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Rapid Responses: Rapid Responses published:
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New research, confusing nomenclature, diagnostic criteria - a winning synergy
- Kate Duprey (1 May 2005)
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Prejudice based medicine
- N Portman (1 May 2005)
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Failure to consider the issue of differential diagnosis now inexcusable.
- Angela P. Kennedy (3 May 2005)
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BCDC
- Douglas T Fraser (3 May 2005)
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Three important criticisms
- Charles Bernard Shepherd (6 May 2005)
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Nutritional deficiencies found in ME/CFS patients.
- Ellen C G Grant (7 May 2005)
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Re: Nutritional deficiencies found in ME/CFS patients.
- Di newman (9 May 2005)
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Nutritional deficiencies and food and chemical allergies in ME/CFS patients.
- Ellen C G Grant (9 May 2005)
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Temporomandibular Joint dysfunction as a Differential Diagnosis in ME/CFS patients
- Mohamed Amir (5 September 2006)
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Kate Duprey, Journalist freelance 66202
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Dr. Viner and psychological specialist Dr. Christie’s ABC section on adolescents very ably presents the "psychosocial" component of biopsychosocial medicine Charles Engel outlined in his seminal 1977 study re Rather casually put, Engel’s theory is "a little social with your bio is good medicine." Indeed. As with the many other approaches to overall health care, empirically balanced with appropriate checks and balances guarding against misdiagnosis, whether bio or psychosocial, it is a concept well deserving of public discussion and further public edification. Psychologist Carol Tarvis has published some fascinating explorations in this area. In my personal opinion, her book on anger as a cultural expression is phenomenal. I highly recommend it. Dr. Harriet Lerner has also published work on girls and adolescents that may be of tangential interest. However, what was not entirely clear to me in this specific article by Drs. Viner and Christie’s was the actual topic since two separate entities were referenced in the same article. I read numerous references to "fatigue," as a nondiagnostic term meaning different things to different people, as well as being a common symptom of many different biological illnesses, and some psychiatric constructs as well. From a scientific viewpoint however, what specifically threw me, was the lack of differentiation by Drs. Viner and Christie between the separate entities of unspecified chronic "fatigue" and "chronic fatigue syndrome" where "fatigue" is specifically defined as "postexertional fatigue." At least by the Centers for Disease Control (CDC) in the United States. I decided to do a few more background checks. Further fact checking verified that current ICD classification by the World Health Organization in Geneva, formally classifies "undifferentiated fatigue, " “fatigue disorders” as well as the term "neurasthenia," under F48.0 Mental and Behavioural Disorders. I also checked for both "chronic fatigue syndrome" and fibromyalgia often listed with chronic fatigue syndrome, under this classification, but discovered they are specifically listed under separate biological classifications. Long story short, according to WHO, “chronic fatigue syndrome” is formally classified under diseases of the nervous system along with the terms myalgic encephalomyelitis (ME) and post viral fatigue syndrome, specifically G93.3 and has been since 1992 although the medical designation ME reflects a significant body of neurological research dating back around 70 years. The term, chronic fatigue syndrome didn't arrive on the scene until the late 1980s early 1990s according to research databases and the WHO. Further exploration of the subject revealed confusion regarding an attempted reclassification “chronic fatigue syndrome’ a few years ago by an outlying psychiatric collaborating centre. A technical officer in the Geneva headquarter, Andre L’Hour, in the summer of 2001 confirmed that ICD classifications approved by the World Health Assembly take legal precedence over collaborating centres. Later that year, Dr. B Saraceno publically reconfirmed the separate and exclusionary classifications. In an effort to be thorough, I then did a search of the psychological literature consistently shows that a purely psychosocial diagnosis predicated on psychosomatic attribution including a purely psychiatric diagnosis of FSS is contraindicated if there is a medical cause for common physical symptoms. The bio part of biopsychosocial medicine. The resulting clarification, based on the stated principles of rigorous scientific scrutiny, such discrepancies logically require professional and public re-examination both journalistically and medically as the next step.. The underlying concern I believe, based on another widely known principle, which is the foundation of all rigorous scientific research, states that research results cannot be extrapolated between different cohorts which happens when different criteria are used. Not to mention the sheer annoyance of making meta-analysis impossible. The March 2005 issue of Neuropsychology Review contains a longer, scientifically balanced in-depth discussion of the potential need for subtypes in “Chronic Fatigue Syndrome,” from a biopsychosocial point of view. It includes an interesting section reviewing neurobiological contributions. Even better. research reviewed suggests significant cost savings associated with rapid and accurate diagnosis, as well as basing testing on specific empirically validated medical tests thereby avoiding both cost inflation due to nonspecific testing and the ethical and legal implications and