and neurosyphilis are two examples. As such, these authors do not consider, if future neuroscientific research elucidates a neuropathology for the major mental disorders, whether these disorders would still be under the remit of psychiatrists. If not, perhaps there is little need for clinical psychiatrists to embrace the neurosciences. They further note objections to neurobiological research are based on concerns that the doctor-patient relationship would be fundamentally altered to patients’ detriment. They argue that this is not the case for other medical specialties, where empathy and understanding are still important. However, Kleinman (2) notes that the doctor-patient relationship did indeed become a casualty of an increasingly scientific and technological medicine. They suggest that the neurosciences will reduce the stigma of mental illness. Yet, there is evidence that neurobiological models of mental disorder may actually increase stigmatising attitudes to the mentally ill and clinicians who hold such views less likely to involve patients in decisions about their care (3). They note the contention that physical models have not made any difference to clinical psychiatry. Yet they provide no defence, only an optimistic future prediction that this will happen. It is difficult to object to neurobiological research, but it is important to temper enthusiasm for its potential to revolutionise psychiatry. Not a single patient has benefitted from neurobiological research into psychiatry, and whilst psychopharmacology is one of the success stories of modern psychiatry, our drugs are the result of serendipity rather than a true understanding of the neural and molecular basis of the mental phenomena that underpin the experiences diagnosed as mental disorder. This research is extremely expensive and may be occurring at the cost of social, epidemiological and psychological research which find themselves increasingly difficult to secure funding. In contrast, such research has created evidenced-based interventions for mental illness. For example, the finding that high expressed emotion in families is associated with greater relapse in schizophrenia led to the development of family intervention (4), and the finding that life events of an interpersonal nature were associated with the onset of depression led to the development of interpersonal therapy (5). Perhaps psychiatry cannot afford to be neurophobic, but no evidence for this has thus far been provided. Declaration of interest: None 1. Bullmore E, Fletcher P, Jones PB. Why psychiatry can’t afford to be neurophobic. Br J Psychiatry 2009; 194: 293-295 2. Kleinman A. The illness narratives: suffering, healing and the human condition. Cambridge: Basic Books, 1988 3. Read J, Haslam N, Sayce L, Davies E. Prejudice and schizophrenia: a review of the mental illness is an illness like any other approach. Acta Psychiatr Scand 2006; 114: 303-318 4. Kuipers E, Leff J, Lam D. Family work for schizophrenia: a practical guide. London: Gaskell, 2002 5. Klerman GL, Weissman MM, Rousanville BJ, Chevron ES. Interpersonal psychotherapy of depression. New York: Basic Books, 1984 |
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Sami Timimi, Consultant child and adolescent psychiatrists Lincolnshire Partnership NHS Foundation Trust, Ash Villa, Willoughby Road, Sleaford, NG34 8QA
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stimimi{at}talk21.com Sami Timimi
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Bullmore et al’s (2009) offering is the latest of several articles in the British Journal of Psychiatry that argue that psychiatry depends fundamentally on bio-medical models. Their anxiety that we may be drifting away from a reliance on a belief that mental distress is the consequence of neurological dysfunction, is well placed. The era of evidence based medicine means we need more than fancy, plausible sounding theories to support our beliefs and practices. However, this was the first time I realised that this meant that I am suffering with a disorder – neurophobia. After my initial alarm and search for a viable, evidence based remedy for my condition, I gradually began to relax when I realised that the authors were struggling with a more serious and persistent disorder – BPD (Biobabble Peddling Disorder). For those readers unfamiliar with this syndrome, it has three main symptoms: 1. A ‘see no evil, hear no evil, speak no evil’ attitude to any evidence that contradicts their assumptions. Thus the only ‘evidence’ that Bullmore et al (2009) referred to were papers that support the Kraeplinian idea that schizophrenia is a condition of slow dementia. They conveniently ignored the evidence that antipsychotic use is associated with changes in brain volume (Moncrieff, 2008), which may account for the findings they listed. This is a concern as many who are diagnosed as schizophrenic have not demented and can and do make full recoveries. 