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Schizophrenia and autism
- Stephen MW Hutchison (13 July 2007)
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No evidence that psychodynamic psychotherapy increases risk of relapse
- Mike J Crawford (16 July 2007)
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Delusions are not necessarily false beliefs
- Tom Hughes (20 July 2007)
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Economic Burden of Schizophrenia
- Professor Pranab Kumar Bhattacharya MD(cal),FIcpath(ind), Bhattacharya Rupak BSc(cal), MSC(JU), Bhattacharya Ritwik,B.Com(cal) , Bhattacharya Kausik7/51 Purbapalli, Sodepur, Kolkata-110, Mukherjee Dahlia BA(Hons)Cal Swamiji Nagar, Habra W.B (21 July 2007)
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Aetiology of schizophrenia: Multifactor/Polygenes vs the Speciation Event
- Timothy J Crow (23 July 2007)
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Re: Aetiology of schizophrenia: Multifactor/Polygenes vs the Speciation Event
- Woody Caan (24 July 2007)
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Schizophrenia is more than positive and negative symptoms
- Anthony Harris, Philip Boyce (27 July 2007)
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Viruses and Schizophrenia
- Professor Pranab Kumar Bhattacharya, Manna Asim Kumar MD(cal),Dip BMS(cal), IPGMER, Kol-20, Rupak Bhattacharya Bsc(cal) MSc(JU),Purbapalli, Sodepur, W.B Kol110 (27 July 2007)
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Re: Viruses do not cause schizophrenia
- Timothy J. Crow (1 August 2007)
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Making Schizophrenia worse - iatrogenic inhumanity
- Bob Johnson (3 September 2007)
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Schizophrenia is waking reality processed through the dreaming brain
- Ivan Tyrrell, Joe Griffin (22 November 2007)
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Stephen MW Hutchison, Consultant Physician in Palliative Medicine Highland Hospice, Inverness, IV3 5SB
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I am not a psychiatrist but I was interested to read about the theory that dopamine excess may somehow disproportionately increase the 'salience' of interactions such that features of schizophrenia emerge. My limited understanding of autism is that there is impairment of normal filtering of information, such that there is heightened interpretation. Might this represent some common aetiology in the two conditions? Competing interests: None declared |
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Mike J Crawford, Psychiatrist Imperial College London, Claybrook Centre, 37 Claybrook Road, London W6 8LN
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In their otherwise helpful review of schizophrenia and its treatment Picchioni & Murray (2007) make the claim that psychodynamic psychotherapy may increase the risk of relapse of schizophrenia. In support of this statement the authors reference a systematic review by Malmberg & Fenton (2001). While the authors of this review point out that negative effects associated with this intervention have not been properly investigated, this is an important deficit in many trials of psychological therapies. Malmberg and Fenton found no evidence that psychodynamic psychotherapy is associated with an increased likelihood of relapse. While improvements in mental health and other outcomes were not seen either, the authors state that this could be the result of study sizes and their limited statistical power. They also note that in the only trial to have compared psychodynamic and cognitive approaches those receiving psychodynamic psychotherapy were far less likely to leave the trial early (Gunderson, 1984), and suggest that this approach may therefore be more acceptable to patients. While an evidence base for the use for psychodynamic psychotherapy in schizophrenia does not exist, there is no evidence to suggest that it is any more or less likely to cause relapse than cognitive behaviour therapy or other psychological approaches to helping people with schizophrenia. Gunderson JG, Frank AF, Katz HM, Vannicelli ML, Frosch JP, Knapp PH. Effects of psychotherapy in schizophrenia. II. Comparative outcome of two forms of treatment. Schizophrenia Bulletin 1984;10:564-98. Malmberg L, Fenton M. Individual psychodynamic psychotherapy and psychoanalysis for schizophrenia and severe mental illness. Cochrane Database of Systematic Reviews 2001;3: CD001360 Picchioni MM, Murray RM. Schizophrenia. BMJ 2007; 335: 91-95. Competing interests: None declared |