health costs associated with misdiagnosis. (Also of note is a research study comparing the CFS patient populations selected using three different criteria. This research study by a established group of psychologists can be found in the 2005 February edition of Biological Psychology.) As many are aware, ideological differences are rarely listed as a conflict of interest, after all diversity of thought and inquiry is an informal source of checks and balances, as well as the driving force behind many a medical discovery, both historical and modern. The pace of scientific research is becoming more rapid, as a technical breakthroughs allowing previous knowledge to be reevaluated in a new light. Besides which, financial ties to pharmaceutical corporations and health insurance conglomerations are much more fruitful in general. All flippancy aside, kudos to Drs. Viner and Christie for spotlighting critical differences in the study of “chronic fatigue syndrome” versus the much broader category of “fatigue disorders” thus providing a forum for further clarification and progress. As previously noted by UK psychiatric specialist Simon Wessely, it is simplistic to cast the medical care of humanity solely in psychosocial or biological paradigms. Competing interests: None declared |
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N Portman, Patient Tunbridge Wells, Kent
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It is clear the authors of this paper believe that ME is essentially a psychological illness. Yet disturbingly they also state that "it is essential not to label symptoms as psychological, as this will often alienate the family". This lack of candour is extremely frustrating for patients such as myself who firmly believe that ME is a physical disease, and who are seeking treatments based on a physical model. A number of years ago I was referred to a specialist NHS CFS clinic. I went into the consultation with a list of treatments I was interested in trying. The doctor flatly refused to even discuss any of my suggestions essentially saying that the only treatment available was CBT, take it or leave it. This was after I had been on a waiting list for over a year. After several frustrating experiences such as this, I have now adopted a policy of refusing to have anything to do with doctors who adopt a "biopsychosocial" approach towards treating ME. Unfortunately, when first meeting a doctor, it is often difficult to know whether (s)he falls into this category or not. On too many occasions I have left a consultation feeling that I have been dealing with a slippery politician rather than an objective scientist. Of course psychologists, psychiatrists and other doctors are perfectly entitled to their opinions however misguided, and patients who want to try psychological treatments should be able to do so. But doctors have a duty to be honest with their patients. Attempting to deceive and manipulate patients into accepting treatment approaches they do not believe in is ultimately a waste of time for both parties, and also a scandalous waste of NHS resources. I'm also disappointed to note that, once again, a psychologist is unequivocally stating that ME is perpetuated by deconditioning when not one single scientific study has ever produced evidence to back up this claim. Competing interests: None declared |
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Angela P. Kennedy, Social Sciences Lecturer Essex IG8
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As a sadly frequent occurrence, we are faced here with yet another article where the neurological nature of Myalgic Encephalomyelitis/ICD-10 Chronic Fatigue Syndrome (WHO ICD-10) is ignored, in favour of a vaguely written psychiatric paradigm (Kennedy, 2005) in which a serious, sometimes severely disabling disease with specific signs and symptoms of Central Nervous System Dysfunction (Hyde, 1992, 2003) is subsumed under generalisations of “fatigue and other somatic symptoms“, in which (according to the author‘s beliefs but not supported by evidence) ‘de- conditioning’ and ’psycho-social factors’ are claimed as causes. Simon Wessely may claim (according to Duprey, another RR contributor) that “it is simplistic to cast the medical care of humanity solely in psychosocial or biological paradigms“. But, as he has stated there is no such thing as ME, and has been critiqued for his own and colleague’s overemphasis on the psycho-social, at the expense of the biological, and for his prejudicial descriptions of ME/CFS sufferers (Hooper et al, 2004, Marshall and Williams, 1999, Kennedy, 2005), it would appear to be a case of ’practice what you preach’. Proponents of the psychiatric paradigm- which, with the greatest of respect, Viner and Christie appear to be (unfortunately there is little evidence to suggest otherwise, and here their ‘bio-psychosocial approach’ lays far too much emphasis on the ‘psychosocial’, to the detriment of the biological, a frequent occurrence)- consistently fail to discuss the problem of the issue of ‘fatigue’ as applies to ME/CFS sufferers, thereby incorrectly presenting ‘fatigue’ as merely ‘tiredness’, despite the evidence that the word ‘fatigue’ is inadequate to describe the physical abnormalities (both signs and symptoms) that occur in ME/CFS. In the same context, they fail to acknowledge that ‘fatigue’ (which might mean tiredness, drowsiness, exhaustion, disturbed level of consciousness, weakness, paralysis, or feelings of malaise, depending on how certain illnesses are experienced or linguistically constructed by individuals) is present in MOST organic illnesses, acute and chronic. Indeed: “Fatigue is both a normal and a pathological feature of everyday life’ (Hyde 1992: 11). Proponents of the psychiatric paradigm, in their literature, tend to associate ‘fatigue’ with a psychological state, ignoring the physiological reasons that may contribute to the bodily symptoms in ME/CFS, with the effect that these become generalised, and often trivialised, as ‘fatigue’. As Hyde also points out, to place such an emphasis on such a generalised, unspecific, indefinable and immeasurable term as ‘fatigue’, present in both healthy patients and those with both organic and psychological illness, the elimination of hundreds of other diseases are necessitated. This logistical flaw results in only the most limited investigation being encouraged for ME/CFS patients, and NOT in areas that might yield definitive results, such as certain brain scans (as discussed and referenced in Hyde et al, 1992, Marshall et al, 2001, Carruthers et al, 2003). Particularly relevant to ME/CFS sufferers also is the problem also identified by Hyde (1992: 11-12): ‘…taking the fatigue as the flagship symptoms of a disease not only bestows the disease with a certain Rip Van Winkle humour, but removes the urgency of the fact that most ME/CFS symptoms are in effect CNS symptoms.’ In this context the ramifications of such serious, disabling symptoms as found in ME/CFS are both trivialised and ignored. The problem is compounded by the frequent tendency, by proponents of the psychiatric paradigm themselves and taken up uncritically by others, to use, incorrectly, the term ‘chronic fatigue’ instead of and interchangeably with ‘chronic fatigue syndrome’, even though both terms denote completely different diseases. Chronic Fatigue Syndrome is described in the WHO ICD- 10 as synonymous with (therefore merely another name for) the neurological disease ME, while chronic fatigue is assigned a different category of illness in the ICD-10 (Psychiatric). This incorrect practice of using the terms ‘chronic fatigue’ and ‘chronic fatigues syndrome’ interchangeably and confusingly has a direct relationship to various design flaws in research and the inadequate or dangerous treatment of and perjorative and prejudicial attitudes towards ME/CFS sufferers. Sadly, the Viner et al article is yet another example of this problem. In this paper Viner and Christie claim that Randomised clinical trials in adults have shown that cognitive behaviour therapy and graded exercise programmes are helpful in most patients. This implies that ME/CFS sufferers are to be treated in such a way. As the RCT’s themselves are very small in number, and most research in this area has been criticised for the high drop out rate of patient samples, and the patients excluded from such trials (Carruthers et al, 2003, Kennedy and Bryant, 2004). In promoting GET or GAT for ME/CFS, proponents of the psychiatric paradigm continue to ignore the documented harmful effects and therefore potential dangers of ‘Graded Exercise/’Activity’ for ME/CFS sufferers, for example as demonstrated in Van de Sande (2004) Carruthers et al (2003) 25% Group (2004) Shepherd (2001) Action for ME (2001), as well as the documented bio-medical evidence of, for example, specific cardiac problems in ME/CFS sufferers that provide explanations regarding the post-exertional malaise that leads to such risks (for example, Peckerman et al, 2003). In this context, the claims made by Viner and Christie are untenable. They are also potentially dangerous. At the very least this article should have included an acknowledgement of such risks, for doctors’ protection as practitioners as well as patients’ health. Furthermore, proponents of the psychiatric paradigm of ME/CFS promote the use of Cognitive Behavioural Therapy, NOT as a strategy of coping with one’s illness, but as a ‘cure’ for ME/CFS, (which, it must be remembered, has been both classified and consistently demonstrated as a neurological illness) believing that the multi-system physiological abnormalities (manifesting as symptoms) can be improved to the point of ‘recovery’, merely by challenging the illness beliefs and behaviour of the sufferer (see for example, Sharpe,1996: 248, Stulemeijer et al, 2004). Their rationale for the use of CBT is as a ’cure’ for a neurological illness that they do not even recognise, an illogical position unheard of in regard to medical approaches to any other neurological or other organic illness. Viner and Christie therefore appear to be promoting CBT/GET as treatments that will improve ME/CFS sufferers, without considering the evidence showing the major problems of such an approach. In her Rapid Response, Duprey believes kudos is due to Viner and Christie for ‘spotlighting critical differences in the study of “chronic fatigue syndrome” versus the much broader category of “fatigue disorders” thus providing a forum for further clarification and progress‘. Sadly, there is little evidence of this at all in this article. The major problem with this article, and one which causes enormous risks to patients and serious problems to doctors looking for guidance to treat such patients, is the continued failure to delineate adequately the difference between ME/CFS and idiopathic chronic fatigue, ie, the failure to discuss the problem of differential diagnosis. As this issue is well represented in the literature, a peer review process should have identified this problem, and Viner and Christie themselves should not be ignoring the literature on this issue in the first place. Where was their acknowledgement of the Canadian ME/CFS Case Definition and Treatment protocols (Carruthers et al, 2003)? Where was their acknowledgement of the Jason et article showing how the Canadian Guidelines can improve the differential diagnosis of ME/CFS against other forms of ‘chronic fatigue’? At the very least one would have expected a nod to these important references in an overview article. This continued lack of understanding of the neurological illness ME/CFS is fast becoming inexcusable among those claiming expertise in ‘chronic fatigue syndrome’, and represents a severe abrogation of duty to such patients. Both patients, and doctors seeking guidance on how to care for such patients, deserve better. REFERENCES 25% ME Group, 'Severely Affected ME (Myalgic Encephalomyelitis) Analysis Report on Questionnaire issued January 2004'‘ March 2004. Action for ME, “Severely Neglected - M.E. in the UK” (2001). Carruthers, B. et al (2003) “Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols” Journal