2. A belief that there is jam and honey to come tomorrow. Unfortunately, this tomorrow never seems to arrive. The discoveries that link mental distress to neurological disorder seem always to be about to happen in 20 years time (as it was 20 years ago and no doubt will be in 20 years time). In the meantime we carry on funding research into the biological basis of mental illness, none of which has made a difference to clinical practice. Such a lack of return on massive investment makes the banking crisis look like a pleasant Sunday stroll. 3. A paradoxical belief that we are just like any other branch of medicine, but cannot be judged by the same standards as the rest of medicine. Thus BPDs’ believe that as psychiatrists we deal with ‘illnesses like any other illness’ but that psychiatry should have some special status that makes it exempt from requiring the same standards of evidence found in the rest of medicine. This is understandable, as the lack of empirical evidence to support their theories, means they must resort to reminding everyone about the ‘complexity’ of the disorders and invoking meaningless generalisations such as “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” (Bullmore et al, 2009: 294) as the best they can do for models of mental distress. Having examined the symptoms of neurophobia and compared them to BPD, I have concluded that if I have to have one of these disorders, I’d rather be ‘neurophobic’. Bullmore E, Fletcher P, Jones PB. (2009) Why psychiatry can’t afford to be neurophobic. British Journal of Psychiatry 194(4):293-5. Moncrieff J. (2008) The Myth of the Chemical Cure. Basingstoke: Palgrave Macmillan. |
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Andrew Blewett, Consultant Psychiatrist Devon Partnership NHS Trust
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andrew.blewett{at}nhs.net Andrew Blewett
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Bullmore et al (Why psychiatry can't afford to be neurophobic, British Journal of Psychiatry 2009; 194: 293-295) mount a defence of neuroscience in psychiatry, invoking History, a dawning golden age, Reil and Freud. Whilst ensuring that the curriculum for undergraduates and trainees should accurately reflect what is valuable for doctors wishing to understand and treat mental disorders, they don't fulfil the ambitions of their manifesto. Their argument against neuro-scepticism is weak. Specifically, physical models for mental disorder imply a particular position on psychology which is known as analytical behaviourism, and which effectively denies the existence of mind as a reasonable concept. They may wish to advance this view but either don't realise it or don't say so. Neuroscience is a materialist enterprise that generates and examines hypotheses about brain function, which may inform new ways of looking at mental life: but psychiatry cannot be "based" on neuroscience without becoming neurology. If psychiatrists cease to occupy the no man's land of unknowability, others will. The point about reductionism is a parallel problem. The kind of conversation that psychiatrists engage in with patients could well be better informed by neuroscience, but the reason for contemporary "vague talk about neurotransmitters" is that the innumerable diagnostic categories invented in psychiatry bear no relation to discrete pathognomonic anomalies: nobody would base a diagnosis of schizophrenia on a brain image whether functional or structural. Patients don't need to see their brains light up to know that they are experiencing voices. In psychiatry there is an under-rated crisis of validity, which many get around by claiming that psychiatry is where the rest of medicine was before the discovery of microbes and so on. An alternative view would be that schizophrenia for example is indeed a ‘functional’ disorder: an illness but not a disease, an illness that is culturally plastic and to a great extent subjective in its essence. Finally, the authors claim to refute the allegation that neuroscience is relatively bereft of therapeutic achievement. They fail to provide a single example of a ‘neuroscientific’ novelty since the 1960s, which has transformed any really notable aspect of outcome in psychiatry. The one really big change, de-institutionalisation, could have occurred without any input from neuroscience at all, in fact it was in large part a reaction against biomedicalism. It is doubtful that it would be deemed necessary to place yet another prominent polemical article in the BJPsych in defence of a narrowly conceived neuroscientific hegemony within psychiatry, were this not the case. |
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S M Singh, Assistant Professor in Psychiatry Gian Sagar Medical College, Banur, Punjab, India
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shubhmohan{at}gmail.com S M Singh