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Tom Hughes, Consultant Psychiatrist St Mary's Hospital, Leeds LS12 3QE
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Picchioni and Murray give an excellent review of schizophrenia (1). However, I was disappointed that their definition of delusion was 'a fixedly held false belief that is not shared by others from the patient's community.' Similar definitions appear to be widely taught. A delusion is a belief for which there are no rational grounds, which is held with complete conviction, and which is out of keeping with the person's background (2). The difference is important clinically. Clinicians who favour Picchioni and Murray's definition may find it easy to identify a delusion when the content is outlandish e.g. 'Martians want to kill me', but less easy when the content is commonplace e.g. 'my wife is having an affair'. If a patient is convinced that his wife June is having an affair because he saw an article in the newspaper that morning about a local June Fair, then it is a delusion regardless of whether or not his wife is being unfaithful. Clinicians looking for truth may also find the exercise time- consuming, and expensive to employ private detectives, should June deny an affair. Delusions are generally false beliefs, but are not necessarily so. The important criterion is the grounds upon which the belief is held. (1) Picchioni MM, Murray RM. Schizophrenia BMJ 2007; 335: 91-95. M, Gath D, Mayou R. Oxford Textbook of Psychiatry. 2nd edition. Oxford: Oxford University Press, 1989. Competing interests: None declared |
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Professor Pranab Kumar Bhattacharya MD(cal),FIcpath(ind), Professor Pathology,Incharge HistopathologyUnit, Blood Bank&VCTC,Ex-incha Ronald Ross Malaria Clinic Institute of Post Graduate Medical Education &Research 244A AJC Bose Road, Kolkata-20, W.B, India, Bhattacharya Rupak BSc(cal), MSC(JU), Bhattacharya Ritwik,B.Com(cal) , Bhattacharya Kausik7/51 Purbapalli, Sodepur, Kolkata-110, Mukherjee Dahlia BA(Hons)Cal Swamiji Nagar, Habra W.B
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Schizophrenia has a substantial economic burden to the family members as we feel strongly. The prognosis for persons with this disease is often variable. For some, the disease may be relatively mild with the patients suffering once or for several episodes without requirement of hospitalization. However, the majority of patients with this disease are associated with repeated episodes and worsening of symptoms and outcomes. The combined economic and social costs of schizophrenia place it amongst the world's top ten causes of DALY accounting for an estimated 2.3% of all burdens in the developed countries and 0.85% in the developing countries(1) . At present there is no complete cure for schizophrenia. According to us, the goals of treatment include to improve quality of life, prevention of relapse, re-hospitalization, and rehabilitation. As we consider it that schizophrenia significantly decreases patient’s ability to actively participate in the labor force of the state, to earn his/her lively hood, resulting in high unemployment rate and demands an economic support from the family members, society and government. Most often time these are lacking in the town and urban of industrialized states. Patients of schizophrenia though often has better IQ level in his/her previous settings of life, then even from rest of general population, however though they are engaged in works, who even do work ,often earn an income that is substantially bellow to maintain life. This is more due to drugs (anti psychotic, anti depressive) then due to disease itself. More over the drugs and medicines are often in combinations of drugs and are very costly in open economic market. Complications of drug treatments causes’ further burden to the family. In the state of West Bengal most of patients has to purchase of these drugs even in the public hospital set up when prescribed in OPD basis. As a result, schizophrenia patients contribute to excess mortality in the industrialized state. Another important reason for higher mortality rate of schizophrenia is suicide and cardio logical problems (arrhythmias) from the drugs. The life time risk of suicide in general population in state of West Bengal is 0.5% -01% when in schizophrenia patients 15-25 times higher(2) and life time risk is 9-13%. The proportion of all suicide is attributable to schizophrenia