of Chronic Fatigue Syndrome, Vol. 11(1), pp 7 - 115. Hooper, M. et al “The Mental Health Movement: Persecution of Patients?” (2004) Available on the One Click Website: http://www.theoneclickgroup.co.uk/documents/ME- CFS_docs/The%20Mental%20Health%20Movement%20- %20Persecution%20of%20Patients.pdf Hyde, B. Bastien, S. Jain, A. The Clinical and Scientific Basis of ME/CFS (1992) Nightingale Research Foundation, Canada. Hyde, B, Jain, A. ‘Clinical Observations of Central Nervous System Dysfunction in Post-Infectious, Acute Onset, ME/CFS’ in Hyde et al, 1992. Hyde, B. ‘The Complexities of Diagnosis’ in Jason et al (2003) the Handbook of Chronic Fatigue Syndrome, Wiley and Sons, New Jersey. Jason L.A. Torres-Harding S.R. Jurgens, A. Helgerson, J. "Comparing the Fukuda et al. Criteria and the Canadian Case Definition for Chronic Fatigue Syndrome". Journal of Chronic Fatigue Syndrome 12(1):37- 52, 2004. (a) Kennedy A. ‘When Doctors say ‘psychosomatic‘, what do they mean?’ April 2004. Published in Quest (Newsletter of the National ME/FM Action Network) number 66, Fall 2004. Also available on the One Click Group Website (ME/CFS Documents) http://www.theoneclickgroup.co.uk Kennedy, A. (2004) A SHORT SUMMARY OF THE PSYCHIATRIC PARADIGM OF ME/CFS. Available on the One Click Group Website: http://www.theoneclickgroup.co.uk Kennedy, A. Bryant, J. ‘A Summary of the Inherent Theoretical, Methodological and Ethical Flaws in the PACE Trial’ 21 October 2004. Available on the One Click Website Home page http://www.theoneclickgroup.co.uk Marshall, E. Williams, M. ’Denigration by Design? A Review, with References, of the Role of Dr Simon Wessely in the Perception of Myalgic Encephalomyelitis, 1987 - 1996‘ September 1996, and Marshall, E. Williams, M. ‘Denigration by Design: 1999 Update’ 1999. Available at: http://www.btinternet.com/~severeme.group/introduction.htm Peckerman A, LaManca JJ, Dahl KA, Chemitiganti R, Qureishi B, Natelson BH. "Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome." The American Journal of the Medical Sciences: 2003:326:(2):55-60). Arnold Peckerman, Rahul Chemitiganti, Caixia Zhao, Kristina Dahl, Benjamin H. Natelson, Lionel Zuckier, Nasrin Ghesani, Samuel Wang, Karen Quigley and S. Sultan Ahmed. "Left Ventricular Function in Chronic Fatigue Syndrome (CFS): Data From Nuclear Ventriculography Studiesof Response to Exercise and Postural Stress," Findings presented at the American Physiological Society conference, Experimental Biology 2003, April 11-15, 2003, San Diego Convention Center, San Diego, CA Sharpe, M. C. in Demitrack, M.A. Abbey, S. E (eds.) Chronic Fatigue Syndrome (1996) Guildford Press, New York. Shepherd C. Pacing and exercise in chronic fatigue syndrome. Physiother 2001 Aug;87(8):395-396. Stulemeijer, M. de Jong, L.W.A.M. Fiselier, T.J.W. Hoogveld, SW.B. Bleijenberg, G. 'Cognitive Behaviour Therapy for Adolescents with Chronic Fatigue syndrome: A Randomised Controlled Trial‘ BMJ.com (online) 7th December 2004. Van De Sande, M. ‘ME/CFS Post-Exertional Malaise / Fatigue and Exercise’ Quest (Newsletter of the National ME/FM Action Network) #60, June/July, 2003. Also available on: http://www.mefmaction.net/default.aspx?Page=selectedarticlesmedical Wessely , S. "Microbes, Mental Illness, the Media and ME: the Construction of Disease" Eliot Slater Memorial Lecture, 12 May 1994. Available with comment by Margaret Williams: http://www.meactionuk.org.uk/wessely_speech_120594.htm Angela Kennedy The One Click Group www.theoneclickgroup.co.uk Competing interests: Carer of young woman with ME/CFS; Social Sciences lecturer and researcher; Director of the One Click Group, a political pressure group advocacting for people with ME/CFS. |
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Douglas T Fraser, musician London W6
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Editor, In "Fatigue and Somatic Symptoms", an article which will impact on sick children and their families, Viner and Christie state that "the definition of chronic fatigue syndrome (CFS) in adults has been much debated. The syndrome, often known by patients as myalgic encephalomyelitis or postviral fatigue syndrome, was first commonly described in the 1980s.." Here is one description of ME :- And here is another:- The first of course is Gilliam in 1934, and the second Carruthers et al. in 2003, and I believe they are worth careful comparison. Both of these descriptions apparently came about through the meticulous collation of data from patients. However, with respect to the "much debated" research definitions Viner and Christie mention, Professor Leonard Jason and others have recently appraised the CDC definition, that Viner and Christie recommend in their article, thus : “The Fukuda et al (1994) criteria do not exclude people who have purely psychosocial or psychiatric reasons for their fatigue (and) this broadening of the CFS definition raises questions regarding the extent to which patients with purely psychiatric explanations are erroneously included within the CFS rubric...the erroneous inclusion of people with primary psychiatric conditions in CFS samples will have detrimental consequences for the interpretation of both epidemiologic and treatment efficacy findings”. In view of this it is of course unsurprising and perfectly rational that "many young people and their families are resistant to a psychological explanation for the symptoms and feel that such explanations mean they are not being believed ". It must surely be one of the most appalling and damaging experiences for any child and their family to experience. Viner and Christie also state that ME "was first commonly described in the 1980s". However, thanks to Dr Gordon Parish who has taken the trouble to organise pre-80`s data, and to MERGE where this data can be easily accessed on their website, Viner and Christie might be interested in some details of the sequence of events before the 1980`s, when ME "was first commonly described". [The American term “epidemic neuromyasthenia” refers to a condition similar to “ME”.Icelandic Disease is the original name