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Dear Sir, I read with interest the editorial by Bullmore et al (1) and the responses thereof. I believe that the editorial and the responses raise an important question regarding the ideological basis of psychiatry and the importance of the same. Ideology can be thought of as a way of looking at phenomena and in the absence of being in a state of knowing ‘for sure’, ideology drives the process of identifying, understanding and classifying those phenomena. It has been rightly pointed out that there is an under-rated crisis of validity as regards psychiatric pathological entities (leaving aside for the moment the import and implications of the disease versus disorder versus illness constructs). This crisis is as old as psychiatry and has existed for different reasons depending on the prevailing school of thought at a particular time. This crisis is likely to continue because the basis of these pathologies is unlikely to be elucidated any time soon. As a result, the current format of psychiatric nosology makes no assumptions. It only describes, attempts to classify and it seems useful to use. In such a scenario, it is important that we start with a construct for the ideological basis of psychiatric pathologies. Does the fact that neuroscience explains precious little in psychiatry make it necessarily bad ideology to explain the same? Assuming that psychiatric pathologies exist (quite possibly not in the manner currently classified), a basis in neuroscience for psychiatry is probably the only thing that is likely to ever provide a tangible, evidence based and replicable answer as to its why and how. A mind that is a product of the function of the brain is probably easier to work with than a mind that works on the basis of phantasmal reasons. It has been shown that neuroscientific interpretations of ‘psychological’ interventions such as psychotherapy are compatible. The reasons for the current failure of neuroscience to resolve these questions have been discussed elsewhere. Indeed, it is possible that the optimism regarding the promise that neuroscience seems to offer in psychiatry may be misplaced but as an ideology it is laudable. It is alright for the psychiatrist to occupy the unknown terrain, but the fear of losing out in a turf war to a neurologist should not mean the demise of seeking the truth. A psychiatrist manages a patient with schizophrenia better not because its aetiology is unknown but because she is better trained to do so. 1. Bullmore E, Fletcher P, Jones PB. Why psychiatry can’t afford to be neurophobic. Br J Psychiatry 2009; 194: 293-295 |
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Daniel McQueen, Specialist Registrar in Psychotherapy Cassel Hospital, West London Mental Health Trust
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Daniel.McQueen{at}wlmht.nhs.uk Daniel McQueen
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Psychiatry rests on the biopsychosocial model rather like a three- legged stool, remove any one of the legs and the stool, and psychiatry, fall over. Another three-legged stool might be that of emotion, cognition and behaviour, each is necessary, but insufficient, for understanding humans. In why psychiatry can’t afford to be neurophobic, (Bullmore et al 2009) give a compelling picture of the complexity and explanatory power of genotype and phenotype in modern psychiatry and neuroscience. He expands phenotype to include behaviour and cognition. He also refers to Reil’s vision of psychiatrists as physicians of the mind. Reil (1759-1813) was the creator of the term psychiatry and was concerned with the soul and soul organ, which he considered to be a product of the nervous system (Marneros, 2008). Reil’s conception of the soul would be considerably wider than cognitive function and behaviour. Living during the Romantic period he was concerned with what today might be called emotions, character and self-regulation. It is difficult to do justice to the full breadth of neuroscience in an editorial, however neuroscience and psychiatry are far broader than genes, cognition and the intervening processes. Although the nod is given to psychoanalysis and the importance of “mental, interpersonal, developmental and therapeutic processes”, and “maternal deprivation and child abuse”, there is no reference to emotion and it’s mental representation, affect, and the rapidly growing fields of affective neuroscience, attachment theory, affect regulation, mentalization and developmental psychopathology. Biology, ethology, paleoanthropolgy have shown that social living has been the most important recent evolutionary pressure for brain development (Wills 1993). Subjectivity is intrinsic to, and an emergent property of, our social brain (Solms & Turnbull, 2002). Ethology and attachment theory have shown how emotions are the glue of social interactions; from the moment of birth we are instinctually driven to engage with others: Attachment behaviours, smiling and crying, are genetically programmed. The representation of affect states in self and other (mentalization) is vital to affect regulation and effective social adaptation; affect regulation and mentalization are acquired through secure attachment relationships; and secure attachment, mentalization and self regulation contribute significantly to emotional resilience, which help us to weather the challenges that life presents us reduced with reduced risk of psychiatric illness (Fonagy