through out the world is 9.7% and unlike almost every country in the world the prevalence of suicide in schizophrenia is higher in women than in man and in urban than in rural settings. People with schizophrenia are 24 times more likely to commit suicide than without schizophrenia. State of depression and use of Clozapine may be the cause as per present authors. The health care costs of schizophrenia includes costs of anti psychotic drugs, drugs for adverse or side effects, investigation costs and acute and non acute hospital. In Canada total life time health and non health care costs for schizophrenia borne by federal of govt. is about $2.02 billion of which majority of costs for acute & non acute admission are $ 474 million and $ 761 million respectively and prescription medicine costs $ 1509(3) We are surprised to find that the state govt. of West Bengal do not spend any thing for this disease except free consultation at psychiatric OPD References 1)Kim T Muser, Susan. R; Mc. Gurk. “Schizophrenia”. The Lancet 363; june19; 2063-72;2004 2) Addington DE & Addington JM “Attempted suicide & depression in schizophrenia “Acta Psychiatr Scan 85; 288-91;1992 3) R. Goreree.F, Farahad. N. Burke et al “The economic burden of Schizophrenias in Canada by federal Govt. in 2004 “. Current Medical Research and opinion. 21; no12; 2017-28; 2005 Competing interests: None declared |
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Timothy J Crow, Honorary Director SANE POWIC, University Department, Warneford Hospital, Oxford OX3 7JX
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Timothy J Crow, Email: tim.crow@psych.ox.ac.uk For many years the polygenic-multifactorial view of the aetiology of schizophrenia has found a home at the Institute of Psychiatry from which Picchioni and Murray (14th July 2007 pp91-95) give an eloquent exposition. However, there are problems with the concept 1. No environmental factor is clearly established. Picchioni and Murray put weight on obstetric complications but a follow-up of the 1958 Perinatal Mortality Survey showed no complication of pregnancy or parturition as relevant to the later onset of schizophrenia (1), and the thorough case-control meta-analysis (2) to which Picchioni and Murray refer reveals small and variable effects that may well be attributable to the difficulty of matching cases and controls in individual studies. The authors themselves remark that “The findings from the population based studies were mostly negative and surprisingly contradictory” and later that “At no stage did we suggest that a causal relationship has been established for any one obstetric risk factor”. 2. The polygenes to which they refer but do not name have proven elusive in linkage studies and, if present at all, are remarkably weak in effect. Several genome scans with sample sizes in excess of 300 sibling pairs show negligible agreement between studies (3). 3. Increasing evidence that schizophrenia is part of a spectrum of variation that includes major affective syndromes as well as extending into the general population indicates we are dealing with continua of variation and not discrete categories. The disappearance of pregnancy and birth complications, together with prenatal exposure to influenza, now wisely omitted from the list of early environmental factors leaves the course of “increasingly deviant development … to …frank psychosis” as bereft of precipitants. Undoubtedly there are early deviations and a "neuro-developmental" interpretation is plausible. But causation remains unexplained. There are however uniformities that Picchioni and Murray overlook. Schizophrenic illnesses occur in all populations with an incidence that is more uniform as one moves towards a core syndrome. Thus the apparent genetic influence is remarkably evenly distributed and constant in effect. Structural brain change, eg a degree of ventricular enlargement is a consistent finding. These facts sit uneasily with the polygenic environmental interaction theory. Rather than as a long delayed effect of early environmental insult the onset of psychosis can be seen as reflecting the emergence of variation associated with the latest phylo- and onto-genetic elements in the trajectory of human brain development. Homo sapiens evolved by a great prolongation in the course of maturation and that change reflects a genetic innovation relating precisely to the era of cerebral cortical development in which psychotic symptoms unfold. Thus genetic predisposition to psychosis could reflect variation associated