for the illness] EPIDEMIC 1 1934 Los Angeles City and California State, USA Gilliam AG Epidemiological study of an epidemic diagnosed as poliomyelitis occurring among the personnel of the Los Angeles County General Hospital during the summer of 1934. Public Health Bulletin No. 240, April 1938. [11 related papers] EPIDEMIC 2 1936 Fond-du-Lac, Wisconsin, USA Armstong G Report to the Surgeon General, US Public Health Service of the investigation of an outbreak of “Encephalitis” in the St. Agnes Convent, Fond-du-Lac, Wisconsin, 1936. EPIDEMIC 3 1937 Erstfield, Switzerland Stahel H Die Poliomyelitis — Epidemic bei Stab Geb. IR 37 and Geb Sch Bat II, Erstfeld, 18–30 July, 1937. Die Abortiv — Poliomyelitis. Schweiz Med Wochenschr 1938; 68: 86–91. [one related paper] EPIDEMIC 4 1937 Frohburg Hospital, St. Gallen, Switzerland Gsell O Abortive Poliomyelitis. Verlag Thieme, Leipzig 1938; 13–18. (The three Swiss epidemics 3, 4 and 6 are summarised in review articles by Gsell O (1958) and Parish JG (1978). EPIDEMIC 5 Degersheim, St. Gallen, Switzerland Gsell O Abortive Poliomyelitis. Helv Medica Acta 1949; 16: 170-2 EPIDEMIC 6 1946–47 Iceland Sigurjonsson J Poliomyelitis and Akureyri Disease. Mixed epidemics of poliomyelitis and a disease resembling poliomyelitis with the character of the Akureyri Disease. Nord Med 1959; 61: 174–82. EPIDEMIC 7 1948–49 North Coast Towns, Iceland, Akureyri Nov/Dec 1948, Saudakrokur Dec 1948/Feb 1949, Isafordur Jan/April 1949 Sigurdsson B et al. A disease epidemic in Iceland simulating Poliomyelitis. Am J Hyg 1950; 52: 222–38. [two related papers] EPIDEMIC 8 1949-51 Adelaide, South Australia Pellew RAAA clinical description of a disease resembling poliomyelitis seen in Adelaide, 1949- 51 Med J Aust 1951; 1: 944-6. [3 related papers] EPIDEMIC 9 1950 St. Joseph Infirmary, Louisville, Kentucky, USA Steigman AJ An outbreak of an unidentified illness in the Nurses Training School of St. Joseph Infirmary, Louisville, in Kentucky in October 1950. Report to the National Foundation of Infantile Paralysis, 1951. (Data summarised by Henderson DA, Shelokov A, see Review article 2, 1959). [one related paper] EPIDEMIC 10 1950 New York State White DN, Burtch RB Iceland Disease — a new infection simulating Acute Anterior Poliomyelitis. Neurology 1954; 4: 506–16. [one related paper] EPIDEMIC 11 1952 Middlesex Hospital Nurses Home, London, England Acheson ED Encephalomyelitis associated with Poliomyelitis Virus. Lancet 1954; 2: 1044–8. Acheson ED Outbreak at the Royal Free. Lancet 1955; 2: 395. EPIDEMIC 12 1953 Copenhagen, Denmark Fog AT Neuritis Vegitiva (Epidemica?). Ugeskr Laeger 1953; 115: 1244–51.[two related papers] EPIDEMIC 13 Lakeland, Florida, U.S.A. Henderson DA, Shelokov A Epidemic neuromyasthenia-clinical syndrome? N EngI J Med 1959; 260: 757- 64. EPIDEMIC 14 1953 Whitley Hospital, Coventry And Coventry District, England Macrae AD, Galpine JF An illness resembling Poliomyelitis observed in nurses. Lancet 1954; 2: 350–2. EPIDEMIC 15 1953 Chestnut Lodge Hospital, Rockville, Maryland, USA Shelokov A, Habel K, Verder E, Welsh W Epidemic neuromyasthenia. An outbreak of poliomyelitis-like illness in Student Nurses. N Engl J Med 1957; 257: 345–55. Hardtke EF Iceland disease in Indiana. J Indiana State Med Assoc 1955; 48: 245–50. {Case also described by Acheson ED, see Review article 1, 1959). EPIDEMIC 16 1953 Jutland, Denmark Pedersen EP Epidemic encephalitis in Jutland. A clinical survey for the years 1952–54. Dan Med Bull 1956; 3: 65–75. EPIDEMIC 17 1954 Tallahassee, Florida, USA Bond JO A new clinical entity? Lancet 1956; 2: 256. EPIDEMIC 18 1954 Seward, Alaska Deisher JB Benign myalgic encephalomyelitis (Iceland Disease) in Alaska. Northwest Med 1957; 56: 1451–6. EPIDEMIC 19 1954 British Army, Berlin, Germany Sumner DN Further outbreak of a disease resembling poliomyelitis. Lancet 1956; 1: 764–6.[one related paper] EPIDEMIC 20 1954 Liverpool, England Comparative epidemiology: see Official Public Health report for Epidemic 24 (1955). EPIDEMIC 21 1955 Dalston, Cumbria, England Wallis AL An unusual epidemic. Lancet 1955; 2: 290. (Further details in Letters, Lancet 1955; 2: 1091 and Lancet 1956; 2: 146).. [two related papers] EPIDEMIC 22 1955 Royal Free Hospital, London, England Anon Infectious mononucleosis. Br Med J 1955; 2: 309–10. [14 related papers] EPIDEMIC 23 1955 Perth, Western Australia Steen AS Virus epidemic in recurrent waves. BMJ 1956; 1: 235. EPIDEMIC 24 1955 Gilfach, Geoh, Wales Jones TD Virus epidemic in recurrent waves. BMJ 1956; 1: 348. [two sproradic case papers London&Boscombe]] EPIDEMIC 25 1955 Addington Hospital, Durban and Durban City, South Africa Hill RCJ Memorandum on the outbreak amongst the nurses at Addington Hospital, Durban. S Afr Med J 1955; 29: 344–5. [three related papers,one sporadic] EPIDEMIC 26 1955–56 Segbwema, Sierra Leone, Oct 1955 – Oct 1956 Rose JR A new clinical entity? Lancet 1956; 2: 197. Rose JR An outbreak of encephalomyelitis in Sierra Leone. Lancet 1957; 2: 914–16. EPIDEMIC 27 1955–56 Patreksfordur and Thorshofn, Iceland, Oct 1955 – April 1956 Sigurdsson B, Gudnadottir M, Petursson G Response to poliomyelitis vaccination. Lancet 1958; 1: 370–1. EPIDEMIC 28 April 1955 – Sept 1957 NW London, England Ramsay AM, O’Sullivan E Encephalomyelitis simulating poliomyelitis. Lancet 1956; 1: 761–6. [two related papers] EPIDEMIC 29 Ridgefield, Connecticut, USA Henderson DA, Shelokov A, Heller JH, Stafford T Unpublished data, quoted by Henderson DA, Shelokov A. Epidemic neuromyasthenia N EngI J Med 1959; 260: 757–64. EPIDEMIC 30 1956 30Punta Gorda, Florida, USA Poskanzer DC, Henderson DA, Kunkle BS, Kalter SS, Clement WB, Bond JO Epidemic neuromyasthenia. An outbreak in Punta Gorda, Florida. N EngI J Med 1957; 257: 356–64. EPIDEMIC 31 1956 Newton-le-Willows, Lancashire, England Lyle WH Lymphocytic meningo-encephalitis with myalgia and rash. Lancet 1956; 2: 1042–3. [two related papers] EPIDEMIC 32 1956 Pittsfield, Williamstown, Massachusetts, USA Deutaman W, Davis RK (Unpublished - Data included in survey in Henderson and Shelokov. N Eng J Med 1959; 260: 757–64 