et al. 2004; Sroufe et al. 2005). The danger of seeming to neglect the importance of emotion and relating (whilst emphasising the importance of cognition, molecules and genes) in psychiatry is that we risk promoting the disengagement from neuroscience that Bullmore argues so passionately against. Bullmore, E., Fletcher, P., Jones, P.B. (2009). Why psychiatry can’t afford to be neurophobic. The British Journal of Psychiatry, 194;293-295. Fonagy, P., Gergely, G., Jurist, E., & Target, M. (2004). Affect Regulation, Mentalization, and the Development of the Self. London: Karnac. Marneros, A. (2008). Psychiatry’s 200th birthday. The British Journal of Psychiatry, 193: 1-3. Solms, M., & Turnbull, O. (2002). The Brain and the Inner World. New York: Other Books. Sroufe, L. A., Egeland, B., Carlson, E. A., & Collins, W. A. (2005). The Development of the Person. The Minnesota Study of Risk and Adaptation from Birth to Adulthood. New York: Guilford. Wills, C. (1993). The runaway brain. London: Harper Collins. |
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Carl F Johansson, CT1 Psychiatry Charing Cross Training Scheme
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doctorfreddie{at}gmail.com Carl F Johansson
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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 a Descartian dualistic viewpoint one must be optimistic that all mental life will eventually be mapped onto a neuronal substrate. Proponents of both approaches would do well to familiarise themselves with 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. He pointed 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 not mutually 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 References: 1. Bullmore E, Fletcher P, Jones P. Why psychiatry can’t afford to be neurophobic 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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Hugh M Jones, Consultant Psychiatrist South London and Maudsley NHS Foundation Trust
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hugh.jones{at}slam.nhs.uk Hugh M Jones
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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 might more 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 working less 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 wrongly still 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 to be neurophobic . British Journal of Psychiatry 194 293-295 |
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Dusan Kecmanovic, Consultant psychiatrist and Visiting professor, University of Belgrade Kecmanovic Clinic, Sydney, Australia
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dkecmanovic{at}mail2me.com.au Dusan Kecmanovic
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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 to communicate 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 whether medical or psychosocial causal explanation have a greater influence on the stigma 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 Psychiatric Treatment (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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Ian P Burges Watson, psychiatrist (retired) , Adrian J Bradley
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paddyandjudy{at}clearmail.com.au Ian P Burges Watson, et al.
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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 stigmatisation of 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 result of 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 responses in 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 illness. 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 stress disorder: facts and fiction. Current Opinion in Psychiatry 2008; 21(1):74-77. Declaration of interest: None I Paddy Burges Watson MD MRCPsych Research Fellow, University of Taswmania Adrian J Bradley Bsc (Hons) PhD LLB. Sen .Lecturer School of Biomedical Sciences The University of Queensland Correspondence: P Burges Watson, PO Box 5, Kettering, Tasmania, Australia 7155. E-mail: paddyandjudy@clearmail.com.au |
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Prof K.A.L.A. Kuruppuarachchi MD,FRCPsych(UK), Professor of Psychiatry Faculty of Medicine, University of Kelaniya, Ragama, Sri Lanka
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lalithkuruppu{at}lycos.com Prof K.A.L.A. Kuruppuarachchi MD,FRCPsych(UK)
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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 in the 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, course of the illness and the treatment outcome in many psychiatric ailments such as 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 in the 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 and postgraduate) 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 important area which will eventually benefit the patients all over the world. References: 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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