with the gene(s) responsible for changes in hominid evolution relative to the common great ape precursor. Specifically a component of that variation is related to the cerebral torque, the feature that appears characteristic of the human brain and its capacity for language (4). In support of this view are some specific morphological findings – asymmetries of pyramidal cell density in dorsolateral prefrontal cortex were found to be to the left in 9 out of 10 normal individuals, but to the right in 8 out of 10 individuals with schizophrenia (5). Again changes in the left medial temporal lobe eg the para-hippocampal gyrus, appear to be relatively consistent in post-mortem and imaging (6) studies, and there are reports of arcuate bundle deficiencies selective to the left side (7,8), and a striking report of loss of asymmetry of dopamine uptake processes in the striatum that cleanly separates patient and control groups (9). Thus the alternative to the polygenic-multifactor view is that the variation relates to the most recent change in human phylogeny, specifically to the genetic event that transformed a prior species, eg Homo Heidelbergensis into Homo sapiens (10). The variation associated with this genetic change (the Xq21.3 to Yp duplication and its subsequent re-arrangements on the Y are suggested as having a primary role in the hominid lineage) may well depend on the interaction between X and Y chromosomes and relate to what is now described as “meiotic suppression of unpaired chromosomes”, an epigenetic process associated with modifications of the histones that constitute the skeleton of chromosome structure. In this case the increased risk (that applies mainly to first-degree relatives) would be expected to be limited to one, or at most, two generations rather than fixed in the gene sequence for many. In this mechanism I propose lies variation that relates not only to schizophrenia but to the diversity of human psychological development that includes other psychopathological deviations, eg the autistic spectrum, other psychoses and deviations in personality. According to this view the variation relates to a particular genetic mechanism, is a consequence of a singular and relatively recent (maybe 160 KYA) event in our evolutionary history, and is a component of the diversity associated with the cerebral characteristic (that I take to be the torque) that defines the species and gives us our unique social and communicative creativity. References (1) Done DJ, Johnstone EC, Frith CD, Golding J, Shepherd PM, Crow TJ. Complications of pregnancy and delivery in relation to psychosis in adult life: data from the British perinatal mortality survey sample. Br Med J 1991; 302:1576-1580. (2) Cannon M, Jones PB, Murray RM. Obstetric complications and schizophrenia; historical and meta-analytic review. Am J Psychiatry 2002; 159:1080-1092. (3) Crow TJ. How and why genetic linkage has not solved the problem of psychosis: review and hypothesis. Am J Psychiatry 2007; 164:13-21. (4) Crow TJ. Schizophrenia as the price that Homo sapiens pays for language: a resolution of the central paradox in the origin of the species. Brain Res Reviews 2000; 31:118-129. (5) Cullen TJ, Walker MA, Eastwood SL, Esiri MM, Harrison PJ, Crow TJ. Anomalies of asymmetry of pyramidal cell density and structure in doroslateral prefrontal cortex in schizophrenia. Brit J Psychiatry 2006; 188:26-31. (6) Honea R, Crow TJ, Passingham D, Mackay CE. Regional deficits in brain volume in schizophrenia: a meta-analysis of voxel-based morphometry studies. Am J Psychiatry 2005; 162:2233-2245. (7) Burns J, Job D, Bastin ME, Walley H, Macgillivray T, Johnstone EC et al. Structural disconnectivity in schizophrenia: a diffusion tensor magnetic resonance imaging study. Brit J Psychiatry 2003; 182:439-443. (8) Hubl D, Koenig T, Strik W, Federspiel A, Kries R, Boesch C et al. Pathways that make voices: white matter changes in auditory hallucinations. Arch Gen Psychiatry 2004; 61:658-668. (9) Hsiao M-C, Lin K-J, Liu C-Y, Kai-Yuan T, Tzu-Chen Y. Dopamine transporter change in drug-naïve schizophrenia: an imaging study with 99mTc-TRODAT-1patients. Schiz Res 2003; 65:39-46. (10) Williams NA, Close J, Giouzeli M, Crow TJ. Accelerated evolution of Protocadherin11X/Y: A candidate gene-pair for cerebral asymmetry and language. Am J Med Genet (Neuropsychiatric Genet) 2006; 141B:623-633. Competing interests: None declared |
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Woody Caan, Professor of public health Anglia Ruskin University, Cambridge CB1 1PT, UK.