and 814–18). EPIDEMIC 33 Coventry, England Galpine JF, Brady C Benign myalgic encephalomyelitis. Lancet 1957; 1: 757–8 and Br Med J 1957; 2: 645. [two related papers] EPIDEMIC 34 1957 Brighton, South Australia Hicks DA A new clinical entity. Lancet 1957; 1: 686. [four unrelated papers] EPIDEMIC 35 1958 Athens, Greece Daikos G, Paleologue A, Garzonis S, Bousvaros GA, Papadoyannakis N Arch Med Sci, Athens 1958; 14: 617. [one related two unrelated papers] EPIDEMIC 36 1959 Newcastle upon Tyne, England Pool JH, Walton JN, Brewis EG, Uldall PR, Wright AE, Gardner PS Benign myalgic encephalomyelitis in Newcastle-upon-Tyne. Lancet 1961; 1: 733–7. [five other papers mainly on sporadic] EPIDEMIC 37 1961–62 New York State Albrecht RM, Oliver VL, Poskanzer EC Epidemic neuromyasthenia. Outbreak in a convent in New York State. JAMA 1964; 187: 904–7. EPIDEMIC 38 1964–66 NW London Scott BD Epidemic malaise. Br Med J 1970; 1: 170. Ramsay AM [five other papers] EPIDEMIC 39 Franklin, Kentucky, USA Miller G, Chamberlin R, McCormack WM An outbreak of neuromyasthenia in a Kentucky Factory — the possible role of a brief exposure to organic mercury. Am J Epidemiol 1967; 86: 756–64. [one other paper] EPIDEMIC 40 1965–66 Galveston County, Texas Johnson JM, Micks DW Epidemic neuromyasthenia Variant? Texas Reports on Biology and Medicine 1967; 25: 484. [two other papers] EPIDEMIC 41 1968 Fraidek, Lebanon Mourad S, Chidiac J Benign myalgic encephalomyelitis in Lebanon. Leb Med J 1969; 22: 735–40. EPIDEMIC 42 1969 Medical Centre, State University of New York, USA Damadian R Unidentified symptom complex. N Engl J Med 1969; 280: 1131. Correspondence: Trimble G. Epidemic Neuromyasthenia. N Engl J Med 1969; 281: 105. Fisher CM. On Damidian’s Ache, 281: 106. Epidemic Neuromyasthenia, 281 : 797–8. Steigman AJ, Hart RH, Adamson JR EPIDEMIC 43 1970 Lackland Air Force Base, Texas, USA Graybill JR, Silva J, O’Brian MS, Reinarz JA Epidemic neuromyasthenia. A Syndrome or disease? JAMA 1972; 219: 1440–3. EPIDEMIC 44 1970–71 Hospital for Sick Children, Great Ormond Street, London, England Dillon MJ, Marshall WC, Dudgeon JA, Steigman AJ Epidemic neuromyasthenia: outbreak among nurses at a children’s hospital. Br Med J 1974; 1: 301–5. Correspondence: Br Med J 1974; 1: 574–5, Wallis GG, Perry FS. 2: 276, Parish JG. 559, Dillon MJ. [one related paper, one other] EPIDEMIC 45 1976 Southwest Ireland Corridan JP Myalgic encephalomyelitis. J Irish Med Ass 1976; 69: 414. [two related papers, one other] EPIDEMIC 46 1977 Dallas Fort Worth, Texas, USA Shelokov A, Currie DM, Nelson M. “Epidemic neuromyasthenia’ Texas 1977. Postgrad Med J 1978; 54: 741 (Abstract). [twenty-two other papers and letters] EPIDEMIC 47 1979 Southampton, England May PGR, Donnan SPB, Ashton JR, Ogilvie MM, Rolles CJ Personality and medical perception in benign myalgic encephalomyelitis. Lancet 1980; 2: 1122–4. Correspondence: [six other papers] It seems to me that if other clinicians were to rely on diagnostic equipment that is as faulty and unreliable as the CDC and Oxford "CFS" criteria, not a few of them would be seeking alternative employment by this point, or at least suing the manufacturers. Douglas Fraser Dr J. Gordon Parish (Epidemics) http://www.meresearch.org.uk/melibrary/publications/Research%20Publications%20on%20ME%20epidemics%201934 -1980.pdf Gilliam AG (1938) Epidemiological study of an epidemic, diagnosed as poliomyelitis, occurring among the personnel of the Los Angeles County General Hospital during the Summer of 1934. Public Health Bulletin, US Treasury Department, No 240, pp 1-90, Washington DC, United States Government Printing Office. Postviral Fatigue Syndrome (Myalgic Encephalomyelitis), Edited by Rachel Jenkins & James Mowbray, John Wiley & Sons, Chichester 1991 ISBN 0 471 92846 Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocol Carruthers et al. Journal of Chronic Fatigue Syndrome 2003;11:7-115 http://www.meresearch.org.uk/melibrary/information/definition.html The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis, Iceland Disease and Epidemic Neuromyasthenia E.D. Acheson, D.M., M.R.C.P. American Journal of Medicine, Vol. 26, Issue 4, Pages 569–595. http://www.meresearch.org.uk/melibrary/information/Acheson%20- %20Am%20J%20Med.pdf U.S. Case Definition of Chronic Fatigue Syndrome: Diagnostic and Theoretical Issues Leonard A. Jason Caroline P. King Judith A. Richman Renee R. Taylor Susan R. Torres Sharon Song Journal of Chronic Fatigue Syndrome (The Haworth Medical Press, an imprint of The Haworth Press, Inc.) Vol. 5, No. 3/4, 1999, pp. 3-33. http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0004D&L=co- cure&P=R621 Variability in diagnostic criteria for chronic fatigue syndrome may result in substantial differences in patterns of symptoms and disability.Journal: Eval Health Prof 2003 Mar;26(1):3-22 Authors: Jason LA, Helgerson J, Torres-Harding SR, Carrico AW, Taylor RR. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=12629919&dopt=abstract The specificity of the CDC-1994 criteria for chronic fatigue syndrome: comparison of health status in three groups of patients who fulfil the criteria. Kennedy G, Abbot NC, Spence V, Underwood C and Belch JJF http://www.meresearch.org.uk/research/sponsored/comparison.html Chronic Fatigue Syndrome: The Need for Subtypes Authors: Jason, Leonard 1; Corradi, Karina 2; Torres-Harding, Susan 2; Taylor, Renee 3; King, Caroline 4 Source: Neuropsychology Review, March 2005, vol. 15, no. 1, pp. 29-58(30) Publisher: Kluwer Academic Publishers Competing interests: None declared |
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Charles Bernard Shepherd, Medical Adviser ME Association, 4 Top Angel, Buckingham MK18 1TH