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Prof. Crow has added a vital dimension to this aetiology, that of Developmental Trajectories at individual and species levels. [1] His evolutionary approach to schizophrenia resonates with Nobel Laureate John Nash Jr.'s recent address to the American Psychiatric Association. The advantage for humanity in having potential 'diversity' in mental development is huge, in our 'complex' and changeable environment. [2] Within each lifecourse there may be critical stages of mental development [3] probed in natural experiments with drugs (including cannabis, LSD, or cocaine) or in whole cohorts exposed to the horrors of war, forced migration or imprisonment. Crow's Oxford contemporary Gordon Claridge used to give students vivid accounts of the 'Seven Day Psychosis' observed during military service, and its resemblance to a 'Bad Trip' after LSD. The conceptual bridge between Crow's model and Picchioni and Murray [4] is in the latter's observation that people 'try to make some sense' of their psychotic experiences. Crow describes the unique essence of homo sapiens as 'communicative'. [1] What if communication is only part of that evolutionary leap of imagination? In H.G. Wells' 'Island of Dr. Moreau' the talkative chimp pesters the shipwrecked sailor for some Big Thinks he associates with being a man. Is communication just a small step in what Viktor Frankl called 'The Will to Meaning'? [5] We seem to be hard wired to try to make sense of our lives, but psychosis can subvert this in any member of our species. Prof. Crow, Prof. Nash, Dr. Frankl (and Dr. Moreau) all teach us: Are We Not Men? [1] Crow TJ. Aetiology of schizophrenia: multifactor/polygenes vs the speciation event. BMJ rapid response 23 July 2007. [2] Moran M. Nash suggests schizophrenia may serve adaptive function. Psychiatric News 6 July 2007 http://pn.psychiatryonline.org/cgi/content/full/42/13/2 (accessed 23 July 2007). [3] Caan W. Wider implications for our understanding of 'mental illness'. BMJ rapid response 3 December 2004. [4] Picchioni MM, Murray RM. Schizophrenia. BMJ 2007; 335: 91-95. [5] Frankl VE. The Will To Meaning. New York: Meridian, 1988. Competing interests: None declared |
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Anthony Harris, Senior lecturer Department of Psychiatry, Westmead Hospital, PO Box 533, Wentworthville, NSW 2145, Australia, Philip Boyce
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Dear Sir, We read with interest the review of schizophrenia by Picchioni and Murray and would like to question their description of the disease and the symptoms they review. We were surprised that the authors omitted to mention the cognitive dysfunction present in the disease. These deficits in attention, concentration, memory (especially verbal memory) and executive function, are now well recognised (1) and along, with negative symptoms are the most important determinants of function and outcome (2, 3). Indeed they are far more likely to predict eventual outcome than the positive symptoms of schizophrenia upon which the article dwells in some detail (2). These deficits are present from the time of first presentation to services (4), are stable over time and persist (5). For medical practitioners to understand the profound difficulty that patients with schizophrenia frequently have in negotiating our world, an understanding of their marked cognitive difficulties is essential. Such symptoms can often explain the poor functional outcome of patients even when the positive symptoms of the disease have been controlled. If one’s basic cognitive functions are impaired return to school, training or employment and indeed the ability to negotiate the complexities of health and welfare services are severely impacted upon, making full recovery unlikely. An understanding of the treatment of cognitive dysfunction is only beginning. Second generation antipsychotics do have a modest advantage over first generation antipsychotics in treating cognitive dysfunction (6). Cognitive remediation, a new psychotherapy, show more promise with a number of approaches showing a greater effect size than pharmacotherapy (7). However as with any psychotherapy within public mental health services the greatest struggle may not be the development of an effective treatment but its provision in services already stretched by providing the most basic support and treatment. Reference List 1. R. W. Heinrichs, K. K. Zakzanis, Neuropsychology 12, 426 (1998). 2. M. F. Green, American Journal of Psychiatry 153, 321 (1996). 3. M. F. Green, R. S. Kern, D. L. Braff, J. Mintz, Schizophrenia Bulletin 26, 119 (2000). 4. D. Fitzgerald et al., Australian and New Zealand Journal of Psychiatry 38, 501 (2004). 5. A. L. Hoff et al., American Journal of Psychiatry 156, 1336 (1999). 6. C. R. Bowie, K. Jaga, Expert Review of Neurotherapeutics. 7(3):281-7, (2007). 7. E. W. Twamley, D. V. Jeste, A. S. Bellack, Schizophrenia Bulletin 29, 359 (2003). Competing interests: None declared |
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Professor Pranab Kumar Bhattacharya, Professor of Pathology, Incharge Unit, Blood Bank& VCTC, Cytogenetics,Ronald Ross Malaria Clinic Institute of Post Graduate Medical Education & Research, 244A AJC Bose Road, Kolkata-700020, W.B,, Manna Asim Kumar MD(cal),Dip BMS(cal), IPGMER, Kol-20, Rupak Bhattacharya Bsc(cal) MSc(JU),Purbapalli, Sodepur, W.B Kol110
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Associations of schizophrenia and viral exposer during the 2nd trimester of pregnancy (an important period of development of Hippocampus of human brain) are found by several researches. Disorganization of hippocampus neurons was also reported by several authors. Neuronal disarray had been attributed to abnormal prenatal migration of neuroblasts into hippocampal primordium. Hippocampal volume and pyramidal cell density when was measured in each of the four sections of corne ammonis by means of a semi automated computerized system, schizophrenia patients had consistent lower cell density in hippocampus(unpublished data by authors) Virus implicated are influenza virus(1), type-1 herpes simplex virus(3), cytomegalo virus(4), hepatitis B virus(2), human endogenous retrovirus(5). Serological data from human studies in serum, CSF, proliferative responses in peripheral blood mononuclear cells(PBMSC), Western blot analysis, electrochemiluminescence immunoassay show that exposer to environmental trauma including viruses particularly during 2nd trimester of pregnancy increases the risk for later development of schizophrenia References-: 1) Mednick SA, Maclion.RA, HullenonMO, Bonnet D “ Adult Scizophrenia following prenatal exposer to an influenza epidemic “ Arch.Gen. Psychiatry 45;189-92;1988 2)O reilly RL “ viruses & schizophrenia” Aust. NEZ Psychiatry 28;222- 28;1994 3) Bartava L Rajenij, Pogady J “ Herpes simplex antibodies in the CSF of Scizophrenia patients “Acta Virol 155;661-66;1987 4) Albrecht.P, Torrey EF, Boone.E etal “ Raised Cytomegalo virus antibody level in CSF of schizophrenic patients” Lancet 2;769-72;1980 5) Karlson H Bachmann.S, Schorder.J etal “ Retroviral RNA identified in the CSF and brain of individual with schizophrenia” Proc. Natl. Acad. Sci. 98;4634-39;2001 Correspondence Professor Pranab Kumar Bhattacharya MD(cal) FICpath(ind)
Competing interests: None declared |
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Timothy J. Crow, Honorary Director SANE POWIC, Warneford Hospital, Oxford OX3 7JX
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In my opinion the scope for virus causation of schizophrenia and the evidence of structural change in the hippocampus are both less than Professor Bhattacharya supposes. Concerning the viral theory I write from the perspective of having been one of its most enthusiastic advocates (Crow, 1983). Up until 1983 I agreed with Torrey and Hare that the possibility that schizophrenia was caused by a virus had been greatly neglected. Specifically, I argued that there was evidence for horizontal transmission ie contagion. But I convinced myself that this was not the case on the basis of the finding that when two siblings develop the disease they do so at the same age and not the same time (Crow and Done, 1986). Co-incidentally other evidence that my colleagues and I thought we had of infection became explicable on other grounds (Crow, 1984). Subsequently a case was made by Mednick et al for prenatal exposure to influenza as Prof Bhattacharya reminds us. That case was severely damaged in my view, by evidence that we were able to glean from the UK National Child Development Survey that mothers who had suffered from influenza in the second trimester did not have an excess of children who later developed schizophrenia (Crow and Done, 1992). There were three cases, which was exactly population expectation when by the predictions of the proponents of the hypothesis there should have been 28! That I suggest was as decisive a refutation as you could hope for. I see no compelling evidence for other agents as early causative factors. Concerning the hippocampus as a target of the disease process my colleagues and I completed a series of detailed post-mortem studies. We found no evidence of a change in structure, as assessed by the size of the hippocampus or its individual subfields, the density of the constituent cells or the size of those cells (Walker et al, 2002). Nor do we see evidence of cellular disorientation. The hippocampus in our view is normal. It is on the basis of findings such as these that I am convinced that an evolutionary explanation is required, and that the primary changes are in the cerebral cortex. This is the structure that has changed most recently in human evolution, and it has done so by the introduction of the cerebral torque. It is to the developmental control of this sapiens specific feature that we should look in our search for an explanation. Crow, T. J. (1983) Is schizophrenia an infectious disease? Lancet, 342: 173-175. Crow, T. J. (1984) A re-evaluation of the viral hypothesis: Is psychosis a result of retroviral integration at a site close to the cerebral dominance gene? British Journal of Psychiatry, 105: 243-253. Crow, T. J., and Done, D. J. (1986) Age of onset of schizophrenia in siblings: a test of the contagion hypothesis. Psychiatry Research, 18: 107-117. Crow, T. J. and Done, D. J. (1992). Prenatal exposure to influenza does not cause schizophrenia. British Journal of Psychiatry, 161: 390- 393. Walker, MA et al (2002) Estimated neuronal populations and volumes of the hippocampus and its subfields in schizophrenia. American Journal of Psychiatry, 159: 821-828 Competing interests: None declared |