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EDITOR- The ME Association has three criticisms of the review of fatigue and somatic symptoms in adolescents by Viner and Christie. (1) First is the failure to clearly differentiate between the fatigue that occurs in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) from that which is found in many other conditions. The fatigue in ME/CFS is exercise-induced, affects both physical and mental functioning, and is accompanied by the highly characteristic post-exertional malaise whereby relatively small amounts of activity on one day can result in a significant exacerbation in all ME/CFS symptoms some time later. The fatigue is profound and disabling. Second is the seriously flawed conclusion that the illness is principally perpetuated by '...physical deconditioning, sleep disturbance and psychosocial factors'. The simple fact is that nobody yet knows the underlying cause/s of ME/CFS, and while psychological and social factors may play a role - as in any chronic medical condition - there is compelling evidence of abnormalities in brain, muscle, endocrine and immune system function. (2) These findings cannot simply be explained by a psychosomatic model. Neither is it consistent with published evidence (3) to conclude that deconditioning is a significant perpetuating factor. Third is the way in which the positive results of clinical trials involving controversial approaches to management such as cognitive behaviour therapy (CBT) and graded exercise therapy (GET) have not been balanced by negative evidence from patients - as was noted in feedback to the Chief Medical Officer's report. (4) With CBT, only 7% found this approach to be "helpful"; 26% said it made their condition "worse"; and 67% reported "no change". With GET, 35% found it "helpful"; 50% said it made their condition "worse"; and 15% reported "no change". Not surprisingly, doctors have recently been reminded by their insurance organisations that prescriptions for exercise must be given with exactly the same care as drugs - something we believe is not happening in practice. The ME Association strongly endorses the view of Viner and Christie that the diagnosis should be considered and confirmed as soon as possible. In the case of children and adolescents this can often be done within a three month period from onset of symptoms - there is no need to wait for six months as stipulated in international research criteria. (5) And evidence recently collected for the ME Alliance report into early diagnosis (6) found that while 29% of children and adolescents waited for between six months and a year, 45% waited for more than a year - a situation which is clearly unacceptable. Yours sincerely Dr Charles Shepherd
References 1 Viner R and Christie D. ABC of adolescence: Fatigue and somatic symptoms. British Medical Journal 2005; 330: 1012 - 1015 (30 April 2005) 2 Shepherd C and Chaudhuri A. ME/CFS/PVFS - An exploration of the key clinical issues. ME Association 2005. Available on-line at: http://www.meassociation.org.uk. 3 Bazelmans E, et al. Is physical deconditioning a perpetuating factor in chronic fatigue syndrome? A controlled study on maximal exercise performance and relations with fatigue, impairment and physical activity. Psychological Medicine 2001; 31: 107 - 114. 4 CFS/ME Working Group. Report of the CFS/ME Working Group: report to the chief medical officer of an independent working group. 2002. Available on-line at: http://www.doh.gov.uk - search under CFS/ME. 5 Fukuda K, et al. The chronic fatigue syndrome. A comprehensive approach to its definition and study. Annals of Internal Medicine 1994; 121: 953 - 959. 6 ME Diagnosis: Delay Harms Health. ME Alliance 2005. Available on- line at the ME Association website. Competing interests: None declared |
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Ellen C G Grant, physician Kingston-upon-Thames, KT2 7JU, UK
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Dr Charles Shepherd writes that, “The simple fact is that nobody yet knows the underlying cause/s of ME/CFS, and while psychological and social factors may play a role - as in any chronic medical condition - there is compelling evidence of abnormalities in brain, muscle, endocrine and immune system function”. Why therefore does he not recommend therefore that patients with myalgic encephalitis or chronic fatigue syndrome have relevant diagnostic tests? Myalgic- about muscles- should indicate testing for correctable magnesium deficiencies in sweat and red blood cells.1,2 Encephalitis – about the brain- should indicate teats for sweat or white blood cell tests for zinc deficiency and red cell superoxide dismutase tests for copper or manganese deficiencies. These common deficiencies disrupt brain, muscle, endocrine and immune system function. Mervyn Werbach's detailed review of the literature suggests a number of marginal nutritional deficiencies may have etiologic relevance. These included deficiencies of various B vitamins, vitamin C, magnesium, sodium, zinc, L-tryptophan, L-carnitine, coenzyme Q10, and essential fatty acids. Objective testing, he writes, should identify them and their resolution should be assured by repeat testing following initiation of treatment.3 Magnesium supplementation improved parameters of oxidant-antioxidant balance in patients with chronic fatigue syndrome in a series of patients in which 75% were females.4 In my experience ME/CFS is common with use of hormonal contraceptives and the symptoms often signal zinc, copper, magnesium, selenium and glutathione deficiencies. Patients can notice immediate benefits from repletion of copper and zinc deficiencies. Magnesium deficiencies can take longer to be repleted. It would be useful for patients’ help groups to have advisors who are experienced in the field of Nutritional Medicine. 1 Cox IM, Campbell MJ, Dowson D. Red blood cell magnesium and chronic fatigue syndrome. Lancet 1991; 337: 757-60. 2 Howard JM, Davies S, Hunnisett A. Magnesium and chronic fatigue syndrome. Lancet 1992; 340: 426. 3 Werbach MR. Nutritional strategies for treating chronic fatigue syndrome. Altern Med Rev 2001; 6: 4-6. 4 Manuel y Keenoy B, Moorkens G, et al. Magnesium status and parameters of the oxidant-antioxidant balance in patients with chronic fatigue: effects of supplementation with magnesium. J Am Coll Nutr 2000; 19: 374-82. Competing interests: None declared |