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Bob Johnson, Consultant Psychiatrist PO38 9AA
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What a toxic fiasco – surely at the start of the twenty-first century we can do better than Picchioni and Murray’s review of schizophrenia1. Doubtless their review faithfully reflects current views of psychosis – but what an awesomely impoverished view that is. When the term ‘medical model’ is deployed to abuse psychiatry, then some effort to restore medicine’s good name should at least be attempted. Sadly those accusing present-day psychiatry of reducing sufferers to ‘mindless unfeeling robots’ will find ample supporting evidence here. But first, why no reference to the abundant data that neuroleptics prolong psychoses? For 50 years there has been a continuous stream of damning evidence – from the Nine Hospital Study2 when after 12 months the non-drugged group were twice as healthy, through WHO studies in the 1970s3 where if you developed schizophrenia in countries too poor to afford neuroleptics you went back to work within 3 years, to the latest4 where stopping medication improved recovery rates eight-fold. You’ll be much better off going against what the doctor says – hardly the best basis for any medical practice. Even flimsier whiffs of iatrogenic damage should be intolerable in any medical speciality, especially one as important as psychiatry. Whichever way you define psychosis, and the definitions offered are unhelpful, it is self-evidently a disease of the mind. Yet this most important of all human organs, is never mentioned. Half baked philosophy, such as the banal obfuscation about ‘mindbody dualism’ in DSM–IV5, doesn’t help – but if doctors use their own minds to puzzle out diagnoses, surely they should afford the same courtesy to their clients. Not only are sufferers from schizophrenia presented as mindless – they are also seen as emotionless. In the opening sentences of their review, everyone is allowed to feel fear – except the sufferers themselves. And yet this is the key to the disease, as also to its cure – eliminate the fear by extending the ‘healing hand of kindness’, and recovery rates rocket, as they did in 17966. Recent fMRI studies7 indicate how fear degrades cognition. Reducing fear allows sufferers to blossom. When psychiatrists reintroduce emotions into their practice, as I was trained to do8, their tasks become infinitely more rewarding. Robots and automatons are incapable of intent, let alone consent. Yet consent is the foundation stone of democracy, indeed of civilisation, and thereby also of the stable mind. By enlisting it, rational thought becomes available in even the severest psychosis – a happy outcome that remains unobtainable as long as doctors refuse to allow themselves to talk openly about infantile terrors and traumagenesis. Picchioni and Murray’s review is based on meta-analyses. A rather different perspective emerges in a public debate9. Here parents and others eloquently describe their suffering, and the damage done by medication. Also on display is a psychiatric nihilism bordering on the inhumane – enough to make you wince. Psychiatry should be queen of all medical specialities, but first it must eliminate every last thing portraying human beings as ‘mindless unfeeling robots’. Dr Bob Johnson
1 Marco M Picchioni and Robin M Murray Clinical Review of Schizophrenia BMJ 2007;335:91-95 (14 July), doi:10.1136/bmj.39227.616447.BE 2 cited in Robert Whitaker 2002, Mad in America, Basic Books, New York, ISBN 0738203858 3 Robert Whitaker 2002, op cit 4 Martin Harrow and Thomas Jobe. “Factors involved in outcome and Recovery in Schizophrenia patients Not on Antipsychotic Medications: A 15-Year Multifollow up Study”. The Journal of Nervous and Mental Disease, 2007; 195:406-414. 5 Diagnostic and Statistical Manual of Mental Disorders. 4th Edition, American Psychiatric Association 1994 (DSM-IV), xxi. 6 Robert Whitaker 2002 “The healing hand of kindness”. op cit, ch 2. 7 Dean Mobbs, et al. When Fear Is Near: Threat Imminence Elicits Prefrontal- Periaqueductal Gray Shifts in Humans Science 24 August 2007:Vol. 317. no. 5841, pp. 1079 – 1083 DOI: 10.1126/science.1144298 8 Bob Johnson, 2005. Emotional Health Trust Consent Publishing, Isle of Wight, UK. ISBN 978-0-9551985-0-2 9 Public Debate 2006, ‘Psychiatric drugs do more harm than good’, transcribed at www.TruthTrustConsent.com Competing interests: None declared |
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Ivan Tyrrell, Principal of MindFields College MindFields College, Chalvington, East Sussex, BN27 3TD, Joe Griffin
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When innate emotional needs – human givens – are not being met well, people start to worry excessively and are then prone to becoming depressed. Our observations of hundreds of depressed patients had confirmed that excessive worry puts huge stress on the REM sleep mechanism. (Stop them worrying and the depression lift.) This led us to hypothesise that schizophrenia develops in those particularly imaginative, highly sensitive people who become so stressed that the REM sleep discharge mechanism cannot take the strain, and so their ability to separate waking reality from the metaphorical reality of the dream world (where the metaphors themselves seem totally real), becomes impaired. When they wake up, they cannot properly switch out of the REM state and become stuck in it. Naturally their thinking is then predominantly driven from the right hemisphere, the part of the brain most active in metaphorical pattern matching and dreaming. Many of their bodily behaviours could be expected to derive from those found in normal dreaming. In other words, the left hemisphere’s role, which is normally to analyse and organise reality in a rational way, and is predominantly in charge during wakefulness, has been usurped. The delicate working partnership of the brain’s hemispheres has shattered. This, to our minds, provides a plausible way of explaining the wide variety of psychotic symptoms. The phenomenon of ‘word salad’ – the loosening of meaningful associations between words and phrases that results in people talking in a stream of apparent nonsense – is just what one might expect if the left hemisphere of the brain were to be out of sync with the metaphorical mind of the right hemisphere, as the latter would continue to generate associations without waiting for the left hemisphere to check them out and articulate them. Catatonia, where patients can stand, sit or lie motionless for long periods in strange postures, oblivious to pain, is what the body also does during REM state dreaming, when the anti-gravity muscles are paralysed. Indeed, resistance to pain is often observed among schizophrenic patients and is even more marked during severe episodes. This is easily understood when we realise that, in dreaming also, cut off from all sensation, we experience no physical pain. That, too, is a REM state phenomenon (and is why hypnotised people can have major surgery painlessly without anaesthetic, as we have discussed). Hearing voices is entirely predictable from our theory too. Talking is primarily a left hemisphere activity, whereas right hemisphere activity is mainly concerned with processing pattern matching and tagging emotions to those patterns to prompt action. We don’t talk when the right hemisphere is dominant during dreaming in REM sleep, although talking whilst in slow-wave sleep is common (but the content rarely seems to make sense to the awake mind.) However, during a psychotic episode, if the person were in the REM state awake, there would still be some logical activity and thinking taking place in the left hemisphere. But, because the REM state is not anticipating any input from the left hemisphere, it has to interpret those thoughts metaphorically and comes up with the image of alien voices, which can seem to be commenting on the person’s every move, or haranguing them or giving ‘instructions’. (It might be expected that such thoughts would often be critical because the left hemisphere would, to some degree, still be able to analyse what was going on and ‘logically’ know that the behaviour is not normal.) This could further be interpreted metaphorically by the right hemisphere as being spied upon, or being persecuted, or that aliens are inside their head or that they are being followed everywhere by strange ‘rays’ that know everything they are doing. (Neurophysiological evidence confirms that, when schizophrenic people are hearing voices, the speech centres in the left neocortex are activated. And other researchers have observed and filmed REM activity when patients hear voices.) The visual hallucinations or delusions associated with psychosis are also totally characteristic of the dream state, the function of which is to generate such hallucinatory realities. Neuroscientists have shown the same neuronal pathways are activated in psychotic episodes. Whilst dreaming we all believe completely in the reality of our dreams, just as the schizophrenic person believes in their reality. It has long been suggested that there is a connection between creativity and mental illness. Certainly, people prone to schizophrenia tend to come from creative families. And even if they themselves are not productively creative, then high rates of creativity are found among their siblings and other relatives. Furthermore, creative people tend to be more sensitive to the emotional environment around them and are less robust in withstanding hostility, intolerance or criticism. Indeed, the higher the level of emotional criticism within the family context, the higher the rate of schizophrenic and depressive relapses. When people go into a psychotic REM trance due to emotional arousal any criticism may well be acting like a post-hypnotic suggestion, compounding the condition. When treatment for people suffering psychotic breakdowns concentrates on getting the patient's innate emotional needs met, a much higher rate of recovery is seen. Ivan Tyrrell and Joe Griffin Competing interests: None declared |
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