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Di newman, disabled with M.E.(ICD-10) M.E. and (ICD-10) CFS, Representative (Cambridgeshire)
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I read this with interest, as someone diagnosed "80% disabled with Myalgic Encephalomyelitis," some 11 years ago, also suffered appalling "food intolerances." To the extent of quite severe reactions to certain foods e.g.wheat, yeast, gluten, diary products, within minutes of being comsumed. In addition, reaction to most chemicals, smoke, petrol fumes, etc. These, fortunately, over the years, have lessened to some degree - mostly due to dietary changes and other allowences, throughout my daily life. My understanding of those "intolerances / reactions," incidentally, is down to changes within "the brain-barrier, hypothalamus and Hypocampus," as demonstrated by many of the Good and the Great Myalgic Encephalomyelitis and(ICD-10)Chronic Fatigue Syndrome consultants and specialists in the field of Microbiology, Neurology, Virology, Haematology, Endocrinology etc. E.g. Spence, Gow, Hyde, Carruthers, Simpson, Mowbray, Streeten, Ramsay, Dowsett, Cheney, Goldstein, Bell, Richardson, Parish, Chaudhuri, Behan and Behan, Defreitas, Peterson, Costa - work done over numerous years showing the cause and impact on the whole system - causing a cascade of symptoms e.g. changes to brain -including metabolism (various scans: gEEG etc); cardiac and cardiovascular (e.g. including orthostatic hypotension etc); vascular; neuroimmune; blood, limbic; peripheral nerve - systems. Those specialist research areas, span many years and the authors - world renown. Their qualifications and training, of the highest levels, not to mention, commitment have shown the cause and impact of Myalgic Encephalomyelitis and (ICD-10) Chronic Fatigue Syndrome M.E. and (ICD-10) CFS). What we need to do is to take account of those former studies and build from it into a 21st treatment and management - not just discard that research - or keep returning to the drawing board (or appearing to be lost, on route to it :o). So there is no need with this continuing old chestnut "we do not know the causes of M.E." - it's all there in the Medical Library Books - and in the public arena! There is no "mystery" about M.E. and(ICD-10) CFS! Like you, have joined the queue of the "Puzzled" (in fact, some years ago!). As far as the "reasoning" behind promoting the concept that "no further investigations are needed." Indeed, there is none to be found - how can any reasoning of the basis / effect / treatment of a condition classified as neurological - affecting the immune, vascular and endorine, etc systems be based on mere "assumption" only!? How on earth can there be any real knowledge and figures on severity; differential diagnosis; levels of disability; extent of impact on the body systems e.g. heart, nervous system - icluding the "brain-gut" dysruption found in M.E. (ICD- 10) CFS as seen in MS, Ataxia and many other neurological conditions (whom, unlike M.E., incidentally, are given dietary advice by their NHS consultants and types of treatments - which take into account of system - hypersensitvity, e.g. medication,on the already dysfunctional systems, etc and, are often given complementary medicine advice and treatment, within the NHS. Furthermore, not forgetting the Basal Ganglia dysfunction, presenting symptoms in neurological conditions - yet often seen in M.E. and (ICD-10- CFS) as "only a psychiatric / mental problem." where antidepressants, including SSRIs are then seen the only "treatment" offered, often prescribed at inappropriate high doses, causing adverse drug reactions and worsening of symptoms / severe relapses. So yes, I too, are more than mystified and suspect the matter will only be resolved, at policy level, when and where, such are addressed. Competing interests: None declared |
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Ellen C G Grant, physician Kingston-upon-Thames, KT2 7JU, UK
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The key to this muddle in ME/CFS, and many other illnesses, is that zinc, magnesium and copper deficiencies adversely affect the normal functioning of every cell in the body. Deficiencies of these extremely important essential enzyme co-factors impair gut absorption and immunity. This in turn increases the numbers of commonly eaten foods causing allergies or intolerances and further loss of these vitally important nutrients. Competing interests: None declared |
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Mohamed Amir, Dental Surgeon Putney, London SW15 1JT
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I accidently came across this article by Viner & Christie while doing some research. I have also read the responses with great interest. There is a cursory mention of temporomandibular joint (TMJ) disorders in the article. My experience of treating many patients with CFS is that this aspect must always be excluded in the differential diagnosis as it gives similar symptomatology as many other causal relationships. Asking the patient if they have any jaw pain is not sufficient. Palpation of the Lateral Pterygoid muscle by running a gloved finger on the buccal aspect of the upper molar teeth backwards and upwards will often produce acute pain in most patients. The pain might be worse on one side than the other. Evidence of jaw clicking, limited mouth opening (Normal 50mm), deviation of the lower jaw on slowly opening the mouth, tooth grinding and jaw clenching while asleep should be enquired into. A history of orthodontic or wisdom tooth extractions is also often indicative of TMJ dysfunction. Dental splints over the teeth provide limited and symptomatic relief and should not be percieved as "TMJ treatment under control" as the proper dental management of such patients is far more complex. I shall be grateful if this can be brought to the attention of those in medicine that the patients so depend on. It might even give some an alternative to "psychosocial" relationships. Competing interests: TMJ treatment |
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